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At least 40% of allergic patients are sensitized to grass pollen allergens and more than 95% of them display IgE reactivity to group I allergens [3–6].. More-over, insect cell-expressed

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expression of the major Timothy grass pollen allergen,

Phl p 1

Tanja Ball1,2, William Edstrom2, Ludwig Mauch3, Jacky Schmitt3, Bernd Leistler3, Helmut Fiebig4, Wolfgang R Sperr5, Alexander W Hauswirth5, Peter Valent5, Dietrich Kraft1, Steven C Almo2 and Rudolf Valenta1

1 Department of Pathophysiology, Center for Physiology and Pathophysiology, Medical University of Vienna, Austria

2 Albert Einstein College of Medicine, Department of Biochemistry, NY, USA

3 Pharmacia Diagnostics, Freiburg, Germany

4 Allergopharma KG, Reinbek, Germany

5 Division of Hematology, Department of Internal Medicine I, Medical University of Vienna, Austria

Type I allergy is an IgE-mediated hypersensitivity

dis-ease affecting more than 25% of the population [1,2]

Grass pollen allergens belong to the group of most

fre-quently recognized allergenic components [3] At least

40% of allergic patients are sensitized to grass pollen

allergens and more than 95% of them display IgE reactivity to group I allergens [3–6] Group 1 allergens represent a family of glycoprotein allergens of approximately 30 kDa that occur as cross-reactive antigens in almost all grasses and corn species [6,7]

Keywords

allergen; allergy; epitope; eukaryotic

expression; Phl p 1

Correspondence

R Valenta, Division of Immunopathology,

Department of Pathophysiology, Center for

Physiology and Pathophysiology, Medical

University of Vienna, Waehringer Guertel

18–20, A-1090 Vienna, Austria

Fax: +43 1 40 400 5130

Tel: +43 1 40 400 5108

E-mail: rudolf.valenta@meduniwien.ac.at

(Received 6 August 2004, revised 21

September 2004, accepted 22 September

2004)

doi:10.1111/j.1432-1033.2004.04403.x

Approximately 400 million allergic patients are sensitized against group 1 grass pollen allergens, a family of highly cross-reactive allergens present in all grass species We report the eukaryotic expression of the group 1 aller-gen from Timothy grass, Phl p 1, in baculovirus-infected insect cells Domain elucidation by limited proteolysis and mass spectrometry of the purified recombinant glycoprotein indicates that the C-terminal 40% of Phl p 1, a major IgE-reactive segment, represents a stable domain This domain also exhibits a significant sequence identity of 43% with the family

of immunoglobulin domain-like group 2⁄ 3 grass pollen allergens Circular dichroism analysis demonstrates that insect cell-expressed rPhl p 1 is a folded species with significant secondary structure This material is well behaved and is adequate for the growth of crystals that diffract to 2.9 A˚ resolution The importance of conformational epitopes for IgE recognition

of Phl p 1 is demonstrated by the superior IgE recognition of insect-cell expressed Phl p 1 compared to Escherichia coli-expressed Phl p 1 More-over, insect cell-expressed Phl p 1 induces potent histamine release and leads to strong up-regulation of CD203c in basophils from grass pollen allergic patients Deglycosylated Phl p 1 frequently exhibits higher IgE binding capacity than the recombinant glycoprotein suggesting that rather the intact protein structure than carbohydrate moieties themselves are important for IgE recognition of Phl p 1 This study emphasizes the important contribution of conformational epitopes for the IgE recognition

of respiratory allergens and provides a paradigmatic tool for the structural analysis of the IgE allergen interaction

Abbreviations

PrPhl p 1, prokaryotic recombinant Phl p 1; ErPhl p 1, eukaryotic recombinant Phl p 1; GST, glutathione S-transferase.

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They are exclusively expressed in mature pollen grains

where they are localized mainly in the cytoplasm [8]

Using immuoelectronmicroscopy two mechanisms for

the release of group 1 allergens have been

demonstra-ted First, contact of intact pollen grains with mucosal

surfaces (e.g nasal epithelium) leads to hydration and

rapid diffusion of the allergens [9] Second, it has been

demonstrated that rain water induces the expulsion of

respirable micron size allergen-containing particles

from grass pollens [10,11] The small size of these

sub-cellular particles allows them to reach the deeper

air-ways and may explain the frequent occurrence of

heavy asthma attacks after rainfalls [12,13]

cDNAs coding for group 1 allergens from several

grasses have been isolated and showed high sequence

similarity [14–20] The recombinant group 1 allergen

from Timothy grass, rPhl p 1, expressed in Escherichia

coli contained many of the T cell epitopes of natural

group 1 allergens and cross-reacted with the naturally

occuring isoallergens from Timothy grass and other

grass species [6,21,22] However, several

post-transla-tional modifications (e.g glycosylation, occurrence of

hydroxyprolines) and the formation of disulphide

bonds have been described for group I allergens

[23,24] These modifications do not occur when

pro-teins are expressed in prokaryotic expression systems

and hence E coli-expressed group 1 allergens exhibit

impaired structural and immunological properties The

importance of conformational epitopes for IgE

recog-nition of group I allergens is highlighted by IgE

com-petition experiments using recombinant fragments of

Phl p 1 representing continuous IgE epitopes as even

a mixture of several major IgE-epitope-containing

rPhl p 1 fragments does not completely inhibit IgE

binding to intact Phl p 1 [25]

To obtain properly folded rPhl p 1, the cDNA

cod-ing for the mature allergen was expressed in

baculo-virus-infected insect cells An expression strategy was

chosen which led to the secretion of the recombinant

allergen into the cell culture supernatants rPhl p 1

was purified to homogeneity, characterized by mass

spectro-metry and the presence of post-translational

modification (i.e glycosylation) was investigated The

secondary structure content of insect cell-expressed

rPhl p 1 was examined by circular dichroism analysis

and diffraction quality crystals of the recombinant

allergen were grown The IgE binding properties of

insect cell-expressed Phl p 1 were compared with those

of E coli-expressed and natural Phl p 1 by competition

studies performed under native conditions and the

importance of glycosylation for IgE reactivity was

examined by enzymatic deglycosylation of insect

cell-expressed Phl p 1 Finally, the biological activity of

insect cell-expressed and E coli-expressed Phl p 1 was compared in histamine release experiments and by CD203c expression in basophils from grass pollen allergic patients [26] The finding that proper folding

of insect-cell expressed Phl p 1 is related to increased IgE reactivity and allergenic activity is discussed as a general feature of respiratory allergens and has rele-vance for the development of allergy vaccines which are based on the reduction of allergen fold

Results

Comparison of natural and recombinant group 1 grass pollen allergens

Although the majority of rPhl p 1 was detected in the insoluble pellet fraction of infected insect cells, up to 0.75 mgÆL)1of soluble rPhl p 1 could be purified from the culture supernatant by Ni2+-affinity chromato-graphy under nondenaturing conditions Purified insect cell-expressed Phl p 1 migrated at slightly higher molecular mass than the natural Phl p 1, E coli-expressed Phl p 1 and the Phl p 1-homologous allergen from rye grass (Lol p 1) (Fig 1A) Insect cell-expressed Phl p 1 as well as natural group 1 allergens (nPhl p 1 and nLol p 1) reacted with a rabbit antiserum raised against purified E coli-expressed Phl p 1 (Fig 1B) but not with the corresponding preimmune serum (Fig 1C) A band of approximately double the molecular mass as the purified allergens, possibly rep-resenting a dimer, was detected in the bacterial and insect cell-expressed Phl p 1 and, to a lower degree, in the nPhl p 1 preparations

Biochemical and biophysical characterization

of insect-cell expressed Phl p 1 The molecular mass of insect cell-expressed Phl p 1 was determined by mass spectrometry to be 28 122 Dalton (data not shown) The difference of 956 Da between the calculated (27 166 Da) and the deter-mined molecular mass is attributed to glycosylation Limited proteolysis in combination with mass spectro-metry was performed to identify structural domains [27,28] Fundamental to this approach is the notion that protection against proteolysis is conferred in regions of the protein that are within a rigid struc-ture, while proteolytic cleavage of a multiple-domain protein is biased towards solvent accessible regions (i.e exposed loops, interdomain linker chains) We identified two proteolytically stable structural domains

of rPhl p 1 by limited proteolysis, one comprising C78–K118 and a second domain spanning from

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K147–K241 (data not shown) The latter corresponds

to the region homologous to group 2 allergens To

confirm that the difference between the calculated

and determined molecular mass is due to

glycosyla-tion of the insect cell-expressed Phl p 1, glycan

detec-tion was performed (Fig 2A) Nitrocellulose-blotted

insect cell-expressed Phl p 1, but not E coli-expressed

Phl p 1 showed a positive staining for glycan moieties

(blue color) Also, a nonglycosylated control protein,

creatinase, and the marker proteins gave negative

reaction in the glycan staining and appear brown

(Fig 2A) Finally, enzymatic deglycosylation with

PNGase F resulted in a reduction of molecular mass

of insect cell-expressed Phl p 1 as visualized by

SDS⁄ PAGE (Fig 2B)

Insect cell-expressed Phl p 1 represents a folded

protein with considerable b-sheet structure that

crystallizes as thin plates

Insect cell- and E coli-expressed Phl p 1 were analyzed

by circular dichroism (CD) spectroscopy to determine

their secondary structural content (Fig 3) The CD

spectrum of insect cell-expressed, eukaryotic Phl p 1

(ErPhl p 1) suggested the presence of substantial

anti-parallel b-sheet, while the CD spectrum for the Phl p 1

expressed in bacteria (prokaryotic: PrPhl p 1) indicated

a considerable amount of unordered structure The

characteristics of the CD spectrum of insect

cell-expressed Phl p 1 indicates structural similarity with

Phl p 2, an almost exclusively b-sheet containing

aller-gen with 43% sequence identity to the C-terminal third

of Phl p 1 [29,30] Thermal denaturation of insect

cell-expressed Phl p 1 was monitored by far-UV CD in the

range of 20C to 90 and showed an irreversible

unfolding transition, with a melting point of  42 C

(data not shown) Only the properly folded insect cell-expressed but not the E coli-expressed Phl p 1 afforded crystals These crystals belonged to the ortho-rhombic space group P212121 and diffracted X-rays to

a resolution of 2.9 A˚ (Fig 4)

Phl p 1 and Phl p 2 belong to different clusters of proteins as determined by phylogenetic analysis Amino acid sequences of seven group 1 pollen aller-gens and four group 2⁄ 3 allergens were subjected to phylogenetic analysis using the phylip 3.6a2 package (http://evolution.genetics.washington.edu/phylip.html) (Fig 5) The allergens formed three main clusters, one comprising Zea m 1 and Cyn d 1, a second consisting

of Lol p 3, Dag g 3, Lol p 1, Phl p 1, Ory s 1 and Tri a 3 and a third cluster including Lol p 2, Hol l 1, Phl p 2 and Pha a 1 Although Phl p 1 and Phl p 2 are derived from Phleum pratense and share high sequence identity, the phylogenetic analysis shows that they are less related to each other than group 1 and group 2⁄ 3 allergens from different species

Insect cell-expressed Phl p 1 contains the IgE epitopes of natural Phl p 1

A comparison of the IgE binding capacity of E coli-and insect cell-expressed Phl p 1 under nondenaturing conditions in a dot-blot assay showed that insect cell-expressed Phl p 1 was more potent than the E coli-derived allergen (Table 1) IgE competition studies performed under native conditions confirmed this result (Fig 6A) Preincubation of sera from four grass pollen allergic patients with E coli-expressed Phl p 1 completely inhibited IgE binding to the very same pro-tein, but not to the insect cell-expressed Phl p 1 An

Fig 1 Coomassie staining and immunoreactivity of purified recombinant and natural group 1 allergens (A) Coomassie stained SDS ⁄ PAGE containing natural Lol p 1 (nLol p 1), natural Phl p 1 (nPhl p 1), eukaryotic recombinant Phl p 1 (ErPhl p 1) and bacterial recombinant Phl p 1 (PrPhl p 1) B and C represent immunoblots probed with rabbit anti-(Phl p 1 Ig) antiserum and the corresponding preimmune serum, respect-ively.

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almost complete reduction of IgE binding to insect

cell-expressed Phl p 1 was only observed for serum of

patient 2, whereas considerable IgE reactivity of sera

1, 3 and 4 to insect cell-expressed Phl p 1 was observed

despite preincubation with an excess of E coli-expressed Phl p 1

Whether insect cell-expressed Phl p 1 contains the IgE epitopes of a natural Phl p 1 preparation was inves-tigated by IgE competition experiments (Fig 6B) Pre-incubation of sera from grass pollen allergic patients with insect cell-expressed Phl p 1 led to a strong or complete inhibition of IgE reactivity to natural Phl p 1 (Fig 6B)

Next we studied the influence of glycosylation on the IgE binding capacity of insect cell-expressed Phl p 1 (Fig 6C) Five out of 10 patients showed stronger IgE reactivity to deglycosylated insect cell-expressed Phl p 1 than to the untreated protein (Fig 6C, 1, 2, 3, 5, 7) Three patients exhibited com-parable IgE reactivity to both protein forms (Fig 6C,

#4, 9, 10) and two sera reacted stronger with the gly-cosylated allergen version (Fig 6C, 6, 8) Finally, we studied the possible presence of cross-reactive IgE epi-topes between Phl p 1 and Phl p 2 Preincubation of sera from pollen allergic patients with insect cell-expressed, E coli-expressed Phl p 1 or an unrelated control allergen (birch pollen allergen, rBet v 1) had

no effect on IgE binding to rPhl p 2 (data not shown)

Allergenic activity of insect cell-expressed Phl p 1 The allergenic activity of insect cell-expressed Phl p 1 was analyzed by basophil histamine release (Fig 7) and CD203c expression (data not shown) Basophils from two grass pollen allergic patients were exposed to different concentrations of E coli- or insect cell-expressed Phl p 1 (Fig 7A,B) In both patients, insect cell-expressed Phl p 1 was more potent, inducing hista-mine release at lower concentrations (10)3lgÆmL)1) than E coli-expressed Phl p 1 (10)2lgÆmL)1) Meas-urement of CD203c expression on blood basophils of three Phl p 1 allergic patients confirmed these results Incubation with insect cell-expressed Phl p 1 always led to stronger upregulation of CD203c than incuba-tion with E coli-expressed Phl p 1 (data not shown)

A

B

Fig 2 Biochemical and biophysical characterization of insect cell-expressed Phl p 1 (A) Glycan detection Nitrocellulose blotted insect cell-expressed rPhl p 1 (ErPhl p 1), rPhl p 1 expressed in bacteria (PrPhl p 1), Creatinase and marker proteins (M) were sim-ultaneously stained for sugar moieties (blue) and reactive amino groups (fluorescent) Molecular masses are indicated on the left margin (B) SDS ⁄ PAGE containing insect cell-expressed Phl p 1 before (ErPhl p 1-) and after (ErPhl p 1 +) enzymatic deglycosyla-tion Lane M: Molecular mass marker.

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Phl p 1 represents one of the most important respiratory

allergens known to date As Phl p 1 is a glycoprotein

containing seven cysteines, we expressed the allergen in

eukaryotic insect cells to obtain a post-translationally

modified and folded protein As demonstrated by mass

spectrometry, glycan detection and deglycosylation

experiments, insect cell-expressed Phl p 1 was obtained

as a glycoprotein The seemingly correct folding of

insect cell-expressed Phl p 1 is demonstrated by the

fol-lowing experiments: insect cell-expressed Phl p 1 but

not E coli-expressed Phl p 1 exhibited a secondary

structure consisting mainly of b-sheets when analyzed

by CD spectroscopy Furthermore, only insect

cell-expressed Phl p 1 grew diffraction quality crystals

and thus will yield the three-dimensional structure of this allergen

Phl p 1 belongs to the group 1 family of highly cross-reactive grass pollen allergens The C-terminal domains

of these allergens display sequence similarity to group

Fig 3 Comparison of E coli- and insect cell-expressed Phl p 1 by

circular dichroism spectroscopy Far-UV CD spectra of E.coli- (grey)

and insect cell-expressed Phl p 1 (black), expressed as mean

resi-due ellipticity (y-axis), were recorded at 20 C in the wave length

range displayed on the x-axis.

Fig 4 Crystal growth of insect cell-expressed Phl p 1.Phl p 1

crys-tallizes as thin plates of 0.35 · 0.35 · 0.15 mm.

Fig 5 Analysis of the sequence and phylogenetic relationship among group 1 and group 2 ⁄ 3 allergens from various grass spe-cies A phylogenetic tree was reconstructed on the basis of amino-acid sequences of group 1 (Zea m 1: Zea mays, Cyn d 1: Cynodon dactylon, Pha a 1: Phalaris aquatica, Hol l 1: Holcus lanatus, Ory s 1: Oryza sativa, Lol p 1: Lolium perenne, Phl p 1: Phleum pra-tense) and group 2 ⁄ 3 allergens (Lol p 3: Lolium perenne, Dag g 3: Dactylis glomerata, Lol p 2: Lolium perenne, Tri a 3: Triticus aesti-vum, Phl p 2: Phleum pratense) using the PROTDIST and KITSCH program of the PHYLIP package.

Table 1 Comparison of the IgE binding capacity of E coli- and insect cell-expressed Phl p 1 IgE reactivity to recombinant Phl p 1, expressed in E coli (PrPhl p 1) and baculovirus-infected insect cells (ErPhl p 1).

Patient number

IgE binding (c.p.m.) IgE binding (c.p.m.)

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2⁄ 3 grass pollen allergens, another family of major grass

pollen allergens that exhibit an immunoglobulin-like

fold composed almost exclusively of b-sheet structure

[29,30] As shown by circular dichroism spectroscopy,

Phl p 1 showed also almost exclusively b-sheet

secon-dary structure The results from limited proteolysis

com-bined with mass spectrometry indicated a two domain

organization of the protein with a C-terminal portion

homologous to group 2 allergens Despite these findings,

Phl p 1 and Phl p 2 appear to represent

immunological-ly independent allergens because significant

crossreactiv-ity of IgE antibodies was not observed and both

proteins belonged to different phylogenetic clusters

The analysis of Phl p 1 IgE epitopes using

recom-binant allergen fragments had indicated the presence

of several continuous IgE epitopes, of which the most prominent could be allocated to the C-terminal por-tion of Phl p 1 [25] We have identified this porpor-tion

as an intact domain by the limited proteolysis experi-ment suggesting that intact and folded Phl p 1 domains represent the primary targets for patients’ IgE antibodies The latter assumption is also suppor-ted by the fact that only an incomplete inhibition of IgE reactivity to the Phl p 1 allergen could be obtained after preincubation of patients’ sera with small recombinant protein fragments suggesting the importance of conformational IgE epitopes [25] Therefore, we further tested the importance of struc-tural integrity on IgE binding capacity and allergenic activity of Phl p 1 by comparing insect cell-expressed

A

B

C

Fig 6 (A) Superior IgE binding capacity of insect cell- vs E coli-expressed rPhl p 1 Sera from four grass pollen allergic patients were prein-cubated with bacterially expressed rPhl p 1 and exposed to dot-blotted bacterial recombinant (PrPhl p 1+) or eukaryotic recombinant Phl p 1 (ErPhl p 1+) PrPhl p 1- and ErPhl p 1- show the IgE binding without preadsorption of sera (B) Inhibition of IgE binding to natural Phl p 1 (nPhl p 1) by insect cell-expressed Phl p 1 Sera from three grass pollen allergic patients (1–3) were tested for IgE reactivity to nitrocellulose-dotted eukaryotic recombinant Phl p 1 (ErPhl p 1) and natural Phl p 1 (nPhl p 1) Sera were preadsorbed with BSA (A), natural Phl p 1 (B), or insect cell-expressed Phl p 1 (C) (C) IgE binding capacity of deglycosylated insect cell-expressed Phl p 1.IgE reactivity of 10 sera from grass pollen allergic patients (1–10) to untreated (–) and deglycosylated (+) Phl p 1 is shown.

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Phl p 1 with E coli-expressed Phl p 1 This

compar-ison revealed a higher IgE-binding capacity and more

pronounced allergenic activity of insect cell-expressed

rPhl p 1 compared to E coli-expressed rPhl p 1, as

determined by basophil activation assays

Deglycosy-lation experiments demonstrate that the higher

IgE-binding capacity and increased allergenic activity of

insect cell-expressed Phl p 1 is due to intact structural

integrity rather than to IgE recognition of

carbo-hydrate moieties In fact, we found that

deglycosyla-tion rather increased the IgE binding capacity of

Phl p 1 This may be due to the exposure of protein

epitopes by removing carbohydrates from a

poten-tially hyperglycosylated insect cell-expressed Phl p 1

On the other hand, it is unlikely that the authentic,

plant-derived carbohydrates represent per se

import-ant targets for patients’ IgE import-antibodies because insect

cell-expressed Phl p 1 showed almost identical IgE

reactivity as natural Phl p 1

The importance of native tertiary structure for the IgE recognition of Phl p 1 seems to be a general princi-ple applicable to the most common respiratory aller-gens For example, it has been demonstrated that disruption of native structure by fragmentation has led

to a strong reduction of the IgE binding capacity and allergenic activity of the major birch pollen allergen, Bet v 1 [31], the cross-reactive calcium-binding allergens Aln g 4 [32] and Phl p 7 [33], the major mite allergen Der p 2 [34], and the major bovine allergen, Bos d 2 [35] We consider the possibility that respiratory aller-gens may predominantely contain conformational IgE epitopes as important for at least three reasons First, it indicates that respiratory sensitization occurs preferen-tially against intact and folded protein antigens which elute from respirable particles (e.g pollen, mite faeces, animal dander) Second, our study emphasizes that it is important to choose an optimal expression strategy for obtaining native properly folded recombinant allergens which closely mimic the immunological properties of the natural counterparts for diagnostic purposes

Finally, and perhaps most importantly, IgE recogni-tion of mainly conformarecogni-tional epitopes has important implications for the design of safe allergy vaccines with reduced allergenic activity Disruption of the native structure of respiratory allergens allows for the main-tenance of important T cell epitopes of a given allergen and simultaneously preserves sequences relevant for the induction of protective antibody responses [36] Con-trolled reduction of the fold of respiratory allergens by recombinant DNA technology or synthetic peptide chemistry thus seems to be a generally applicable strat-egy for the generation of recombinant allergy vaccines with reduced allergenic activity [37]

Experimental procedures

Materials, patients’ sera and antibodies The Sf9 cell line was purchased from the German Collec-tion of Microorganisms and Cell Cultures (Braunschweig, Germany) After informed consent was obtained, sera were collected from Phl p 1 allergic patients, following the Helsinki guidelines Allergenic patients were characterized

by case history, skin prick test, and the demonstration of allergen-specific serum IgE antibodies by RAST (Pharmacia Diagnostics, Uppsala, Sweden) Natural group 1 grass pollen allergens from Timothy grass (nPhl p 1) and rye grass (nLol p 1) were purified as described [38] Purified

E coli-expressed rPhl p 1, rPhl p 2 and rBet v 1 were obtained from BIOMAY (Vienna, Austria) A rabbit anti-Phl p 1 antiserum was obtained by immunizing rabbits with purified rPhl p 1 using complete Freunds’ adjuvant (Charles

Fig 7 Induction of basophil histamine release with recombinant

Phl p 1 preparations Granulocytes from patients (A, B) allergic to

grass pollen were incubated with various concentrations (x-axis) of

bacterial rPhl p 1 (PrPhl p 1) and eukaryotic rPhl p 1 The percentage

of histamine released into the supernatant is displayed on the y-axis.

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River, Kissleg, Germany) Alkaline phosphatase-conjugated

goat anti-(rabbit Ig) and rabbit anti-(mouse Ig) serum was

pur-chased from JacksonImmunoResearch Laboratories (West

Grove, PA, USA), a mouse monoclonal anti-Hexahistidine

antibody was obtained from Dianova (Hamburg, Germany)

The125I-labeled anti-human IgE immunoglobulins were

pur-chased from Pharmacia Diagnostics

Construction of recombinant baculovirus

The Phl p 1-encoding cDNA [16] was PCR amplified and

cloned into the BamHI and KpnI restriction sites of the

pBacPAK8 vector (Clontech Inc., Palo Alto, CA, USA),

containing the baculovirus-derived ecdysteroid

UDPgluco-syltransferase signal peptide [39] for enhanced secretion of

the recombinant protein into the culture supernatant and a

C-terminal His6-tag The pBacPAK8 construct was

con-firmed by DNA sequencing and cotransfected with the

line-arized pBacPAK6 viral DNA (Clontech Inc., Palo Alto,

CA, USA) into Sf9 insect cells The clones with the highest

level of protein secretion were chosen by Western blotting

for virus amplification

Expression and purification of rPhl p 1 from

baculovirus-infected insect cells

The expression of rPhl p 1 in insect cells was optimized by

infecting Sf9 cells with different amounts of virus and by

expression for various periods Aliquots of the culture

sup-ernatants and cell pellets were analyzed by SDS⁄ PAGE and

immunoblotting with a rabbit anti-Phl p 1 antiserum and

a monoclonal hexahistidine antibody Rabbit

anti-rPhl p 1 Igs were detected with an alkaline phosphatase

(AP)-labeled goat (rabbit Ig) antiserum Bound

hexahistidine Igs were detected with AP-labeled rabbit

anti-mouse Igs

Optimal expression of Phl p 1 was achieved by infection

of 2· 106 Sf9 cells per mL with recombinant baculovirus

at a multiplicity of infection (MOI) of 5 with culturing in

3 L spinner⁄ flasks in Insect-Xpress medium (BioWhittaker

Inc., Walkersville, MD, USA) containing 2% fetal bovine

serum At day two postinfection, supernatants were

separ-ated by centrifugation (8000 g, 4C, 30 min) and dialyzed

against start buffer [50 mm sodium phosphate (pH 8.0),

300 mm NaCl] at 4C overnight Insect cell-expressed

rPhl p 1 was purified using Ni-nitrilotriacetic acid superflow

matrix (Qiagen, Hilden, Germany) under nondenaturing

conditions by stepwise elution with increasing (20–250 mm)

imidazole concentrations The eluted samples were dialyzed

against 10 mm Tris HCl (pH 8.0), 100 mm NaCl and

con-centrated by Centricon ultrafiltration (Millipore, Bedford,

MA, USA) Protein concentrations of purified samples were

estimated using BCA reagent (Pierce Chemicals, Rockford,

IL, USA) and UV absorption at 280 nm The molar

extinc-tion coefficient of the protein was calculated from the tyro-sine and tryptophan content [40]

Mass spectrometry Purified baculovirus-expressed Phl p 1 was analyzed by LC-MS (Liquid Chromatography-Mass Spectrometry) using a VYDAC (Hesperia, CA, USA) C4 column on a Waters HPLC 2690 (Waters Corp., Milford, MA, USA) which fed into an electrospray Thermo Finnigan LCQ quadrupole ion-trap mass spectrometer (ThermoQuest Inc., San Jose, CA, USA)

Limited proteolysis followed by LC-MS Purified baculovirus-expressed Phl p 1 was subjected to lim-ited proteolysis by trypsin, Arg-C, Lys-C, Asp-N and Glu-C Ten microliter aliquots containing 18 lm rPhl p 1 were diges-ted with protease in the following ratios 1 : 5, 1 : 15, 1 : 50,

1 : 150 and 1 : 500 (protease:rPhl p 1; w⁄ w) for 1 h at room temperature Proteolysis was halted by freezing at )70 C Aliquots were analyzed by SDS⁄ PAGE Samples showing multiple bands, indicative for successful partial digest were then selected for further investigation by LC-MS A Vydac C18 column was used on a Waters HPLC 2690 (Waters Corp.) followed by electrospray into a Thermo Finnigan LCQ Ion Trap Mass Spectrometer (ThermoQuest Inc.) The spectra were deconvoluted using Thermo Finnigan’s xcali-bursoftware and the spectra were also verified by hand cal-culations of charge states The proteolytic fragments were identified using the paws software program (version 8.1.1, for Macintosh; Genomic SolutionsTM, Ann Arbor, MI, USA; http://bioinformatics.genomicsolutions.com/paws.html)

Detection of glycoproteins and deglycosylation treatment

Purified E coli- and insect cell-expressed Phl p 1 proteins were separated by SDS⁄ PAGE and transferred to nitrocellu-lose followed by detection of sugars using a DIG glycan⁄ pro-tein double labeling kit (Boehringer Mannheim GmbH, Mannheim, Germany) Briefly, glycans were oxidized to pro-duce aldehyde groups allowing the covalent attachment of the steroid hapten digoxigenin (DIG) The latter was then detected using horseradish peroxidase-conjugated anti-digo-xigenin Igs yielding a blue color reaction Creatinase and bacterial rPhl p 1 were used as nonglycosylated controls which were stained by labeling of amino groups with fluo-rescein and detection with alkaline phosphatase-conjugated anti-fluorescein Igs (Boehringer) giving a brown color reac-tion Enzymatic deglycosylation was performed with gluta-thione S-transferase (GST)–PNGase F (Hampton Research,

CA, USA) by using reaction ratios of GST–PNGase F:glyco-protein of 1 : 2 Deglycosylation was carried out for 15 h at

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room temperature in 10 mm Tris (pH¼ 8.0), 100 mm NaCl.

The GST–PNGase F was removed from the target protein

using glutathione-Sepharose

Circular dichroism (CD) measurements

All recombinant proteins were subjected to CD analysis to

access stability and secondary structure composition Far

UV-CD spectra were collected on a Jasco-J720

spectropola-rimeter (Jasco, Tokyo, Japan) at room temperature, at final

protein concentrations of 10–25 lm in either 0.5 or

0.01 mm path-length quartz cuvettes The molar ellipticity

was calculated according to [h]¼ ⁄ 10cl, where h is the

ellip-ticity, l is the cuvette path-length in cm and c is the protein

concentration in molÆL)1 Three independent measurements

were recorded and averaged for each spectral point in all

experiments Thermal denaturation was monitored in the

range of 20C to 90 C The reversibility of the unfolding

process was checked by measuring the CD signal upon

cooling to the starting temperature

Phylogenetic analysis of the relationships among

group 1 and group 2/3 allergens from various

grass species

Multiple alignment of sequences homologous to Phl p 1 as

identified by a BLAST search [41] was generated by using

clustalx [42] A distance matrix among sequences was

constructed using the protdist program of the phylip

3.6a2 [43,44] package The distance matrix was used as

input to the KITSCH program from the phylip package

for the construction of a phylogenetic tree This program

implements the Fitch–Margoliash least-squares methods

with the assumption of an evolutionary clock

SDS/PAGE analysis and immunoblotting

Samples were resolved on 12.5% polyacrylamide gels under

reducing conditions Proteins were stained with Coomassie

blue or transferred to nitrocellulose membranes [45]

Blot-ted proteins were probed with sera from Phl p 1 allergic

patients¢, anti-His Igs, rabbit anti-Phl p 1 antiserum and

the corresponding preimmune serum Patients’ bound IgE

antibodies were detected with 125I-labeled anti-human IgE

[46], anti-His Igs with AP-conjugated rabbit anti-(mouse

Ig), and bound rabbit Igs with an AP-conjugated goat

anti-(rabbit IgG) serum [47]

IgE-binding capacity and cross-reactivity

of allergens as determined by nondenaturing

dot-blot experiments

The IgE reactivity of the recombinant Phl p 1 molecules

was determined by dot-blot under conditions of antigen

excess [7] Three micrograms of the purified recombinant proteins were dotted onto nitrocellulose strips and incuba-ted with sera from Phl p 1 allergic patients Bound IgE antibodies were detected with125I-labeled anti-(human IgE) Igs (Pharmacia) and quantified by c-counting (Wallac, LKB, Turku, Finland) [25]

IgE inhibition experiments under conditions of antigen excess were performed as described [7] Patients’ sera were incubated with 5 lgÆmL)1 of each allergen (or the same amount of BSA for control purposes) overnight at 4C The next day, preincubated sera were exposed to 3 lg of nitrocellulose-dotted natural Phl p 1, rPhl p 2, E coli and baculovirus expressed Phl p 1 Bound serum IgE was detec-ted as described for the IgE immunoblotting and quantified

by c-counting [25]

Basophil activation experiments Granulocytes were isolated from heparinized blood samples

of individuals allergic to Phl p 1 by dextran sedimentation The capacity of E coli- and insect cell-expressed Phl p 1 to induce basophil degranulation was tested by incubation of granulocytes with various concentrations of the purified proteins and by measuring histamine released into the cell-free supernatant by radioimmunoassay (Immunotech, Marseille, France) Histamine release was measured in trip-licates and expressed as a percentage of total histamine determined after cell lysis, as described [48] Up-regulation

of CD203c expression on basophils after allergen exposure was measured as described [26]

Acknowledgements

We acknowledge the skillful technical assistance of Miriam Gulotta regarding the circular dichroism experiments This study was supported by grants Y078GEN, F01801, F01809, J1835 and J2122 of the Austrian Science Fund, by the CeMM Project of the Austrian Academy of Sciences, and by a research grant from BIOMAY, Vienna, Austria

References

1 Wills-Karp M, Santeliz J & Karp CL (2001) The germ-less theory of allergic disease: revisiting the hygiene hypothesis Nat Rev Immunol 1, 69–75

2 Wu¨thrich B, Schindler C, Leuenberger P & Ackermann-Liebrich P (1995) Prevalence of atopy and pollinosis in the adult population of Switzerland (SAPALDIA study) Swiss Study on Air Pollution and Lung Diseases

in Adults Int Arch Allergy Immunol 106, 149–156

3 Andersson K & Lidholm J (2003) Characteristics and immunobiology of grass pollen allergens Int Arch Allergy Immunol 130, 87–107

Trang 10

4 Johnson P & Marsh DG (1965) ‘Isoallergens’ from rye

grass pollen Nature (London) 206, 935–937

5 Freidhoff LR, Ehrlich-Kautzky E, Grant JH, Meyers

DA & Marsh DG (1986) A study of human immune

response to Lolium perenne (rye) pollen and its

compo-nents, Lol, p 1 and Lol, p 2 (rye 1 and rye 2)

J Allergy Clin Immunol 78, 1190–1201

6 Laffer S, Duchene M, Reimitzer I, Susani M,

Mannhal-ter C, Kraft D & Valenta R (1996) Common

IgE-epi-topes of recombinant Phl p 1, the major timothy grass

pollen allergen and natural group I grass pollen

isoaller-gens Mol Immunol 33, 417–426

7 Niederberger V, Laffer S, Froeschl R., Kraft D,

Rumpold H, Kapiotis S, Valenta R & Spitzauer S

(1998) IgE antibodies to recombinant pollen allergens

(Phl p 1, Phl p 2, Phl p 5, and Bet v 2) account for a

high percentage of grass pollen-specific IgE J Allergy

Clin Immunol 101, 258–264

8 Grote M, Dolecek C, vanRee R., Kraft D, Scheiner O

& Valenta R (1994) Immunogold electron microscopic

localization of timothy grass (Phleum pratense) pollen

major allergens Phl p 1 and Phl p 5 after anhydrous

fixation in acrolein vapor J Histochem Cytochem 42,

427–431

9 Vrtala S, Grote M, Duchene M, vanRee R., Kraft D,

Scheiner O & Valenta R (1993) Properties of tree and

grass pollen allergens; reinvestigation of the linkage

between solubility and allergenicity Int Arch Allergy

Immunol 102, 160–169

10 Grote M, Vrtala S, Niederberger V, Wiermann R,

Valenta R & Reichelt R (2001) Release of

allergen-bearing cytoplasm from hydrated pollen: a mechanism

common to a variety of grass (Poaceae) species

revealed by electron microscopy J Allergy Clin Immunol

108, 109–115

11 Taylor PE, Flagan RC, Valenta R & Glovsky MM

(2002) Release of allergens as respirable aerosols: a link

between grass pollen and asthma J Allergy Clin

Immu-nol 109, 51–56

12 Suphioglu C, Singh MB, Taylor P, Bellomo R, Holmes

P, Puy R & Knox RB (1992) Mechanism of

grass-pol-len-induced asthma Lancet 339, 569–572

13 Knox RB, Suphioglu C, Taylor P, Desai R., Watson

HC, Peng JL & Bursill LA (1997) Major grass pollen

allergen Lol p 1 binds to diesel exhaust particles:

impli-cations for asthma and air pollution Clin Exp Allergy

27, 246–251

14 Perez M, Ishioka GY, Walker LE & Chesnut RW

(1990) cDNA cloning and immunological

characteriza-tion of the rye grass allergen Lol p 1 J Biol Chem 265,

16210–16215

15 Broadwater AH, Bedinger PA, Rubinstein AL, Chay

CH & Klapper DG (1993) Zea m 1, the maize homolog

of the allergen-encoding Lol p 1 gene rye grass Gene

131, 227–230

16 Laffer S, Valenta R, Vrtala S, Susani M, vanRee R, Kraft D, Scheiner O & Ducheˆne M (1994) Complemen-tary DNA cloning of the major allergen Phl p 1 from timothy grass (Phleum pratense); recombinant Phl p 1 inhibits IgE binding to group 1 allergens from eight dif-ferent grass species J Allergy Clin Immunol 94, 689– 698

17 Suphioglu C & Singh MB (1995) Cloning, sequencing and expression in Escherichia coli of Pha a 1 and four isoforms of Pha a 5, the major allergens from canary grass pollen Clin Exp Allergy 25, 853–865

18 Xu H, Theerakulpisut P, Goulding N, Suphioglu C, Singh MB & Bhalla PL (1995) Cloning, expression and immunological characterization of Ory s 1, the major allergen of rice pollen Gene 164, 255–259

19 Smith PM, Suphioglu C, Griffith IJ, Theriault K, Knox

B & Singh MB (1996) Cloning and expression in yeast Pichia pastorisof a biologically active form of Cyn d 1, the major allergen from Bermuda grass pollen J Allergy Clin Immunol 98, 331–343

20 Schramm G, Bufe A, Petersen A, Haas H, Schaak M & Becker WM (1997) Mapping of the IgE-binding epi-topes on the recombinant major group 1 allergen of vel-vet grass pollen, rHol 1 1 J Allergy Clin Immunol 99, 781–787

21 Vrtala S, Susani M, Sperr WR, Valent P, Laffer S, Dolecek C, Kraft D & Valenta R (1996) Immuno-logical characterization of purified recombinant timothy grass pollen (Phleum pratense) allergens (Phl p 1, Phl p 2, Phl p 5) J Allergy Clin Immunol 97, 781–787

22 Schenk S, Breiteneder H, Susani M, Najafian N, Laffer

S, Duchene M, Valenta R, Fischer G, Scheiner O, Kraft

D & Ebner C (1995) T-cell epitopes of Phl p 1, major pollen allergen of timothy grass (Phleum pratense): evi-dence for cross-reacting and non-crossreacting T-cell epitopes within grass group 1 allergens J Allergy Clin Immunol 96, 986–996

23 Petersen A, Becker WM, Moll H, Blu¨mke M & Schlaak

M (1995) Studies on the carbohydrate moieties of the timothy grass pollen allergen Phl p 1 Electrophoresis

16, 869–875

24 Petersen A, Schramm G, Schlaak M & Becker WM (1998) Post-translational modifications influence IgE reactivity to the major allergen Phl p 1 of timothy grass pollen Clin Exp Allergy 28, 315–321

25 Ball T, Fuchs T, Sperr WR, Valent P, Vangelista L, Kraft D & Valenta R (1999) B cell epitopes of the major timothy grass pollen allergen, Phl, p 1, revealed

by gene fragmentation as candidates for immunother-apy FASEB J 13, 1277–1290

26 Hauswirth AW, Natter S, Ghannadan M, Majlesi Y, Schernthaner GH, Sperr WR, Buehring HJ, Valenta R

& Valent P (2002) Recombinant allergens promote expression of CD203c on basophils in sensitized indivi-duals J Allergy Clin Immunol 110, 102–109

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