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Báo cáo khoa học: N-Methylation in polylegionaminic acid is associated with the phase-variable epitope of Legionella pneumophila serogroup 1 lipopolysaccharide pptx

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In the present study, an isogenic mutant strain, termed 5215, was constructed by deletion of genes involved in the biosynthesis of the mAb 2625 epitope.. NMR spectroscopic studies reveal

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N-Methylation in polylegionaminic acid is associated

serogroup 1 lipopolysaccharide

Identi®cation of 5-( N , N -dimethylacetimidoyl)amino- and 5-acetimidoyl

( N -methyl)amino-7-acetamido-3,5,7,9-tetradeoxynon-2-ulosonic acid

in the O-chain polysaccharide

Oliver Kooistra1, Edeltraud LuÈneberg2, Yuriy A Knirel1,3, Matthias Frosch2and Ulrich ZaÈhringer1

1 Research Center Borstel, Center for Medicine and Biosciences, Borstel, Germany; 2 Institute for Hygiene and Microbiology, University of WuÈrzburg, Germany; 3 N D Zelinsky Institute of Organic Chemistry, Russian Academy of Sciences, Moscow, Russia

Previously, a phase-variable epitope was detected in the

virulent wild-type strain RC1 of Legionella pneumophila

serogroup 1 subgroup OLDA using a

lipopolysaccharide-speci®c monoclonal antibody, mAb 2625 [LuÈneberg, E.,

ZaÈhringer, U., Knirel, Y A., Steinmann, D., Hartmann, M.,

Steinmetz, I., Rohde, M., Kohl, J & Frosch, M (1998)

J Exp Med 188, 49±60] In the present study, an isogenic

mutant strain, termed 5215, was constructed by deletion of

genes involved in the biosynthesis of the mAb 2625 epitope

Mutant 5215 was as virulent as the parental wild-type RC1

but did not bind mAb 2625 The two strains showed no

di€erence in the core oligosaccharide and lipid A but in

the O-chain polysaccharide structure, which is a

homo-polymer of

5-acetimidoylamino-7-acetamido-3,5,7,9-tetra-deoxy-D-glycero-D-galacto-non-2-ulosonic acid (a derivative

of legionaminic acid) NMR spectroscopic studies revealed a hitherto unknown modi®cation of bacterial polysaccharides

in the wild-type strain, namely N-methylation of the 5-ace-timidoylamino group on a single legionaminic acid residue that is located, most likely, proximal to the core oligosac-charide Two major N-methylated substituents, the (N,N-dimethylacetimidoyl)amino and acetimidoyl(N-methyl) amino groups, could be allocated to the long- and middle-chain O-polysaccharide species, respectively N-Methylation

of legionaminic acid that was absent from the isogenic mutant 5215 and from the spontaneous phase variant 811, correlated with the presence of the mAb 2625 epitope Keywords: N-methylation; lipopolysaccharide; O-chain polysaccharide; phase variation; Legionella pneumophila

Legionella pneumophila is a facultative intracellular parasite

and the cause of legionellosis, a pneumonia with sometimes

fatal progression [1] The reservoirs of legionellae are

natural or man-made water systems and their natural hosts

are various amoebae species [2] In the human lung

L pneumophila invades and replicates within alveolar

macrophages [3] The serogroup-speci®c antigens of the

Gram-negative legionellae reside in the lipopolysaccharide (LPS) of the outer membrane [4,5]

The chemical structure of L pneumophila serogroup (Sg) 1 LPS has been extensively studied [6±12] (Fig 1) The O-chain polysaccharide (OPS) of the LPS is an a-(2 ® 4)-linked homopolymer of the 5-N-acetimidoyl-7-N-acetyl derivative of 5,7-diamino-3,5,7,9-tetradeoxynon-2-ulosonic acid, termed legionaminic acid [7] Initially, the

D-glycero-L-galacto con®guration was ascribed to legionam-inic acid [7], but this was later revised ®rst to theL-glycero

-D-galacto con®guration [13,14] and, ®nally, to the

D-glycero-D-galacto con®guration [15,16] Similarities in the biosynthesis pathway of legionaminic acid and neuram-inic acid (5-amino-3,5-dideoxy-D-glycero-D -galacto-non-2-ulosonic acid) have been described previously [17] In strains belonging to the Pontiac group, e.g Philadelphia 1 [5,18], polylegionaminic acid is quantitatively 8-O-acetylated [7,19], but in other Sg 1 strains of the non-Pontiac group, including those of subgroup OLDA [5,18], it is only speci®cally 8-O-acetylated at a few legionaminic acid residues [12] In the Pontiac group, the 8-O-acetyl has been identi®ed as a part of the epitope of LPS-speci®c mono-clonal antibodies mAb 2 and mAb 3/1 [18,19], and the 8-O-acetyl transferase-encoding gene lag-1 has been described previously [20] In L pneumophila Sg 1 LPS, the OPS is

Correspondence to U ZaÈhringer, Forschungszentrum Borstel,

Zentrum fuÈr Medizin und Biowissenschaften, Parkallee 22, D-23845

Borstel, Germany Fax: + 49 4537 188612, Tel.: + 49 4537 188462,

E-mail: uzaehr@fz-borstel.de

Abbreviations: LPS, lipopolysaccharide; OPS, O-chain polysaccharide;

PS, polysaccharide; Sg, serogroup; GPC, gel-permeation

chromatog-raphy; HMBC, heteronuclear multiple-bond correlation; DEPT,

distortionless enhancement by polarization transfer; Kdo,

3-deoxy-D -manno-oct-2-ulosonic acid; Rha, L -rhamnose; BYCE, bu€ered

charcoal yeast extract.

Note: part of this study was presented at the 20th International

Carbohydrate Symposium, Hamburg, Germany, August

13±September 1, 2000.

(Received 8 August 2001, revised 13 November 2001, accepted 16

November 2001)

Eur J Biochem 269, 560±572 (2002) Ó FEBS 2002

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linked to a terminal nonreducing L-rhamnose residue

(RhaII) of the core oligosaccharide [9,10] (Fig 1) The

LPS core oligosaccharide lacks heptose and phosphate,

contains abundant 6-deoxy sugars and N-acetylated amino

sugars, and is highly O-acetylated [8±10,12] Lipid A of

L pneumophila Sg 1 consists of unusual long-chain and

branched fatty acids [6,8], which may account for its low

endotoxic potential [21±23]

Recently, phase-variable expression of an LPS epitope of

L pneumophila has been reported [24] The LPS

phase-variant strain 811 was isolated from the virulent wild-type

strain RC1 (Sg 1, subgroup OLDA), and found to be

avirulent and serum sensitive [24] The altered LPS

pheno-type could be distinguished with the aid of the LPS-speci®c

monoclonal antibody mAb 2625, which bound to wild-type

RC1 but not to phase variant 811 Revertants from strain

811 retain all phenotypic characteristics of the wild-type

[24] We have recently shown that phase variation in

L pneumophila depends on chromosomal excision and

insertion of an unstable 29-kb genetic element of

presum-ably phage origin [25] The 29-kb sequence is located in a

de®ned and conserved site within the chromosome of the

virulent wild-type strain RC1 In contrast, in the

phase-variant strain 811, the 29-kb element is excised from the

chromosome and replicates as a high copy plasmid resulting

in the avirulent phenotype [25]

In another study, we characterized a 32-kb gene locus

responsible for LPS biosynthesis in L pneumophila [17]

Complementation of the spontaneous stable LPS mutant

strain 137 that did not bind mAb 2625 was achieved with a

gene from the avirulent parental wild-type strain 5097 The

gene, designated ORF 8, was able to restore mAb 2625

binding and exhibited homologies to bacterial methyl

transferase genes [17]

Until now, the structure of the mAb 2625 epitope was not

known, because in previous studies no structural difference

could be detected between the LPS of wild-type RC1 and

phase variant 811 [24] or between the LPS of the avirulent

wild-type 5097 and the corresponding mutant 137 [17] As

the mAb 2625 LPS epitope was found to be associated with

alteration in virulence and serum resistance upon phase

variation [24], we were interested in the elucidation of its

chemical structure The aim of this study was to identify the

mAb 2625 epitope and to correlate it to virulence For this

purpose, the isogenic mutant 5215 was generated by deletion of the LPS biosynthesis operon ORF 8±12 in the virulent wild-type RC1 With the aid of this genetically de®ned mutant that did not bind mAb 2625, we were able to correlate the mAb 2625 epitope to N-methylation of the 5-acetimidoylamino group on legionaminic acid, a modi®-cation that has not been found to date in bacterial polysaccharides Studies of binding of mAb 2625 to the N-methylated legionaminic acid derivatives is described in the accompanying paper [26]

M A T E R I A L S A N D M E T H O D S

Bacterial strains and cultivation

L pneumophila wild-type strain RC1 (Sg 1, subgroup OLDA) is a virulent patient isolate that binds mAb 2625 [17,24] The unstable phase-variant strain 811 derived from strain RC1 is avirulent and does not bind mAb 2625 [24] Phase variation is mediated by chromosomal insertion and excision of a 29-kb genetic element of presumably phage origin It is presumed that a regulatory factor is affected upon phase variation leading to numerous phenotypic alterations [25]

L pneumophila wild-type strain 5097 (Sg 1, subgroup OLDA) was obtained from the American Type Culture Collection, Rockville, MD (ATCC 43109) Strain 5097 is not virulent (presumably due to long-term passage on arti®cial media) and binds mAb 2625 The spontaneous stable mutant strain 137 that does not bind mAb 2625 was derived from strain 5097 [17] A point mutation in ORF 8 resulting in a frame shift with presumably polar effects is responsible for loss of the mAb 2625 epitope in mutant strain 137 [17] All strains were grown on buffered charcoal yeast extract (BCYE) agar with a-growth supplement (Merck)

Construction of theL pneumophila ORF 8±12 mutant strain 5215 from wild-type strain RC1

For deletion of the ORF 8±12 operon, a 7150 bp HpaI±SpeI restriction fragment from pEL28 (covering position 456 of ORF 7 to position 710 of ORF 13) was ligated into the HincII site of pBC From the resulting plasmid pMH546

Fig 1 Schematic representation of the L pneumophila serogroup 1 lipopolysaccharide structure Adapted from [6±12,15,16,20] Sugar abbreviations: GlcN3N, 2,3-diamino-2,3-dideoxy- D -glucose; Kdo, 3-deoxy- D -manno-oct-2-ulosonic acid; Man, D -mannose; GlcNAc, 2-acetamido-2-deoxy- D -glucose (N-acetyl- D -glucosamine); QuiNAc, 2-acetamido-2,6-dideoxy- D -glucose (N-acetyl- D -quinovosamine); Rha, L -rhamnose; Leg and 4e-Leg, derivatives of legionaminic and 4-epilegionaminic acid, respectively OAc stands for O-acetyl group.

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(Fig 2) a 3-kb NsiI fragment (covering position 275 of ORF

8 to position 399 of ORF 11) was deleted and a kanamycin

resistance cassette was inserted inverse to the direction of

transcription of ORFs 8±12 The kanamycin cassette was a

1282 bp EcoRI restriction fragment from plasmid pUC4K

(Pharmacia) Orientation of the insertion was con®rmed by

sequence analysis The resulting construct was termed

pMH549 (Fig 2) The entire 5.5-kb insert of pHM549

was excised with NotI±ApaI (restriction sites of the multiple

cloning site of pBC) and ligated into the EcoRV site of

plasmid vector pLAW344 [27], resulting in plasmid pMH12

(Fig 2) pLAW344 harbours the sacB gene and allows

counter-selection for homologous recombination pMH12

was introduced into L pneumophila strain RC1 by

elec-troporation and bacteria were plated on BYCE agar

supplemented with kanamycin (50 lgámL)1) Grown

trans-formants were harvested, suspended in sterile distilled water,

and plated on BCYE agar supplemented with kanamycin

and 5% sucrose for selection of homologous recombination

by double cross-over Homologous recombination was

con®rmed by Southern blot and PCR analysis in the

resulting mutant strain, termed 5215

Isolation and fractionation of LPS

LPS from wild-type RC1, mutant 5215, and phase variant

811 was extracted from enzyme-digested cells by a modi®ed

phenol/chloroform/petroleum ether procedure as described

previously [6,7] The LPS yields from dry cells were 9, 16,

and 6% (w/w), respectively

Fractionation of the intact LPS by OPS chain-length was

achieved by gel-permeation chromatography (GPC) in

10 mM Tris buffer (pH 8.0) containing 1 mM EDTA, 0.25% (w/w) sodium deoxycholate, 0.2 M NaCl, and 0.02% (w/w) NaN3 as described previously [28] Brie¯y,

5 mg LPS were dissolved under ultrasonication in 3.5 mL

5 mM EDTA and 2% (w/w) sodium deoxycholate Non-soluble material was removed by centrifugation and discarded The sample was applied to a column (2.5 ´ 120 cm; Bio-Rad) of Sephacryl S-200 HR (Pharma-cia) using the buffer mentioned above at a pump rate of

10 mLáh)1and a differential refractometer for monitoring (Knauer) Fractions of  3 mL were collected

SDS/PAGE and Western blot SDS/PAGE was carried out in 14% polyacrylamide gels using a Mini-Protean II system (Bio-Rad) LPS bands were visualized by the silver-staining technique described else-where [29] For extracted LPS samples, 100 lL stock-solution (2 mgámL)1) was mixed with 100 lL sample solution [30] and incubated at 95 °C for 5 min Then, 0.75 lL (0.75 lg LPS) of this solution was applied per lane For fractionated LPS, 1 mL of each fraction was dried in an evaporation centrifuge, dissolved in 100 lL water, mixed with 100 lL sample solution [30], and incubated at 95 °C for 5 min The sample volume applied per lane varied from 0.25 to 2.5 lL, depending on the refraction index of the corresponding fraction in GPC

For Western blot analysis of extracted LPS samples, 2 lg LPS per lane were applied to 12.5% polyacrylamide gels The sample volume of fractionated LPS applied per lane in Western blot analysis varied from 0.75 to 7.5 lL and was three times as high as that in silver-stained SDS/PAGE

Fig 2 Schematic depiction of plasmid constructs employed for generation of the ORF 8±12 mutant 5215 For detailed description see Materials and methods On top of the plasmids a schematic diagram of the 32-kb gene locus of L pneumophila wild-type RC1 required for LPS biosynthesis is depicted (adopted from [17]) The direction of the operons is indicated by arrowheads and designation of selected ORFs are shown above gene blocks.

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Western blotting onto nitrocellulose ®lter membranes was

carried out as described previously [31] Immunostaining

was performed subsequently with mAb 2625 [24] or mAb

LPS-1 (Progen) and alkaline phosphatase-conjugated goat

anti-(mouse Ig) Ig (Dianova) [24]

Chemical analysis

GLC was performed with a Hewlett-Packard Model 5890

Series II instrument equipped with a 30-m capillary column

of SPB-5 (Supelco) using a temperature gradient

150 ® 320 °C at 5 °Cámin)1 Monosaccharides were

analysed by GLC as the alditol acetates after hydrolysis

with 0.1MHCl for 48 h at 100 °C for neutral sugars [32] or

with 10MHCl for 30 min at 80 °C for amino sugars [33]

Following hydrolysis, sugars were dried, reduced with

NaBH4, and acetylated with acetic anhydride in pyridine

(30 min, 85 °C) Total hexosamine was determined by the

Morgan±Elson reaction after acid hydrolysis (4M HCl,

16 h, 100 °C) [34] 3-Deoxy-D-manno-oct-2-ulosonic acid

(Kdo) was determined by the thiobarbituric acid assay

according to the modi®ed method [35] Quanti®cation of

total phosphate was carried out by the ascorbic acid method

[36] Fatty acids of the lipid A portion were analysed by

GLC and combined GLC-MS as the methyl esters after

methanolysis (2MHCl/MeOH, 24 h, 120 °C) and

trimethyl-silylation with N,O-bis-(trimethylsilyl)-tri¯uoroacetamide

as described previously [6,37]

Preparation, modi®cation, and fractionation of the OPS

LPS each of wild-type RC1, mutant 5215, and phase variant

811 (750, 300, and 450 mg, respectively) was degraded at

100 °C for 4 h with 0.1M NaOAc/HOAc buffer (pH 4.4,

10 mgámL)1LPS), and the resultant lipid A precipitate was

removed by centrifugation (5000 g, 30 min) The

superna-tant was lyophilized and desalted by GPC on a column

(2.5 ´ 50 cm; Bio-Rad) of Sephadex G-50 (S) (Pharmacia)

using 50 mMpyridinium/acetate buffer (pH 4.3) and

mon-itoring with a differential refractometer (Knauer) to give the

corresponding polysaccharide (PS) portion

PS was de-O-acetylated with 20% (v/v) aqueous NH4OH

at 37 °C for 16 h (10 mgámL)1 PS); the following

lyo-philization and desalting as described above yielded

PSNH4OH To obtain PSNH4OH devoid of core sugars,

PSNH4OHwas treated with 48% (v/v) aqueous hydro¯uoric

acid (HF) at 4 °C for 7 days [38] (10 mgámL)1PSNH4OH),

the reagent was removed under a stream of nitrogen, and

the resultant PSNH 4 OH/HFwas desalted as above

PSNH 4 OH/HFwas fractionated by tandem GPC on two

directly connected columns (2.5 ´ 120 cm each; Bio-Rad) of

Toyopearl TSK HW-50 (S) (Supelco) and Fractogel TSK

HW-40 (S) (Merck) Pyridinium/acetate (50 mM) buffer

(pH 4.3) containing 10% (v/v) acetonitrile was used for

elution at a pump rate of 15 mLáh)1 and a differential

refractometer (Knauer) for monitoring Fractions of  3 mL

were collected, appropriately combined into six pools, and

lyophilized

NMR spectroscopy

1H NMR, 2D 1H,1H NMR (COSY and NOESY with

mixing time 300 ms), and H-detected 1H,13C NMR

(HMQC and HMBC) spectra were recorded with a Bruker Avance DRX-600 spectrometer.13C NMR and DEPT-135 NMR spectra were recorded with a Bruker Avance DPX-360 spectrometer Standard Bruker software was used

to acquire and process the NMR data Samples were lyophilized three times from2H2O and measured in2H2O (2H, 99.996%; Cambridge Isotope Laboratories) at 27 °C Chemical shifts were referenced to external acetone (dH

2.225 p.p.m.; dC31.45 p.p.m.)

R E S U L T S

Construction and characterization of the ORF 8±12 mutant strain 5215 from wild-type strain RC1 Genes involved in formation of the LPS epitope bound by mAb 2625 were identi®ed on a LPS biosynthesis gene cluster and assigned to the ORF 8±12 operon [17] ORF 8 showed homologies to bacterial methyl transferases [39,40], ORF 9 exhibited sequence similarities to Neu5Ac condensing enzymes (e.g SiaC of Neisseria meningitidis [41]), and ORF 11 showed vague homologies to plant methyl transferases [42] The proteins encoded by the remaining ORFs 10 and 12 showed no homologies to known amino-acid sequences The only ORF 8±12 mutant accessible was mutant 137 derived from the avirulent wild-type 5097 Therefore, the isogenic ORF 8±12 deletion mutant 5215 was constructed from wild-type RC1 by homologous recombi-nation (Fig 2) in order to compare the LPS structures of wild-type RC1, the genetically de®ned mutant 5215, and the phase variant 811 Unexpectedly, virulence and serum resistance were not affected in mutant 5215, when compared

to the parental wild-type RC1 (data not shown), which revealed that the mAb 2625 LPS epitope itself is not associated with virulence of L pneumophila strain RC1 Characterization of LPS from wild-type RC1

and mutant 5215

In silver-stained SDS/PAGE (Fig 3A), LPS from wild-type RC1 and mutant 5215 displayed no difference in banding pattern Both LPS showed a characteristic bimodal distri-bution by OPS chain-length In Western blot analysis, LPS from mutant 5215 did not bind to mAb 2625 (Fig 3B) but bound to mAb LPS-1 in a different manner compared to LPS from wild-type RC1 (Fig 3C) MAb LPS-1 is known

to recognize speci®cally a conserved epitope located in the outer core region of the LPS from L pneumophila Sg 1 strains [12,24,43]

Chemical analyses of both wild-type RC1 and mutant

5215 LPS revealed L-rhamnose, D-mannose, Kdo, and amino sugars, i.e total hexosamine according to the Morgan±Elson reaction after acid hydrolysis (total of 2,3-diamino-2,3-dideoxy-D-glucose, 2-amino-2-deoxy-D -glucose, and 2-amino-2,6-dideoxy-D-glucose), in the molar ratios of  2 : 2 : 2 : 5 According to GLC data, the ratio of 2-amino-2-deoxy-D-glucose and 2-amino-2,6-dideoxy-D -glucose was the same in the LPS from wild-type RC1 and mutant 5215 Comprehensive analysis by NMR spectros-copy and MALDI-TOF MS revealed no difference in composition and structure of the core oligosaccharides isolated from wild-type RC1 and mutant 5215 [12] NMR spectroscopy revealed that the lipid A backbone is a

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1,4¢-bisphosphorylated (1¢ ® 6)-linked disaccharide of

2,3-diamino-2,3-dideoxy-D-glucose in both wild-type RC1

and mutant 5215 [44] Fatty acid composition of lipid A of

both strains was almost identical as well [44]

Investigations of the core oligosaccharide [12] and the

lipid A backbone [44] of the LPS from phase variant 811

revealed that both were unchanged compared to wild-type

RC1 However, lipid A of phase variant 811 contained

3-hydroxylated fatty acids of different chain-length

compared to lipid A of wild-type RC1 [44]

Fractionation of LPS by GPC

To determine the location of the mAb 2625 epitope, LPS

from wild-type RC1 and mutant 5215 was fractionated by

GPC on Sephacryl S-200 HR The refraction index elution

pro®le of the GPC of wild-type RC1 LPS (Fig 4A)

indicated the same characteristic bimodal distribution of

long and short O-chain LPS species as in SDS/PAGE

(Fig 3A) A similar pro®le showing a low amount of long

O-chain LPS species and a relatively high amount of short

O-chain LPS species was observed for mutant 5215 LPS

(Fig 5A) Silver-stained SDS/PAGE after GPC of the

wild-type RC1 LPS revealed 33 fractions (nos 96±128) containing

LPS species with different OPS chain-lengths (Fig 4B)

A ladder-like pattern was observed with differences of up

to 10 sugar residues within each fraction and with

overlap-ping about 6±8 residues in each pair of neighbouring

fractions

In Western blot analysis, mAb 2625 bound only to the

wild-type LPS species from fractions 96±116, and did not

bind to LPS molecules below a certain size, i.e a certain

OPS chain-length (Fig 4C) In contrast, mAb LPS-1

exclusively bound to the LPS species from fractions

113±126, and did not bind to LPS molecules above a

certain size (Fig 4D) This rather sharp margin clearly

showed that the mAb 2625 epitope is only present or accessible in LPS species having a speci®c OPS chain-length

of  15 and more residues of legionaminic acid

Fig 4 Fractionation of LPS from L pneumophila wild-type RC1 by gel-permeation chromatography on Sephacryl S-200 HR Part of refraction index elution pro®le of LPS (A) Silver-stained SDS/PAGE (B) and Western blot with mAb 2625 (C) and mAb LPS-1 (D) of fractionated LPS The dotted lines in the top panel indicate fractions and the dashed lines in the lower panels indicate the borders of di€erent, appropriately aligned SDS/polyacrylamide gels or Western blots.

Fig 5 Fractionation of LPS from L pneumophila mutant 5215 by gel-permeation chromatography on Sephacryl S-200 HR Part of refraction index elution pro®le of LPS (A) Western blot with mAb 2625 (B) of fractionated LPS The dotted lines in the top panel indicate fractions and the dashed lines in the lower panel indicate the borders of di€erent, appropriately aligned Western blots.

Fig 3 Silver-stained SDS/PAGE (A) and Western blot with mAb 2625

(B) and mAb LPS-1 (C) of L pneumophila LPS from wild-type RC1

(lane 1) and mutant 5215 (lane 2) In A, 0.75 lg LPS per lane was

applied, and 2 lg LPS in B and C.

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As followed from Fig 3, all LPS-containing fractions

(nos 96±128) from mutant 5215 bound mAb LPS-1

(Fig 5B)

Preparation and characterization of OPS

An OPS attached to the core oligosaccharide (PS) was

prepared by mild acid hydrolysis of LPS from each strain

(wild-type RC1, mutant 5215, and phase variant 811) to

cleave the lipid A moiety followed by GPC on Sephadex

G-50 (S) Based on the ®nding that the OPS is linked to the

terminalL-rhamnose residue of the LPS core

oligosacchar-ide (RhaII) [9] and the observation that 48% aqueous HF

selectively cleaves the glycosidic linkage of 6-deoxy sugars in

polysaccharides [38], a protocol was elaborated to remove

core oligosaccharide constituents from PS When the intact

LPS was treated with 48% aqueous HF and separated by

SDS/PAGE, Western blot analysis revealed that although

the OPS of the LPS was partially cleaved, the mAb 2625

epitope in the remaining LPS species was not affected After

de-O-acetylation of the LPS, the HF treatment completely

cleaved the OPS of the LPS In this case, silver-stained

SDS/PAGE showed only low-molecular-mass molecules

resembling rough-type LPS, which did not react with mAb

2625 in Western blot In contrast to the glycosidic linkage of

6-deoxy sugars, e.g.L-rhamnose [38], that of legionaminic

acid and its N-linked substituents are stable under the same

conditions [14]

Therefore, PS was de-O-acetylated, treated with 48%

aqueous HF, and the resultant modi®ed polysaccharide

(PSNH4OH/HF) was fractionated by tandem GPC on

Toyo-pearl TSK HW-50 (S) and Fractogel TSK HW-40 (S) to

separate long-, middle-, and short-chain OPS species The

middle-chain species were present in a low amount (e.g see

pool III in Fig 6) Only a negligible difference in the elution

pro®les of PSNH 4 OH/HFfrom wild-type RC1, mutant 5215,

and phase variant 811 was observed

OPS from each strain separated into pools I to VI (Fig 6) were investigated by1H NMR spectroscopy The1H NMR spectra (only pools I, III, and V are shown in Fig 7) indicated that legionaminic acid with its major substituents, 5-N-acetimidoyl and 7-N-acetyl groups (Fig 8, structure 1) remained intact (see also Tables 1 and 2) The only anomeric proton signals present in the spectra were those

of twoL-rhamnose residues (RhaIH1 dH5.06 and RhaIIH1

dH 4.99; Fig 9A±C), which was in accordance with identi®cation of onlyL-rhamnose by GLC analysis of the alditol acetates derived from PSNH4OH/HF Therefore, the isolated PSNH4OH/HF species from all three strains were composed of legionaminic acid and L-rhamnose, whereas the major portion of the core oligosaccharide was cleaved

by HF treatment A 1H,13C HMQC experiment demon-strated that PSNH4OH/HF contained at the reducing end either an Rha disaccharide ® 3)-a-L-RhaII-(1 ® 3)-L-RhaI

( 70%) or a single Rha residue ® 3)-L-RhaII( 30%), in both cases the reducing Rha residue being predominantly, but not exclusively, a-con®gured The disaccharide was identi®ed by the H1 chemical shift of RhaII (compare published data [9]) and a characteristic down®eld displacement of the C1 signal from dC95.17 in nonlinked Rha to dC103.21 in a-linked RhaII(compare to published data in [45])

Identi®cation of N-methylated derivatives

of legionaminic acid N-Methyl groups in bacterial polysaccharides occur rarely [46] and published data are only scarce Therefore, careful NMR spectroscopic analysis was used to elucidate the structure of N-methylated derivatives of legionaminic acid Comparison of the1H NMR spectra of the OPS of pool III from all three investigated strains revealed four signals between 2.9 and 3.3 p.p.m (all singlets; Fig 9, panels A and D), whose presence correlated with the reactivity of mAb

2625 with LPS in Western blot The signals were observed in long- and middle-chain OPS from wild-type RC1, but in no OPS from mutant 5215 (Fig 9, panels B and E) In phase variant 811, these signals were recognized in the OPS of the same pools as in wild-type RC1 but were 10- to 20-fold less intense (Fig 9, panels C and F) Except for the region of the four signals, the 1H NMR spectra of the polysaccharides from all three strains were almost identical (compare Fig 9, panels A±C) The middle-chain OPS of pool III from wild-type RC1 having 15±20 residues of legionaminic acid was the smallest one that displayed these signals and, moreover, the relative intensity of these signals was the highest compared to other pools from the same strain Therefore, further structural investigation was performed with this preparation

The 1H NMR chemical shifts and the grouping of the signals in pairs (one pair at dH3.30 and 3.19, and the other at

dH3.03 and 2.95; see below) resembled those of N-methyl groups in stereoisomers of N-acetimidoyl-N-methylglycine (N-acetimidoylsarcosine) at dH3.70 (E) and dH3.60 (Z) [47] The corresponding13C NMR chemical shifts (one pair at dC

42.95/42.89 and 40.74/40.60, and the other at dC33.73 and 32.56, respectively) and a DEPT-135 NMR experiment con®rmed N-linked methyl groups The 1H,13C HMQC experiment revealed also a third, minor pair of signals at dH

2.97 and 2.94 and dC30.93 and 29.86, which were partially

Fig 6 Fractionation of OPS (PS NH4OH/HF ) from L pneumophila

wild-type RC1 by tandem gel-permeation chromatography on Toyopearl TSK

HW-50 (S) and Fractogel TSK HW-40 (S) Pools I, III, and V

corre-spond to long-, middle-, and short-chain PS NH4OH/HF , respectively;

pools II, IV, and VI correspond to intermediate fractions.

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superimposed on the signals of the major higher-®eld pair in

the1H NMR spectrum (Fig 10, right panel)

In the1H,13C HMBC spectrum (Fig 10, left panel), the

proton signals of the major lower-®eld pair at dH3.30 and

3.19 cross-correlated to the lower-®eld carbon signals at dC

40.74/40.60 and 42.95/42.89 Furthermore, both proton

signals correlated to the signals of the same nonprotonated

carbon (dC167.03) and the same C-methyl group (dC16.63)

of an N-acetimidoyl group In a NOESY experiment, the

two N-methyl signals correlated to each other These data

suggested that both N-methyl groups are linked to the same

nitrogen of an N-acetimidoyl group, i.e that an

(N,N-dimethylacetimidoyl)amino group is present (Fig 8,

structure 2) This group is linked to C5 of a legionaminic

acid residue, which is substituted with a nonmethylated

N-acetimidoyl group in the other legionaminic acid residues

of the OPS

The proton signals of the major higher-®eld pair at dH

3.03 and 2.95 correlated in the1H,13C HMBC spectrum to

different nonprotonated carbon signals at dC169.02 and dC

168.23 and different C-methyl carbon signals at dC20.49

and dC20.21 of another N-acetimidoyl group, respectively

(Fig 10, left panel) In addition, each proton signal

correlated to a signal of a nitrogen-bearing carbon (C5) of

legionaminic acid (dC55.93 and 57.32) Taken these data together, it was concluded that there is present a 5-acetimidoyl(N-methyl)amino group that occurs as two stereoisomers (Fig 8, structure 3) An N-methylacetamido group could be excluded based on identi®cation, using 2D NMR experiments, of a nonmethylated 7-acetamido group

of this particular legionaminic acid residue (Table 2) A methylamino group was excluded based on published data

of the methylamino derivative ofL-fucose in the LPS of Bordetella pertussis strain 1414 [48,49], in which the N-methyl group gave a single singlet in the 1H NMR spectra Similarly, the minor pair of signals at dH2.97 and 2.94 was assigned to a 5-(N-methylacetimidoyl)amino group

A NOESY experiment (Fig 11) was applied to stereo-chemical analysis of the N-methylated acetimidoylamino (acetamidine) groups in 2 and 3, which may occur as stereoisomers due to a partial double-bond character of the linkages at both nitrogens A strong NOE correlation was observed between the lower-®eld signal from each major pair of the N-methyl signals (dH3.30 in 2 and dH3.03 in 3) and the corresponding C-methyl signals of the N-acetimi-doyl group, but only a weak or no cross-peak could be detected for the higher-®eld signal (dH3.19 in 2 and dH2.95

in 3) Hence, the lower- and higher-®eld1H NMR signals of

Fig 7 1D 1 H NMR spectra of the long-, middle-, and short-chain PS NH4OH/HF (pools I, III, and V; panels A±C) from wild-type RC1 The integral traces for selected signals with the corresponding integration values referenced to the anomeric proton signal of Rha II (H1 d H 4.99, integration value set at 0.7) in the ® 3)-a- L -Rha II -(1 ® 3)- L -Rha I disaccharide are superimposed on the spectra The insets show the region between 2.8 and 3.4 p.p.m ex-tended 5-fold Bold numbers refer to struc-tures shown in Fig 8 For abbreviations see legend to Fig 9.

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2 belonged to the N-methyl groups at N1in trans and cis

orientation to N2 of the acetamidine group, respectively

(Fig 8; the descriptors cis and trans for the two N-methyl

groups in 2 are used only to designate their positions relative

to N2and do not refer to stereoisomerism) The lower-®eld

1H NMR signal of 3 belonged to the N-methyl group at N2

in the E isomer and the higher-®eld signal to that in the

Z isomer, in which N1is in trans and cis orientation to C5 of legionaminic acid, respectively (Fig 8)

Like 3, 2 may theoretically occur as two stereoisomers,

E and Z, with regard to the partial double bond at N2, while the NMR spectra showed the presence of only one isomer Molecular modelling data (not shown) suggested that this isomer is 2-E with trans orientation of N1 to C5 as 2-Z would be sterically hindered by interaction of one of the N-methyl groups at N1(that in cis orientation to N2) with the pyranose ring of legionaminic acid

The N-methyl signal in 3 gave strong NOE correlations

to three more proton signals, which were assigned to H4, H7, and either H6 or, less likely, H8 of legionaminic acid The assignment was performed by correlations between signals for H4 (dH3.33 E, dH3.37 Z) and H3ax,3eq(axial:

dH1.86 E, dH1.89 Z, equatorial: dH2.48 E, dH2.51 Z) in COSY, and for H7 (dH3.68 E, dH3.75 Z) and CˆO of the 7-acetamido group (dC175.91 E, dC175.74 Z) in the1H,13C HMBC experiment In addition, signals for H9 (dH 1.17 E, dH 1.16 Z) were found by a weak NOE correlation with the N-methyl group, whereas signals for H6 and H8 appeared to coincide (dH 4.19 E, dH4.13 Z) A signal for H5 of 3 could not be reliably identi®ed, most likely, owing to its coincidence with the H5 signal of the major, non-N-methylated derivative 1 The NOESY data suggested that in the predominant conformation of both 3-E and 3-Z the N-methyl group at N2has an axial (or close to axial) orientation related to the pyranose ring

of legionaminic acid and lies on or close to a plane formed by H4, H6, and H7 In contrast, in 2 no NOE correlation was observed between the N-methyl groups and any proton of legionaminic acid, evidently owing to the remoteness of the N-methyl groups at N1 from the pyranose ring

Long-, middle-, and short-chain PSNH 4 OH/HFfrom wild-type RC1 were investigated by 1D1H NMR spectroscopy and signal integration was performed to calculate the average chain-length of the PSNH 4 OH/HFand the distribution

of N-methylated legionaminic acid derivatives The signal of a-L-RhaIIH1 (dH4.99) in the ® 3)-a-L-RhaII-(1 ® 3)-L -RhaIdisaccharide was used as a reference, because it was the

Fig 8 Structures of

5-acetimidoylamino-7-acetamido-3,5,7,9-tetra-deoxy- D -glycero- D -galacto-non-2-ulosonic acid

(5-N-acetimidoyl-7-N-acetyllegionaminic acid, 1) and its N-methylated derivatives,

5-N-(N,N-dimethylacetimidoyl)-7-N-acetyllegionaminic acid (2-E) and

two stereoisomers of

5-N-acetimidoyl-7-N-acetyl-5-N-methyllegio-naminic acid (3-E and 3-Z).

Table 1 1 H and 13 C NMR chemical shifts for N-methylated acetimidoylamino groups in pool III of the OPS from wild-type RC1 NMe, N-methyl group; NAm CH 3 and NAm CˆN , C-methyl group and nonprotonated carbon of the 5-acetimidoylamino group, respectively ND, not determined.

d H (p.p.m.)

5-N-(N,N-Dimethylacetimidoyl) (2-E) 3.19 (cis) 3.30 (trans) 2.19

5-N-(N-Methylacetimidoyl) (minor) 2.97 (E) 2.94 (Z) 2.25 (E) ND

5-N-Acetimidoyl-5-N-methyl (3) 2.95 (E) 3.03 (Z) 2.30 (E) 2.19 (Z)

d C (p.p.m.)

5-N-(N,N-Dimethylacetimidoyl) (2-E) 40.74 (cis) 42.95 (trans) 16.63 167.03

40.60 (cis) 42.89 (trans)

5-N-Acetimidoyl-5-N-methyl (3) 32.56 (E) 33.73 (Z) 20.21 (E) 20.49 (Z) 168.23 (E) 169.02 (Z)

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only anomeric proton present in a single anomeric

con®g-uration Integration of the signals of 1D1H NMR spectra

(Fig 7) indicated that the average chain-length of long-,

middle-, and short-chain PSNH 4 OH/HF(Fig 6, pools I, III,

and V) is about 40, 18, and 10 legionaminic acid residues

The ratio of the 5-N-(N,N-dimethylacetimidoyl)-7-N-acetyl

and 5-N-acetimidoyl-5-N-methyl-7-N-acetyl derivatives of

legionaminic acid was 1 : 1 in long-chain and 1 : 2 in

middle-chain PSNH4OH/HF, respectively Based on the

rela-tive intensities of the proton signals it was concluded that

only one legionaminic acid residue is N-methylated in each polysaccharide chain above a speci®c length

D I S C U S S I O N

Phase variation in L pneumophila has dramatic effects on the virulence of the bacteria in various in vitro and in vivo models Phase variation can be monitored with the aid of mAb 2625 that is speci®c for an epitope in the LPS of

L pneumophila Sg 1 subgroups OLDA and Oxford The

Table 2 1 H and 13 C NMR chemical shifts for 1 and 3 in the OPS pool III from wild-type RC1 NAc CH 3 and NAc CˆO , C-methyl group and nonprotonated carbon of the 7-acetamido group, respectively ND, not determined.

Derivative of

legionaminic acid d (p.p.m.)

5-N-Acetimidoyl

methyl- (3)

5-N-Acetimidoyl

-7-N-acetyl (1) 174.47 101.86 39.40 71.86 54.30 72.76 55.53 67.92 19.65 23.23 175.32 5-N-Acetimidoyl

-7-N-acetyl-5-N-methyl- (3)

Fig 9 600-MHz 1 H NMR spectra of pool III

of the OPS (PS NH4OH/HF ) from three

L pneumophila strains Left panel: the full spectra of pool III from wild-type RC1 (A), mutant 5215 (B), and phase variant 811 (C) Assignment was made using 2D NMR experiments and published data [7] Right panels: part of spectra of pool III from wild-type RC1 (D), mutant 5215 (E), and phase variant 811 (F) NMe cis and NMe trans , N-methyl groups in 2-E (the descriptors cis and trans designate the positions of the N-methyl groups relative to N 2 ); NMe, N-methyl group in the stereoisomers 3-E and 3-Z; NAc CH 3 and NAm CH 3 , C-methyl groups

of 7-acetamido and 5-acetimidoylamino substituents, respectively Bold numbers refer

to structures shown in Fig 8.

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Fig 10 Sections of 2D 1 H, 13 C HMBC (left panel) and HMQC (right panel) spectra of pool III of the OPS (PS NH 4 OH/HF ) from L pneumophila wild-type RC1 Spectra are aligned in F 1 dimension The corresponding 13 C and 1 H NMR spectra are displayed along F 1 and F 2 axes Spectra were recorded at 600 MHz and 27 °C For abbreviations see legend to Fig 9 Cross-peaks marked by   belong to an unknown minor isomer of legionaminic acid.

Fig 11 Part of a NOESY spectrum of

pool III of the OPS (PS NH4OH/HF ) from

L pneumophila wild-type RC1 The spectrum

was recorded at 600 MHz and 27 °C using a

mixing time 300 ms For abbreviations see

legend to Fig 9 Cross-peaks marked by

  belong to an unknown minor isomer of

legionaminic acid.

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