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The Role of Endotoxin in Infection: Helicobacter pylori and Campylobacter jejuni

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Endotoxins: Structure, Function and Recognition

Part of the book series: Subcellular Biochemistry ((SCBI,volume 53))

Abstract

Both Helicobacter pylori and Campylobacter jejuni are highly prevalent Gram-negative microaerophilic bacteria which are gastrointestinal pathogens of humans; H. pylori colonizes the gastroduodenal compartment and C. jejuni the intestinal mucosa. Although H. pylori causes chronic gastric infection leading to gastritis, peptic ulcers and eventually gastric cancer while C. jejuni causes acute infection inducing diarrhoeal disease, the endotoxin molecules of both bacterial species contrastingly contribute to their pathogenesis and the autoimmune sequelae each induces. Compared with enterobacterial endotoxin, that of H. pylori has significantly lower endotoxic and immuno-activities, the molecular basis for which is the underphosphorylation and underacylation of the lipid A component that interacts with immune receptors. This induction of low immunological responsiveness by endotoxin may aid the prolongation of H. pylori infection and therefore infection chronicity. On the other hand, this contrasts with acute infection-causing C. jejuni where overt inflammation contributes to pathology and diarrhoea production, and whose endotoxin is immunologically and endotoxically active. Futhermore, both H. pylori and C. jejuni exhibit molecular mimicry in the saccharide components of their endotoxins which can induce autoreactive antibodies; H. pylori expresses mimicry of Lewis and some ABO blood group antigens, C. jejuni mimicry of gangliosides. The former has been implicated in influencing the development of inflammation and gastric atrophy (a precursor of gastic cancer), the latter is central to the development of the neurological disorder Guillain-Barré syndrome. Both diseases raise important questions concerning infection-induced autoimmunity awaiting to be addressed.

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Abbreviations

AMAN:

acute motor axonal neuropathy

CAMPs:

cationic antimicrobial peptides

EAN:

experimental ataxic neuropathy

FucT:

fucosyltransferase

Gal:

d-galactose

GalNAc:

N-acetyl-d-glaactosmine

GBS:

Guillain-Barré syndrome

GlcN:

d-Glucosamine

GlcN3N:

2,3-diamino-2,3-dideoxy-d-glucose

H+,K+-ATPase:

H+,K+-adenosine triphosphatase

Ig:

immunoglobulin

LacNAc:

N-acetyl-lactosamine

Le:

Lewis

LOS:

lipooligosaccharide

LPS:

lipopolysaccharide

MFS:

Miller Fisher syndrome

Neu5Ac:

N-acetyl-neuraminic acid

OS:

oligosaccharide

PEtN:

phosphoethanolamine

TLRs:

Toll-like receptors

14:0(3-OH):

(R)-3-hydroxytetradecanoic acid

16:0(3-OH):

(R)-3-hydroxyhexadecanoic acid

18:0(3-OH):

(R)-3-hydroxyoctadecanoic acid

3-(14:0-O)-14:0:

(R)-3-(tetradecanoyloxy)tetradecanoic acid

3-(16:0-O)-14:0:

(R)-3-(hexadecanoyloxy)tetradecanoic acid

3-(12:0-O)-16:0:

(R)-3-(dodecanoyloxy)hexadecanoic acid

3-(14:0-O)-16:0:

(R)-3-(tetradecanoyloxy)hexadecanoic acid

3-(18:0-O)-18:0:

(R)-3-(octadecanoyloxy)octadecanoic acid.

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Acknowledgements

The author gratefully acknowledges Science Foundation Ireland (grant no. 08/SRC/B1393) and the EU Marie Curie Programme (grant no. MTKD-CT-2005-029774) for financial support of his research.

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  1. Laboratory of Molecular Biochemistry, Microbiology, School of Natural Sciences, National University of Ireland, Galway, Ireland

    Anthony P. Moran

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  1. Dept. Biochemistry, Jiangnan University, Wuxi, Jiangsu, 214122, China, People's Republic

    Xiaoyuan Wang

  2. European Southern Observatory (ESO), Karl-Schwarzschild-Str. 2, Garching, 85748, Germany

    Peter J. Quinn

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Moran, A.P. (2010). The Role of Endotoxin in Infection: Helicobacter pylori and Campylobacter jejuni . In: Wang, X., Quinn, P. (eds) Endotoxins: Structure, Function and Recognition. Subcellular Biochemistry, vol 53. Springer, Dordrecht. https://doi.org/10.1007/978-90-481-9078-2_10

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