title: Campylobacter surface-layers (S-layers) and immune evasion.
abstract: Many pathogenic bacteria have evolved mechanisms for evading host immune systems. One evasion mechanism is manifest by the surface layer (S-layer), a paracrystalline protein structure composed of S-layer proteins (SLPs). The S-layer, possessed by 2 Campylobacter species (C. fetus and C. rectus), is external to the bacterial outer membrane and can have multiple functions in immune avoidance. C. fetus is a pathogen of ungulates and immunocompromised humans, in whom it causes disseminated bloodstream disease. In C. fetus, the S-layer is required for dissemination and is involved in 2 mechanisms of evasion. First, the S-layer confers resistance to complement-mediated killing in non-immune serum by preventing the binding of complement factor C3b to the C. fetus cell surface. S-layer expressing C. fetus strains remain susceptible to complement-independent killing, utilizing opsonic antibodies directed against the S-layer. However, C. fetus has also evolved a mechanism for avoiding antibody-mediated killing by high-frequency antigenic variation of SLPs. Antigenic variation is accomplished by complex DNA inversion events involving a family of multiple SLP-encoding genes and a single SLP promoter. Inversion events result in the expression of antigenically variant S-layers, which require distinct antibody responses for killing. C. rectus is implicated in the pathogenesis of periodontal disease and also possesses an S-layer that appears to be involved in evading the human system. Although studied less extensively than its C. fetus counterpart, the C. rectus S-layer appears to confer resistance to complement-mediated killing and to cause the down-regulation of proinflammatory cytokines.
authors: Department of Biochemistry and Molecular Biology, Medical College of Georgia, Augusta, Georgia 30912, USA. stthomps@mail.mcg.edu
authors: Stuart A
authors: SA
authors: Thompson
mesh_terms: D000940:Antigenic Variation / Q000235:genetics*; D000942:Antigens, Bacterial / Q000235:genetics / Q000276:immunology; D001426:Bacterial Proteins / Q000235:genetics / Q000276:immunology*; D001770:Blood Bactericidal Activity; D002168:Campylobacter fetus / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D044883:Campylobacter rectus / Q000235:genetics / Q000276:immunology* / Q000472:pathogenicity; D007446:Chromosome Inversion; D003176:Complement C3 / Q000037:antagonists & inhibitors; D016207:Cytokines / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D004269:DNA, Bacterial / Q000378:metabolism; D015964:Gene Expression Regulation, Bacterial; D006801:Humans; D018836:Inflammation Mediators / Q000037:antagonists & inhibitors*; D008562:Membrane Glycoproteins / Q000235:genetics / Q000276:immunology*; D010510:Periodontal Diseases / Q000276:immunology / Q000382:microbiology*; D010587:Phagocytosis; D014774:Virulence
chemical_list: D000942:Antigens, Bacterial; D001426:Bacterial Proteins; D003176:Complement C3; D016207:Cytokines; D004269:DNA, Bacterial; D018836:Inflammation Mediators; D008562:Membrane Glycoproteins; C055764:S-layer proteins