Ultrastructure and biochemical studies of the flagellar sheath of Helicobacter pylori

Geis, G.; Suerbaum, Sebastian; Forsthoff, B.; Leying, Hermann; Opferkuch, W.

doi:10.1099/00222615-38-5-371

Cited by 107 publications

(79 citation statements)

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“…For example, Helicobacter produces a flagellin that is inherently less stimulatory than that of other organisms, and limits secretion of flagellin monomer into culture supernatants (68). Many species, including Vibrio and Helicobacter cloak their flagella in an outer membrane sheath (69,70). Finally, Pseudomonas strains recovered from cystic fibrosis patients with chronic infections have lost motility and are nonflagellated (71).…”

Section: Discussionmentioning

confidence: 99%

FliC-Specific CD4+ T Cell Responses Are Restricted by Bacterial Regulation of Antigen Expression

Cummings¹,

Barrett²,

Wilkerson³

et al. 2005

The Journal of Immunology

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Salmonella typhimurium, a facultatively intracellular pathogen, regulates expression of virulence factors in response to distinct environments encountered during the course of infection. We tested the hypothesis that the transition from extra- to intracellular environments during Salmonella infection triggers changes in Ag expression that impose both temporal and spatial limitations on the host T cell response. CD4+ T cells recovered from Salmonella immune mice were propagated in vitro using Ag derived from bacteria grown in conditions designed to emulate extra- or intracellular environments in vivo. Extracellular phase bacteria supported a dominant T cell response to the flagellar subunit protein FliC, whereas intracellular phase bacteria were unable to support expansion of FliC-specific T cells from populations known to contain T cells with reactivity to this Ag. This result was attributed to bacterial regulation of FliC expression: transcription and protein levels were repressed in bacteria growing in the spleens of infected mice. Furthermore, Salmonella-infected splenocytes taken directly ex vivo stimulated FliC-specific T cell clones only when intracellular FliC expression was artificially up-regulated. Although it has been suggested that a microanatomical separation of immune T cells and infected APC exists in vivo, we demonstrate that intracellular Salmonella can repress FliC expression below the T cell activation threshold. This potentially provides a mechanism for intracellular Salmonella at systemic sites to avoid detection by Ag-specific T cells primed at intestinal sites early in infection.

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Section: Discussionmentioning

confidence: 99%

FliC-Specific CD4+ T Cell Responses Are Restricted by Bacterial Regulation of Antigen Expression

Cummings¹,

Barrett²,

Wilkerson³

et al. 2005

The Journal of Immunology

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“…Inhibition of the FliA regulon may result from failure of the DflhB : cat mutant to export FlgM via the export apparatus. A sheath contiguous with the outer membrane surrounds the H. pylori flagellum (Geis et al, 1993), but this does not necessarily preclude FlgM secretion, since Vibrio cholerae, which also possesses a sheathed flagellum, secretes FlgM from the cytoplasm via the flagellar protein export apparatus (Correa et al, 2004). The FliA-dependent flaA9-9xylE reporter gene was expressed at levels near those of the wild-type in strains that produced the FlhB N265A or FlhB P266G variants, but these strains appear to be deficient in export of filamenttype substrates (Fig.…”

Section: Discussionmentioning

confidence: 99%

Helicobacter pylori FlhB processing-deficient variants affect flagellar assembly but not flagellar gene expression

2009

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Regulation of the Helicobacter pylori flagellar gene cascade involves the transcription factors s 54 (RpoN), employed for expression of genes required midway through flagellar assembly, and s 28 (FliA), required for expression of late genes. Previous studies revealed that mutations in genes encoding components of the flagellar protein export apparatus block expression of the H. pylori RpoN and FliA regulons. FlhB is a membrane-bound component of the export apparatus that possesses a large cytoplasmic domain (FlhB C ). The hook length control protein FliK interacts with FlhB C to modulate the substrate specificity of the export apparatus. FlhB C undergoes autocleavage as part of the switch in substrate specificity. Consistent with previous reports, deletion of flhB in H. pylori interfered with expression of RpoN-dependent reporter genes, while deletion of fliK stimulated expression of these reporter genes. In the DflhB mutant, disrupting fliK did not restore expression of RpoN-dependent reporter genes, suggesting that the inhibitory effect of the DflhB mutation is not due to the inability to export FliK. Amino acid substitutions (N265A and P266G) at the putative autocleavage site of H. pylori FlhB prevented processing of FlhB and export of filament-type substrates. The FlhB variants supported wild-type expression of RpoN-and FliA-dependent reporter genes. In the strain producing FlhB N265A , expression of RpoN-and FliA-dependent reporter genes was inhibited when fliK was disrupted. In contrast, expression of these reporter genes was unaffected or slightly stimulated when fliK was disrupted in the strain producing FlhB P266G. H. pylori HP1575 (FlhX) shares homology with the C-terminal portion of FlhB C (FlhB CC ) and can substitute for FlhB CC in flagellar assembly. Disrupting flhX inhibited expression of a flaB reporter gene in the wild-type but not in the DfliK mutant or strains producing FlhB variants, suggesting a role for FlhX or FlhB CC in normal expression of the RpoN regulon. Taken together, these data indicate that the mechanism by which the flagellar protein export apparatus exerts control over the H. pylori RpoN regulon is complex and involves more than simply switching substrate specificity of the flagellar protein export apparatus. INTRODUCTIONBacterial flagellar biosynthesis involves transcriptional hierarchies that coordinate flagellar gene expression with assembly. Flagellar gene hierarchies are well characterized in a few bacteria, including Salmonella enterica serovar Typhimurium (S. typhimurium) and Caulobacter crescentus (Chilcott & Hughes, 2000;Wu & Newton, 1997). Flagellar gene regulation in e-Proteobacteria, such as Helicobacter pylori and Campylobacter jejuni, shares some similarities with these established paradigms but also differs significantly. As in S. typhimurium, H. pylori flagellar genes required late in assembly, such as the major flagellin (FlaA) and filament cap protein, are transcribed by s 28 (FliA)-RNA polymerase holoenzyme (Kim et al., 1999;Leying et al., 1992), and, as in C....

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“…Little is known about the composition, formation, or function of flagellar sheaths, which are found in many bacteria, including marine Vibrio species, V. cholerae, B. bacteriovorus, and Helicobacter pylori (reviewed in reference 164). Evidence from these organisms suggests that the sheath contains both lipopolysaccharide and proteins and that it may exist as a stable membrane domain distinct from the outer membrane (42,51,58,69,144). The lipid content of the sheath of B. bacteriovorus is distinct from that of the outer membrane, and the sheath appears to be a highly fluid, symmetric bilayer (179).…”

Section: The Sheathmentioning

confidence: 99%

Polar Flagellar Motility of the Vibrionaceae

McCarter

2001

Microbiol Mol Biol Rev

309

356

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Polar flagella of Vibrio species can rotate at speeds as high as 100,000 rpm and effectively propel the bacteria in liquid as fast as 60 μm/s. The sodium motive force powers rotation of the filament, which acts as a propeller. The filament is complex, composed of multiple subunits, and sheathed by an extension of the cell outer membrane. The regulatory circuitry controlling expression of the polar flagellar genes of members of the Vibrionaceae is different from the peritrichous system of enteric bacteria or the polar system of Caulobacter crescentus. The scheme of gene control is also pertinent to other members of the gamma purple bacteria, in particular to Pseudomonas species. This review uses the framework of the polar flagellar system of Vibrio parahaemolyticus to provide a synthesis of what is known about polar motility systems of the Vibrionaceae. In addition to its propulsive role, the single polar flagellum of V. parahaemolyticus is believed to act as a tactile sensor controlling surface-induced gene expression. Under conditions that impede rotation of the polar flagellum, an alternate, lateral flagellar motility system is induced that enables movement through viscous environments and over surfaces. Although the dual flagellar systems possess no shared structural components and although distinct type III secretion systems direct the simultaneous placement and assembly of polar and lateral organelles, movement is coordinated by shared chemotaxis machinery

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Ultrastructure and biochemical studies of the flagellar sheath of Helicobacter pylori

Cited by 107 publications

References 1 publication

FliC-Specific CD4+ T Cell Responses Are Restricted by Bacterial Regulation of Antigen Expression

FliC-Specific CD4+ T Cell Responses Are Restricted by Bacterial Regulation of Antigen Expression

Helicobacter pylori FlhB processing-deficient variants affect flagellar assembly but not flagellar gene expression

Polar Flagellar Motility of the Vibrionaceae

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