The GroEL-like protein from Campylobacter rectus: immunological characterization and interleukin-6 and -8 induction in human gingival fibroblast

Hinode, D

doi:10.1016/s0378-1097(98)00359-0

Cited by 28 publications

(43 citation statements)

References 17 publications

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“…Bacterial GroEL heat shock proteins are a conserved group of chaperonins whose function to mediate protein folding has made them widely essential to resist various stressors such as extreme temperatures or nutrient limitation (164,265,348). Interestingly, although no member of the GroEL family bears any discernible secretion signal, overwhelming evidence indicates that surface-exposed or secreted GroEL plays a key role in the infection strategies of many bacterial pathogens (35,181,184; reviewed in reference 174). As an example, the corresponding homolog of Legionella pneumophila is known to be displayed on the bacterial surface, where it promotes an invasive phenotype, and the same protein apparently manipulates cellular trafficking, cytoskeleton, and signaling once it is released inside the eukaryotic host cell (recently reviewed in reference 153).…”

Section: The Primary Nichementioning

confidence: 99%

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

2012

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SUMMARY Bartonella spp. are facultative intracellular pathogens that employ a unique stealth infection strategy comprising immune evasion and modulation, intimate interaction with nucleated cells, and intraerythrocytic persistence. Infections with Bartonella are ubiquitous among mammals, and many species can infect humans either as their natural host or incidentally as zoonotic pathogens. Upon inoculation into a naive host, the bartonellae first colonize a primary niche that is widely accepted to involve the manipulation of nucleated host cells, e.g., in the microvasculature. Consistently, in vitro research showed that Bartonella harbors an ample arsenal of virulence factors to modulate the response of such cells, gain entrance, and establish an intracellular niche. Subsequently, the bacteria are seeded into the bloodstream where they invade erythrocytes and give rise to a typically asymptomatic intraerythrocytic bacteremia. While this course of infection is characteristic for natural hosts, zoonotic infections or the infection of immunocompromised patients may alter the path of Bartonella and result in considerable morbidity. In this review we compile current knowledge on the molecular processes underlying both the infection strategy and pathogenesis of Bartonella and discuss their connection to the clinical presentation of human patients, which ranges from minor complaints to life-threatening disease.

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Section: The Primary Nichementioning

confidence: 99%

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

2012

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“…Despite being highly homologous between prokaryotic and eukaryotic cells, hsp60s are strongly immunogenic, and immune responses to microbial hsp60s are speculated to initiate chronic inflammatory diseases in which autoimmune responses to human hsp 60 may be central to pathogenesis (16). Major periodontopathic bacteria such as Porphyromonas gingivalis (13,19), Actinobacillus actinomycetemcomitans (21), Fusobacterium nucleatum (37), Prevotella intermedia (37), Bacteroides forsythus (37), and Campylobacter rectus (11) are reported to produce hsp's homologous to Escherichia coli GroEL. We have previously demonstrated that the frequency of seropositivity and titers of antibodies to human hsp60 and P. gingivalis GroEL were significantly higher in periodontitis patients than in periodontally healthy control subjects (29).…”

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confidence: 99%

Accumulation of Human Heat Shock Protein 60-Reactive T Cells in the Gingival Tissues of Periodontitis Patients

et al. 2002

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Heat shock protein 60s (hsp60) are remarkably immunogenic, and both T-cell and antibody responses to hsp60 have been reported in various inflammatory conditions. To clarify the role of hsp60 in T-cell responses in periodontitis, we examined the proliferative response of peripheral blood mononuclear cells (PBMC), as well as the cytokine profile and T-cell clonality, for periodontitis patients and controls following stimulation with recombinant human hsp60 and Porphyromonas gingivalis GroEL. To confirm the infiltration of hsp60-reactive T-cell clones into periodontitis lesions, nucleotide sequences within complementarity-determining region 3 of the T-cell receptor (TCR) ␤-chain were compared between hsp60-reactive peripheral blood T cells and periodontitis lesion-infiltrating T cells. Periodontitis patients demonstrated significantly higher proliferative responses of PBMC to human hsp60, but not to P. gingivalis GroEL, than control subjects. The response was inhibited by anti-major histocompatibility complex class II antibodies. Analysis of the nucleotide sequences of the TCR demonstrated that human hsp60-reactive T-cell clones and periodontitis lesion-infiltrating T cells have the same receptors, suggesting that hsp60-reactive T cells accumulate in periodontitis lesions. Analysis of the cytokine profile demonstrated that hsp60-reactive PBMC produced significant levels of gamma interferon (IFN-␥) in periodontitis patients, whereas P. gingivalis GroEL did not induce any skewing toward a type1 or type2 cytokine profile. In control subjects no significant expression of IFN-␥ or interleukin 4 was induced. These results suggest that periodontitis patients have human hsp60-reactive T cells with a type 1 cytokine profile in their peripheral blood T-cell pools.

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“…In addition to participating in bacterial adhesion, HSPs have been shown to have cell-cell signaling properties and are able to modulate the activity of host cells. The actions of bacterial HSPs on host cells include inducing the synthesis of pro-inflammatory cytokines (74,75). HSPs have also been reported to promote apoptosis and this effect is likely to inhibit host antibacterial responses (73).…”

Section: Heat-shock Proteinsmentioning

confidence: 99%

Bacterial pathogenesis and mediators in apical periodontitis

2007

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Apical periodontitis is a group of inflammatory diseases caused by microorganisms (mainly bacteria) infecting the necrotic root canal system. The pathogenesis of different types of apical periodontitis and even the same type in different individuals is unlikely to follow a stereotyped fashion with regard to the involved bacterial mediators. Disease pathogenesis is rather complex and involves a multitude of bacteria-and host-related factors. This review article discusses the bacterial pathogenesis of acute and chronic apical periodontitis, with the main focus on the bacterial mediators conceivably involved in the different stages of the infectious process, including secreted products (enzymes, exotoxins, N-formyl-methionyl-leucyl-phenylalanine peptides, heat-shock proteins and metabolic end-products) and structural components (lipopolysaccharide, peptidoglycan, lipoteichoic acid, lipoproteins, fimbriae, flagella, outer membrane proteins and vesicles, DNA, and exopolysaccharides). Knowledge of the bacterial factors involved in the pathogenesis of apical periodontitis is important to the understanding of the disease process and to help establishing proper therapeutic measures to inactivate this bacterial "artillery".

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The GroEL-like protein from Campylobacter rectus: immunological characterization and interleukin-6 and -8 induction in human gingival fibroblast

Cited by 28 publications

References 17 publications

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

Intruders below the Radar: Molecular Pathogenesis of Bartonella spp

Accumulation of Human Heat Shock Protein 60-Reactive T Cells in the Gingival Tissues of Periodontitis Patients

Bacterial pathogenesis and mediators in apical periodontitis

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