Properties of Yersinia enterocolitica porins: interference with biological functions of phagocytes, nitric oxide production and selective cytokine release

Tufano, Maria Antonietta; Rossano, Fabio; Catalanotti, P; Liguori, Giovanna; Marinelli, A.; Baroni, Adone; Marinelli, Paolo

doi:10.1016/0923-2508(94)90185-6

Cited by 32 publications

(28 citation statements)

References 45 publications

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“…The precise role of NO in Yersinia infection has not been clearly defined, although a number of in vitro studies have suggested that the production of NO might contribute to the resolution of the infection (34,42). In the present study, the decreased serum NO production correlated with less efficient bacterial clearance in vivo in TNFRp55Ϫ/Ϫ mice, implying a critical role for NO in resistance to Yersinia infection.…”

Section: Discussionsupporting

confidence: 48%

Tumor necrosis factor receptor p55 controls the severity of arthritis in experimental Yersinia enterocolitica infection

Zhao

Zhang

Chiu

et al. 1999

Arthritis & Rheumatism

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Objective. To dissect the host defense mechanisms in relation to the development of Yersiniaassociated arthritis by evaluating the impact of tumor necrosis factor receptor p55 (TNFRp55) deficiency on Yersinia enterocolitica infection.Methods. TNFRp55؊/؊ and C57BL/6 mice were inoculated intravenously with arthritogenic strain 8081 of Y enterocolitica serotype 0:8. Mice were observed daily for generating survival curves and monitoring arthritis. In subsequent sets of experiments, mice were sacrificed at day 14 after infection for examination of histopathology of joints, bacterial clearance, macrophage microbicidal activity, nitric oxide (NO) production, oxidative burst generation, and cytokine production.Results. There was an 80% mortality rate in TNFRp55؊/؊ mice compared with 25% in the controls at 8 weeks after inoculation with 70 colony-forming units of Y enterocolitica 0:8. Histologic examination of joint tissues revealed that TNFRp55؊/؊ mice developed more severe arthritis, including cartilage degradation and bony destruction, than controls at day 14 after infection. The more extensive joint pathology in TNFRp55؊/؊ mice was correlated with the higher bacterial load in liver, spleen, and lungs, and with the increased levels of interleukin-10. TNFRp55؊/؊ mice displayed impaired intracellular killing of bacteria by macrophages. This was associated with decreased NO production and impaired oxidative burst activity.Conclusion. This study demonstrates that TNF signaling through TNFRp55 controls the severity of Yersinia-induced arthritis and implicates TNF-mediated macrophage microbicidal activity as a central event in this process.

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Section: Discussionsupporting

confidence: 48%

Tumor necrosis factor receptor p55 controls the severity of arthritis in experimental Yersinia enterocolitica infection

Zhao

Zhang

Chiu

et al. 1999

Arthritis & Rheumatism

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“…Tufano and coworkers showed that porins from Yersinia enterocelitica and Helicobacter pylori bind to PMN and that this results in altered cell morphology, reduced surface hydrophobicity, and adherence, accompanied by a reduction of oxidative burst and chemotaxis (56,57). These studies also showed, as we did for gonococcal porin, that the porins of these organisms may inhibit granule exocytosis and the subsequent release of reactive oxygen metabolites.…”

Section: Discussionmentioning

confidence: 99%

Neisseria gonorrhoeaePorin Modifies the Oxidative Burst of Human Professional Phagocytes

et al. 2000

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A hallmark of infection with the gram-negative bacterium Neisseria gonorrhoeae is the local infiltration and subsequent activation of polymorphonuclear neutrophils. Several gonococcal outer membrane proteins are involved in the interaction with and the activation of these phagocytes, including gonococcal porin, the most abundant protein in the outer membrane. Previous work suggests that this porin plays a role in various cellular processes, including inhibiting neutrophils activation and phagosome maturation in professional phagocytes. Here we investigated the ability of porin to modify the oxidative metabolism of human peripheral blood neutrophils and monocytes in response to particulate stimuli (including live gonococci) and soluble agents. The activation of the oxidative metabolism was determined by chemiluminescence amplified with either luminol or lucigenin. We found that treatment of the phagocytes with porin inhibits the release of reactive oxygen species measured as luminol-enhanced chemiluminescence in response to zymosan, latex particles, and gonococci. The engulfment of these particles was not, however, affected by porin treatment. Similar effects of porin on the chemiluminescence response were observed in cytochalasin B-treated neutrophils exposed to the soluble chemotactic peptide N-formylmethionyl-leucyl-phenylalanine. This indicates that porin selectively inhibits granule fusion with those cellular membranes that are in direct contact with porin, namely, the phagosomal and plasma membranes. This porin-induced downregulation of oxidative metabolism may be a potent mechanism by which gonococci modulate oxygen-dependent reactions by activated phagocytes at inflammation sites.Professional phagocytes such as polymorphonuclear neutrophils (PMN) and peripheral blood monocytes play a crucial role in the host defense against infection with microorganisms.

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“…The protein composition of vesicles can vary substantially with the bacterial strain of origin and with the environment (87). Prominent OM proteins such as porins are known to promote proinflammatory activities in a variety of Gram-negative pathogens, including H. pylori, Salmonella, Fusobacterium, and Yersinia species (38,39,126,130,131). Recently, the OM adhesin of N. meningitidis, NadA, was shown to be required for the optimal activation of macrophage responses.…”

Section: Vesicle-mediated Activation Of Inflammation and Innate Immunitymentioning

confidence: 99%

“…Bacteriocin, fimbrial adhesin, pore-forming protein, chitinase (79) Chitinase activity, insecticidal (79) a In addition to proinflammatory properties of endotoxin and porins (130,131). b Abbreviations not defined in the text: AC-Hly, adenylate cyclase-hemolysin; FHA, filamentous hemagglutinin; CDT cytolethal distending toxin; OMP, outer membrane protein; PLC-N, phospholipase, nonhemolytic; UPEC, uropathogenic E. coli; CNF1, cytotoxic necrotizing factor 1; ND, not determined.…”

Section: Xenorhabdus Nematophilusmentioning

confidence: 99%

Virulence and Immunomodulatory Roles of Bacterial Outer Membrane Vesicles

Ellis

Kuehn

2010

Microbiol Mol Biol Rev

807

736

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SUMMARY Outer membrane (OM) vesicles are ubiquitously produced by Gram-negative bacteria during all stages of bacterial growth. OM vesicles are naturally secreted by both pathogenic and nonpathogenic bacteria. Strong experimental evidence exists to categorize OM vesicle production as a type of Gram-negative bacterial virulence factor. A growing body of data demonstrates an association of active virulence factors and toxins with vesicles, suggesting that they play a role in pathogenesis. One of the most popular and best-studied pathogenic functions for membrane vesicles is to serve as natural vehicles for the intercellular transport of virulence factors and other materials directly into host cells. The production of OM vesicles has been identified as an independent bacterial stress response pathway that is activated when bacteria encounter environmental stress, such as what might be experienced during the colonization of host tissues. Their detection in infected human tissues reinforces this theory. Various other virulence factors are also associated with OM vesicles, including adhesins and degradative enzymes. As a result, OM vesicles are heavily laden with pathogen-associated molecular patterns (PAMPs), virulence factors, and other OM components that can impact the course of infection by having toxigenic effects or by the activation of the innate immune response. However, infected hosts can also benefit from OM vesicle production by stimulating their ability to mount an effective defense. Vesicles display antigens and can elicit potent inflammatory and immune responses. In sum, OM vesicles are likely to play a significant role in the virulence of Gram-negative bacterial pathogens.

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Properties of Yersinia enterocolitica porins: interference with biological functions of phagocytes, nitric oxide production and selective cytokine release

Cited by 32 publications

References 45 publications

Tumor necrosis factor receptor p55 controls the severity of arthritis in experimental Yersinia enterocolitica infection

Tumor necrosis factor receptor p55 controls the severity of arthritis in experimental Yersinia enterocolitica infection

Neisseria gonorrhoeaePorin Modifies the Oxidative Burst of Human Professional Phagocytes

Virulence and Immunomodulatory Roles of Bacterial Outer Membrane Vesicles

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