Tumor Necrosis Factor Receptor p55-Deficient Mice Respond to Acute<i>Yersinia enterocolitica</i>Infection with Less Apoptosis and More Effective Host Resistance

Zhao, Yi‐Xue; Lajoie, Ginette; Zhang, Hongwei; Chiu, Brian; Payne, Ursula; Inman, Robert D.

doi:10.1128/iai.68.3.1243-1251.2000

Cited by 28 publications

(20 citation statements)

References 55 publications

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“…Interestingly, when spleen cells taken from TNFR1-deficient mice at day 1 postinfection were cultured in a parallel manner, no enhanced IFN-␥ secretion was observed, suggesting that mechanisms inducing increased IFN-␥ production are activated later in the infection. These data are similar to those reported by Zhao et al for a systemic Yersinia enterocolitica infection model (50). They reported enhanced IFN-␥ production by mitogen-activated splenocytes from TNFR1-deficient animals following infection.…”

Section: Figsupporting

confidence: 81%

Increased Mortality and Dysregulated Cytokine Production in Tumor Necrosis Factor Receptor 1-Deficient Mice following SystemicKlebsiella pneumoniaeInfection

et al. 2003

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A significant clinical complication of pulmonary infections with Klebsiella pneumoniae is peripheral blood dissemination, resulting in a systemic infection concurrent with the localized pulmonary infection. In this context, little is known about the role of tumor necrosis factor receptor 1 (TNFR1)-mediated innate immune responses during systemic Klebsiella infections. Mice lacking TNFR1 were significantly more susceptible to Klebsiella-induced mortality following intravenous inoculation. Bacterial clearance was impaired in TNFR1-deficient mice at early times following infection. Unexpectedly, bacterial burdens at the onset of mortality (days 2 to 3 postinfection) were not higher in mice lacking TNFR1. However, elevated production of liver-associated proinflammatory cytokines (interleukin-12, tumor necrosis factor alpha [TNF-␣[, and gamma interferon [IFN-␥]) and chemokines (MIP-1␣, MIP-2, and MCP-1) was observed within the first 24 h of infection. Additionally, excessive plasma-associated IFN-␥ was also observed late in the course of infection (day 3). Spleen cells from day-3 infected TNFR1-deficient mice secreted markedly enhanced levels of IFN-␥ when cultured in vitro. Additionally, there was a marked increase in the total number of activated lymphocyte subsets as indicated by CD69 upregulation. A notable exception was the sharp decrease in the frequency of splenic NK T cells in infected TNFR1 knockout (KO) mice. Anti-TNF-␣ therapy in TNFR1 KO mice significantly reduced chemokine production and liver injury. Combined, these data indicate a dysregulated antibacterial host response following intravenous Klebsiella infection in the absence of TNFR1 signaling, resulting in heightened cytokine production and hyperactivation of specific splenic lymphocyte subsets.

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Section: Figsupporting

confidence: 81%

Increased Mortality and Dysregulated Cytokine Production in Tumor Necrosis Factor Receptor 1-Deficient Mice following SystemicKlebsiella pneumoniaeInfection

et al. 2003

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“…There is some evidence that TNF-␣ genotypes which seem to be associated with low TNF-␣ production are present at a higher percentage in ReA (180). Also, mice that are knockouts of the p55 receptor are more susceptible to infection by Yersinia and develop more severe arthritis (234). Impaired peripheral-blood T-cell responses to ReA-triggering agents have been demonstrated.…”

Section: Immune Response To Bacteriamentioning

confidence: 97%

HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

2004

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Current evidence supports the concept that reactive arthritis (ReA) is an immune-mediated synovitis resulting from slow bacterial infections and showing intra-articular persistence of viable, nonculturable bacteria and/or immunogenetic bacterial antigens synthesized by metabolically active bacteria residing in the joint and/or elsewhere in the body. The mechanisms that lead to the development of ReA are complex and basically involve an interaction between an arthritogenic agent and a predisposed host. The way in which a host accommodates to invasive facultative intracellular bacteria is the key to the development of ReA. The details of the molecular pathways that explain the articular and extra-articular manifestations of the disease are still under investigation. Several studies have been done to gain a better understanding of the pathogenesis of ReA; these constitute the basis for a more rational therapeutic approach to this disease

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“…One of the underlying mechanisms explaining the salutary course in these mice was a reduction in lymphocyte apoptosis. In addition, TNFR1 -/-mice infected with Yersinia enterocolitica manifest an enhanced clearance of bacteria in association with a decrease in apoptosis of CD4 + lymphocytes (61). The weight of evidence in bacterial disease processes suggests that there is a direct correlation between the magnitude of apoptosis and severity of infection.…”

Section: Figurementioning

confidence: 99%

Apoptosis modulates protective immunity to the pathogenic fungus Histoplasma capsulatum

Allen

Deepe²

2005

Journal of Clinical Investigation

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Pathogen-induced apoptosis of lymphocytes is associated with increased susceptibility to infection. In this study, we determined whether apoptosis influenced host resistance to the fungus Histoplasma capsulatum. The level of apoptotic leukocytes progressively increased in the lungs of naive and immune mice during the course of H. capsulatum infection. T cells constituted the dominant apoptotic population. Apoptosis was diminished in H. capsulatum-infected gld/gld and TNF-α-deficient mice; concomitantly, the fungal burden exceeded that of controls. Treatment of naive and H. capsulatum-immune mice with caspase inhibitors decreased apoptosis but markedly enhanced the severity of infection. Administration of a proapoptotic dose of suramin diminished the fungal burden. The increased burden in recipients of a caspase inhibitor was associated with elevations in IL-4 and IL-10 levels. In the absence of either of these cytokines, caspase inhibition suppressed apoptosis but did not increase the fungal burden. Thus, apoptosis is a critical element of protective immunity to H. capsulatum. Production of IL-4 and IL-10 is markedly elevated when apoptosis is inhibited, and the release of these cytokines exacerbates the severity of infection.

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Tumor Necrosis Factor Receptor p55-Deficient Mice Respond to AcuteYersinia enterocoliticaInfection with Less Apoptosis and More Effective Host Resistance

Cited by 28 publications

References 55 publications

Increased Mortality and Dysregulated Cytokine Production in Tumor Necrosis Factor Receptor 1-Deficient Mice following SystemicKlebsiella pneumoniaeInfection

Increased Mortality and Dysregulated Cytokine Production in Tumor Necrosis Factor Receptor 1-Deficient Mice following SystemicKlebsiella pneumoniaeInfection

HLA-B27-Associated Reactive Arthritis: Pathogenetic and Clinical Considerations

Apoptosis modulates protective immunity to the pathogenic fungus Histoplasma capsulatum

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