Roles of endogenous cytokines in liver apoptosis of mice in lethal Listeria monocytogenes infection

Miura, T

doi:10.1016/s0928-8244(00)00175-9

Cited by 11 publications

(16 citation statements)

References 22 publications

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“…Apoptosis in response to infection with whole, viable L. monocytogenes has been described in hepatocytes [328][329][330], epithelial cells [128], CD4 + T cells, CD8 + T cells, and B lymphocytes [125,130,134], neurons, Purkinje cells [127], dendritic cells [124,331], and natural killer (NK) cells [129] but not in macrophages [8,124,332]. Whether intracellular Listeriae actively impede PCD in macrophages to preserve their intracellular niche is an interesting and unresolved question [333].…”

Section: Streptococcus Sppmentioning

confidence: 99%

“…TNF-α appears to be crucial in directing a separate, CD8 + T-lymphocytemediated PCD pathway in hepatocytes in the absence of perforin and FAS [350]. Miura et al (2000), however, reported that TNF-α and IL-6 play a protective role in mediating survival of hepatocytes during listeriosis [329]. In support of this finding, pancreatic cells in mice lacking TRp55, a key receptor for TNF-α, are prone to PCD triggered by L. monocytogenes [351].…”

Section: Streptococcus Sppmentioning

confidence: 99%

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Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity

Ulett

Adderson²

2006

CIR

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Apoptosis, or programmed cell death (PCD), is an important physiological mechanism, through which the human immune system regulates homeostasis and responds to diverse forms of cellular damage. PCD may also be involved in immune counteraction to microbial infection. Over the past decade, the amount of research on bacteria-induced PCD has grown tremendously, and the implications of this mechanism on immunity are being elucidated. Some pathogenic bacteria actively trigger the suicide response in critical lineages of leukocytes that orchestrate both the innate and adaptive immune responses; other bacteria proactively prevent PCD to benefit their own survival and persistence. Currently, the microbial virulence factors, which represent the keys to unlocking the suicide response in host cells, are a primary focus of this field. In this review, we discuss these bacterial "apoptosis regulatory molecules" and the apoptotic events they either trigger or prevent, the host target cells of this regulatory activity, and the possible ramifications for immunity to infection. Gram-positive pathogens including Staphylococcus, Streptococcus, Bacillus, Listeria, and Clostridia species are discussed as important agents of human infection that modulate PCD pathways in eukaryotic cells.

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Section: Streptococcus Sppmentioning

confidence: 99%

Section: Streptococcus Sppmentioning

confidence: 99%

Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity

Ulett

Adderson²

2006

CIR

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“…In particular, the production of proinflammatory cytokines such as TNF-a and IFN-g and the recruitment of inflammatory monocytes to sites of infection are crucial for the early control of L. monocytogenes (32,33). Infection also leads to robust production of IL-6, and IL-6 deficiency or IL-6 neutralization with Abs results in enhanced susceptibility to L. monocytogenes (6,(34)(35)(36)(37)(38)(39)(40)(41); however, mechanisms of IL-6-mediated protection are so far unclear.…”

mentioning

confidence: 99%

IL-6 Controls the Innate Immune Response against Listeria monocytogenes via Classical IL-6 Signaling

Hoge

Yan

Jänner

et al. 2013

The Journal of Immunology

132

107

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The cytokine IL-6 plays a protective role in immune responses against bacterial infections. However, the mechanisms of IL-6–mediated protection are only partially understood. IL-6 can signal via the IL-6R complex composed of membrane-bound IL-6Rα (mIL-6Rα) and gp130. Owing to the restricted expression of mIL-6Rα, classical IL-6 signaling occurs only in a limited number of cells such as hepatocytes and certain leukocyte subsets. IL-6 also interacts with soluble IL-6Rα proteins and these IL-6/soluble IL-6Rα complexes can subsequently bind to membrane-bound gp130 proteins and induce signaling. Because gp130 is ubiquitously expressed, this IL-6 trans-signaling substantially increases the spectrum of cells responding to IL-6. In this study, we analyze the role of classical IL-6 signaling and IL-6 trans-signaling in the innate immune response of mice against Listeria monocytogenes infection. We demonstrate that L. monocytogenes infection causes profound systemic IL-6 production and rapid loss of IL-6Rα surface expression on neutrophils, inflammatory monocytes, and different lymphocyte subsets. IL-6–deficient mice or mice treated with neutralizing anti–IL-6 mAb displayed impaired control of L. monocytogenes infection accompanied by alterations in the expression of inflammatory cytokines and chemokines, as well as in the recruitment of inflammatory cells. In contrast, restricted blockade of IL-6 trans-signaling by application or transgenic expression of a soluble gp130 protein did not restrain the control of infection. In summary, our results demonstrate that IL-6Rα surface expression is highly dynamic during the innate response against L. monocytogenes and that the protective IL-6 function is dependent on classical IL-6 signaling via mIL-6Rα.

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“…Secretion of TNF-␣ has been shown to be critical for the resolution of a variety of bacterial, fungal, and parasitic infections. The absence of TNF-␣ bioactivity results in significant increases in mortality which correlate with an inability to clear the infectious agent (10,17,22,26,43,45,48). Conversely, excessive TNF-␣ production in the context of systemic bacterial infection, abdominal sepsis, or endotoxemia results in increased mortality and organ injury (20,21,36,46).…”

mentioning

confidence: 99%

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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Roles of endogenous cytokines in liver apoptosis of mice in lethal Listeria monocytogenes infection

Cited by 11 publications

References 22 publications

Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity

Regulation of Apoptosis by Gram-Positive Bacteria: Mechanistic Diversity and Consequences for Immunity

IL-6 Controls the Innate Immune Response against Listeria monocytogenes via Classical IL-6 Signaling

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

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