Inhibition of Neutrophil Migration at the Site of Infection Increases Remote Organ Neutrophil Sequestration and Injury

Mercer-Jones, Mark; Heinzelmann, Michael; Peyton, James C.; Wickel, Dean J.; Cook, Marty; Cheadle, William G.

doi:10.1097/00024382-199709000-00007

Cited by 56 publications

(35 citation statements)

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“…It is therefore conceivable that enhanced production of LTB 4 may also contribute to up-regulation of Mac-1 on IFNARI-deficient neutrophils, thereby further supporting neutrophil migration to the infected peritoneal cavity. Consistent with this notion, Mac-1 was shown to be involved in the immigration of immune cells into the peritoneal cavity during septic peritonitis (36).…”

Section: Discussionmentioning

confidence: 55%

“…2b show that neutrophil production of reactive oxygen intermediates was significantly increased in IFNARI Ϫ/Ϫ mice as compared with wild-type controls. Moreover, cell surface density of the integrin CD11b/CD18 (Mac-1), which has been implicated in neutrophil recruitment during peritonitis (36), was significantly greater on IFNARI-deficient than wild-type neutrophils (Fig. 2c).…”

Section: Enhanced Innate Immune Defense Against Polymicrobial Peritonmentioning

confidence: 95%

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Type I IFN Modulates Host Defense and Late Hyperinflammation in Septic Peritonitis

Weighardt

Kaiser-Moore

Schlautkötter

et al. 2006

The Journal of Immunology

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TLRs are considered important for the control of immune responses during endotoxic shock or polymicrobial sepsis. Signaling by TLRs may proceed through the adapter proteins MyD88 or TIR domain-containing adaptor inducinng IFN-β. Both pathways can lead to the production of type I IFNs (IFN-αβ). In the present study, the role of the type I IFN pathway for host defense and immune pathology in sepsis was investigated using a model of mixed bacterial peritonitis. Systemic levels of IFN-αβ protein were markedly elevated during septic peritonitis. More detailed analyses revealed production of IFN-β, but not IFN-α subtypes, and identified CD11b+CD11c− macrophage-like cells as major producers of IFN-β. The results further demonstrate that in IFN-αβ receptor I chain (IFNARI)-deficient mice, the early recruitment of neutrophils to the infected peritoneal cavity was augmented, most likely due to an increased local production of MCP-1 and leukotriene B4. In the absence of IFNARI, peritoneal neutrophils also exhibited enhanced production of reactive oxygen intermediates and elevated expression of Mac-1. Conversely, administration of recombinant IFN-β resulted in reduced leukotriene B4 levels and decreased peritoneal neutrophil recruitment and activation. Analysis of the cytokine response to septic peritonitis revealed that IFNARI deficiency strongly attenuated late, but not early, hyperinflammation. In accordance with these findings, bacterial clearance and overall survival of IFNARI−/− mice were improved. Therefore, the present study reveals critical functions of the type I IFN pathway during severe mixed bacterial infections leading to sepsis. The results suggest that type I IFN exerts predominantly adverse effects under these conditions.

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Section: Discussionmentioning

confidence: 55%

Section: Enhanced Innate Immune Defense Against Polymicrobial Peritonmentioning

confidence: 95%

Type I IFN Modulates Host Defense and Late Hyperinflammation in Septic Peritonitis

Weighardt

Kaiser-Moore

Schlautkötter

et al. 2006

The Journal of Immunology

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“…Neutrophil apoptosis in patients with both infective and noninfective insultselicited systemic inflammatory response syndrome (SIRS) decreases significantly [125,126]. Because lung and liver damage can be attenuated by antineutrophil treatment, delayed neutrophil death might contribute to the organ damage SIRS [127][128][129]. In addition, a variety of autoimmune/rheumatic diseases such as crystalline arthritis [130,131], inflammatory bowel disease [132], and rheumatoid arthritis [133,134] are associated with the decreased propensity of neutrophils, leading towards apoptosis.…”

Section: Neutrophil Apoptosis In Inflammatory and Immunological Diseasesmentioning

confidence: 99%

Constitutive neutrophil apoptosis: Mechanisms and regulation

2007

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Neutrophil constitutive death is a critical cellular process for modulating neutrophil number and function, and it plays an essential role in neutrophil homeostasis and the resolution of inflammation. Neutrophils die due to programmed cell death or apoptosis. In this article, we review recent studies on the mechanism of neutrophil apoptosis. The involvement of caspase, calpain, reactive oxygen species, cellular survival/death signaling pathways, mitochondria, and BCL-2 family member proteins are discussed. The fate of neutrophils can be influenced within the inflammatory microenvironment. We summarize the current understanding regarding the modulation of neutrophil apoptotic death by various extracellular stimuli such as proinflammatory cytokines, cell adhesion, phagocytosis, red blood cells, and platelets. The involvement of neutrophil apoptosis in infectious and inflammatory diseases is also addressed. Am. J. Hematol. 83:288-295, 2008. V

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“…3B). CD11b is up-regulated rapidly upon neutrophil activation and has been implicated in neutrophil recruitment during peritonitis [28,30].…”

Section: Trifmentioning

confidence: 99%

Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response

Reim

Rossmann-Bloeck

Jusek

et al. 2011

Journal of Leukocyte Biology

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Inhibition of Neutrophil Migration at the Site of Infection Increases Remote Organ Neutrophil Sequestration and Injury

Cited by 56 publications

References 0 publications

Type I IFN Modulates Host Defense and Late Hyperinflammation in Septic Peritonitis

Type I IFN Modulates Host Defense and Late Hyperinflammation in Septic Peritonitis

Constitutive neutrophil apoptosis: Mechanisms and regulation

Improved host defense against septic peritonitis in mice lacking MyD88 and TRIF is linked to a normal interferon response

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