Interleukin-6 Delays Neutrophil Apoptosis

Biffl, Walter L.; Moore, Ernest E.; Moore, Frederick A.; Barnett, Carlton C.; Carl, Virginia S.; Peterson, Verlyn M.

doi:10.1001/archsurg.1996.01430130026005

Cited by 145 publications

(78 citation statements)

References 25 publications

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“…However, after the first week of joint inflammation, PMNs were still present in WT mice but absent in IL-6 Ϫ/Ϫ mice, and this suggests a protective effect of IL-6 on PMN survival. There is compelling evidence that STAT-3 is involved in the survival of PMNs (27,28), possibly by prevention of apoptosis. The role of IL-6 in the clearance of PMNs could, however, be far more complex, with IFN␥ contributing to the IL-6/sIL-6R-mediated clearance of PMNs from the site of inflammation (29).…”

Section: Discussionmentioning

confidence: 99%

Local activation of STAT‐1 and STAT‐3 in the inflamed synovium during zymosan‐induced arthritis: Exacerbation of joint inflammation in STAT‐1 gene–knockout mice

Hooge¹,

Loo²,

Koenders³

et al. 2004

Arthritis & Rheumatism

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Objective. STAT proteins play an important role in cytokine signaling. Some investigators have reported preferential activation of STAT-1, and others have reported preferential activation of STAT-3, in response to endogenous interleukin-6 (IL-6), in patients with rheumatoid arthritis. The present study was undertaken to investigate synovial STAT-1 and STAT-3 activation in an experimental animal model of arthritis.Methods. Zymosan was injected intraarticularly into naive wild-type (WT), IL-6 ؊/؊ , and STAT-1 ؊/؊ mice to induce arthritis. Western blots of synovial lysates were probed with phosphospecific antibodies to detect STAT-1/STAT-3 activation. Inflammation was assessed histologically. Synovial gene expression of the STATinduced feedback inhibitors suppressor of cytokine signaling 1 (SOCS-1) and SOCS-3 in WT and STAT-1 ؊/؊ mice was investigated by reverse transcriptasepolymerase chain reaction.Results. STAT-3 was activated in inflamed synovium of WT mice throughout the course of disease, whereas activated STAT-1 was observed only during the chronic phase. In IL-6 ؊/؊ mice, STAT activation was limited to STAT-3 on day 1. Although macrophage influx was not inhibited, disease went into remission after day 7 in IL-6 ؊/؊ mice. STAT-1 deficiency resulted in exacerbation of chronic joint inflammation and granuloma formation. In STAT-1 ؊/؊ mice, STAT-3 activation in the inflamed joints was unaltered as compared with WT mice. However, synovial SOCS-1, but not SOCS-3, gene expression was markedly reduced in STAT-1 ؊/؊ mice.Conclusion. The results in the IL-6 ؊/؊ mice suggest that STAT-3 is involved in the chronicity of ZIA. Exacerbation of arthritis in STAT-1 ؊/؊ mice suggests an opposing effect of STAT-1, i.e., suppression of joint inflammation. The expression of SOCS-1 could be the underlying mechanism by which STAT-1 controls joint inflammation.

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Section: Discussionmentioning

confidence: 99%

Local activation of STAT‐1 and STAT‐3 in the inflamed synovium during zymosan‐induced arthritis: Exacerbation of joint inflammation in STAT‐1 gene–knockout mice

Hooge¹,

Loo²,

Koenders³

et al. 2004

Arthritis & Rheumatism

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show abstract

“…In order to analyze mitochondrial depolarization, neutrophils were stained with the mitochondrial membrane potentialdependent lipophilic dye, JC-1 (5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolylcarbocyanine iodide) by using a DePsipher™ kit (Trevingen, Gaithersburg, MD, USA) (36). In brief, the neutrophils (10 6 cells/ml) were incubated in the absence or presence of HNP-1 (40 μg/ml) at 37˚C for 18 h in RPMI-1640-10% FBS.…”

Section: Detection Of Mitochondrial Membrane Potential Changementioning

confidence: 99%

“…It could be possible that pro-inflammatory cytokines (such as IL-1ß, TNF-·, IL-8, IL-6, IL-12p70 and MIP-3·) are produced and suppress neutrophil apoptosis during incubation with HNP-1, as these cytokines have the potential to repress neutrophil apoptosis (5,7,27,35,36). In order to test this possibility, we measured the cytokine production by neutrophils and mononuclear cells (10 6 cells/ml) after incubation with HNP-1 (40 μg/ml).…”

Section: Effects Of Hnp-1 On the Expression Of Truncated Bid Andmentioning

confidence: 99%

Evaluation of the effect of α-defensin human neutrophil peptides on neutrophil apoptosis

Nagaoka

Suzuki²,

Murakami³

et al. 2010

Int J Mol Med

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“…They are considered short-lived cells undergoing spontaneous apoptosis in vivo as well as in culture (Savill, 1997). In recent years it has become increasingly evident that culturing PMN in the presence of cytokines extends their life span (Colotta et al, 1992;Klebanoff et al, 1992;Lee et al, 1993;Biffl et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Human Leukocyte Antigen Class II in Stimulated Polymorphnuclear Neutrophils

Abdel-Salam¹

2012

Histocompatibility

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Interleukin-6 Delays Neutrophil Apoptosis

Abstract: Interleukin-6 delays PMN apoptosis, resulting in a larger population of surviving PMNs with a greater collective capacity for superoxide production. This could potentially facilitate PMN-mediated tissue injury and may be a mechanism whereby IL-6 contributes to organ dysfunction.

Cited by 145 publications

References 25 publications

Local activation of STAT‐1 and STAT‐3 in the inflamed synovium during zymosan‐induced arthritis: Exacerbation of joint inflammation in STAT‐1 gene–knockout mice

Local activation of STAT‐1 and STAT‐3 in the inflamed synovium during zymosan‐induced arthritis: Exacerbation of joint inflammation in STAT‐1 gene–knockout mice

Evaluation of the effect of α-defensin human neutrophil peptides on neutrophil apoptosis

Human Leukocyte Antigen Class II in Stimulated Polymorphnuclear Neutrophils

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