Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

Peterson, James W.; Feeback, Kevin D.; Baas, Joel H.; Pizza, Francis X.

doi:10.1152/japplphysiol.01453.2005

Cited by 64 publications

(59 citation statements)

References 46 publications

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“…While our present in vivo experiments do not directly determine the cell types contributing to the elevated cytokine production, previous reports have clearly shown that skeletal (Steensberg et al 2000;Keller et al 2001;Frost et al 2002Frost et al , 2003Lang et al 2003) and cardiac muscle (Saito & Papaconstantinou, 2001;Lang et al 2003;Vona-Davis et al 2003) produce numerous cytokines, including TNFα, IL-1β and IL-6, in response to LPS. Further, the modest inflammatory insult and the absence of elevations in TNFα (Peterson et al 2006) support a very limited influx of inflammatory cells into these tissues. Independent of the cell type producing these cytokines, these data show that the inflammatory environment in both skeletal and cardiac muscle can be impacted by short-term vitamin E administration.…”

Section: Discussionmentioning

confidence: 98%

In vivo vitamin E administration attenuates interleukin‐6 and interleukin‐1β responses to an acute inflammatory insult in mouse skeletal and cardiac muscle

Huey

Fiscus

Richwine

et al. 2008

Experimental Physiology

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Antioxidants are associated with reduced pro-inflammatory cytokine expression in immune cells and isolated tissues; however, no studies have examined whether short-term vitamin E administration is associated with reduced lipopolysaccharide (LPS)-induced cytokine expression in mouse skeletal and cardiac muscle, in vivo. These experiments tested the hypothesis that vitamin E administration attenuates nuclear factor κB (NF-κB), IL-6, IL-1β and tumour necrosis factor α (TNFα) responses in skeletal and cardiac muscle to an inflammatory challenge induced by systemic LPS. We compared IL-6, IL-1β and TNFα mRNA and protein, activated NF-κB and total oxidized proteins in skeletal and cardiac muscle 4 or 24 h after saline or LPS injection in mice receiving vitamin E or placebo for 3 days prior to the insult. Skeletal and cardiac IL-6 mRNA and protein were significantly elevated by LPS in both groups, but responses were significantly lower in vitamin E-compared with placebo-treated mice. In skeletal and cardiac muscle, LPS increased IL-1β mRNA and protein in placebo-but not vitamin E-treated mice. Lipopolysaccharide-induced levels of cardiac IL-1β mRNA and protein and skeletal IL-1β mRNA were lower with vitamin E than placebo. Lipopolysaccharide-induced NF-κB activation and increases in total oxidized proteins were attenuated with vitamin E compared with placebo in both tissues. Vitamin E decreased LPS-induced increases in plasma IL-1β but not IL-6 compared with placebo. The major results provide the first in vivo evidence that short-term vitamin E administration reduces IL-6 and IL-1β responses to LPS in skeletal and cardiac muscle and prevents LPS-induced increases in NF-κB activation and total oxidized proteins.

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Section: Discussionmentioning

confidence: 98%

In vivo vitamin E administration attenuates interleukin‐6 and interleukin‐1β responses to an acute inflammatory insult in mouse skeletal and cardiac muscle

Huey

Fiscus

Richwine

et al. 2008

Experimental Physiology

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“…Following muscle injury, TNF-␣, the chemokines MCP-1, IL-8, and GM-CSF, and COX-2 accelerate muscle repair by recruiting neutrophils and macrophages, reducing the expression of TGF-␤ mRNA, and increasing MyoD mRNA expression (112,113,140,141,161,163). IL-6 does not play an acute role in repairing muscle injury (161), but it is involved in muscle hypertrophy (1,138).…”

Section: Aging Muscle Injury and Inflammationmentioning

confidence: 99%

Aging and its effects on inflammation in skeletal muscle at rest and following exercise-induced muscle injury

Peake

Gatta

Cameron‐Smith

2010

American Journal of Physiology-Regulatory, Integrative and Comp

162

136

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“…These apparently contradictory findings may be reconciled by differential effects depending on concentration and duration, as stimulation of differentiation was observed in response to low levels of TNF-a, whereas high levels of TNF inhibited regeneration and differentiation in a nuclear factor (NF)-kB-dependent fashion, which involved destabilisation of the myogenic regulatory factor MyoD. Some of the beneficial effects of low levels of TNF-a on regeneration may involve macrophage and neutrophil recruitment, as well as myoblast chemotaxis [22,23].…”

mentioning

confidence: 99%

Inflammation: friend or foe of muscle remodelling in COPD?

Langen¹,

Schols²

2007

Eur Respir J

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Tumor necrosis factor-α promotes the accumulation of neutrophils and macrophages in skeletal muscle

Abstract: . Pizza. Tumor necrosis factor-␣ promotes the accumulation of neutrophils and macrophages in skeletal muscle.

Cited by 64 publications

References 46 publications

In vivo vitamin E administration attenuates interleukin‐6 and interleukin‐1β responses to an acute inflammatory insult in mouse skeletal and cardiac muscle

In vivo vitamin E administration attenuates interleukin‐6 and interleukin‐1β responses to an acute inflammatory insult in mouse skeletal and cardiac muscle

Aging and its effects on inflammation in skeletal muscle at rest and following exercise-induced muscle injury

Inflammation: friend or foe of muscle remodelling in COPD?

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