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, and TNF
responses in mouse skeletal and cardiac muscle to an acute inflammatory insult
1 Kinesiology, University of Illinois, Urbana, Illinois, United States
2 Animal Science, University of Illinois, Urbana, Illinois, United States
* To whom correspondence should be addressed. E-mail: khuey{at}uiuc.edu.
Exaggerated pro-inflammatory cytokine responses can be observed with aging, and reduced levels of the anti-inflammatory cytokine IL-10 may contribute to these responses. IL-10 can reduce IL-6, IL-1
, and TNF
expression in non-muscle tissues; however, no studies have examined the combined effects of IL-10 and age on cytokine responses in skeletal and cardiac muscle. These experiments tested the hypothesis that the absence of IL-10, in vivo, is associated with greater IL-6, TNF, and IL-1 responses to an inflammatory challenge in skeletal and cardiac muscle, and that aging exaggerates these responses. We compared IL-6, IL-1 and TNF mRNA and protein levels in skeletal and cardiac muscle of young (4 mon.) and mature (10-11 mon) wildtype (IL-10+/+) and IL-10 deficient (IL-10-/-) mice following lipopolysaccharide (LPS). Skeletal and cardiac IL-6 mRNA and protein were elevated by LPS for IL-10+/+ and IL-10-/- mice with greater responses in the IL-10-/- mice (P<0.01). In skeletal muscle these effects were greater in mature than young mice (P<0.01). IL-1 mRNA and protein responses to LPS were greater in cardiac muscle of young, but not mature IL-10-/- mice as compared to IL-10+/+ (P<0.01) However IL-1 responses were greater in mature than young mice, but only in IL-10+/+ groups (P<0.05). The absence of IL-10 was associated with higher TNF protein levels in cardiac muscle (P<0.05). The results provide the first in vivo evidence that the absence of IL-10 is associated with a greater IL-6 response to LPS in skeletal and cardiac muscles, and in skeletal muscle aging further exaggerates these responses.
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