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Published ahead of print on June 22, 2006, doi:10.1165/rcmb.2006-0103OC

Am. J. Respir. Cell Mol. Biol., Volume 35, Number 6, December 2006, 689-696

A more recent version of this article appeared on December 1, 2006
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Submitted on March 9, 2006
Revised on June 21, 2006

Muscle Wasting and Impaired Muscle Regeneration in a Murine Model of Chronic Pulmonary Inflammation

Ramon C.J. Langen1*, Annemie M.W.J. Schols1, Marco C.J.M. Kelders1, Jos L.J. van der Velden1, Emiel F.M. Wouters1, and Yvonne M.W. Janssen-Heininger2

1 Department of Respiratory Medicine, Maastricht University, Maastricht, The Netherlands, 2 Department of Pathology, University of Vermont, Burlington, VT, USA

* To whom correspondence should be addressed. E-mail: r.langen{at}pul.unimaas.nl.

Muscle wasting and increased circulating levels of inflammatory cytokines, including tumor necrosis factor alpha (TNF{alpha}) are common features of COPD. To investigate if inflammation of the lung is responsible for systemic inflammation and muscle wasting, we adopted a mouse model of pulmonary inflammation resulting from directed over-expression of a TNF{alpha} transgene controlled by the surfactant protein C (SP-C) promoter. Compared to wild type, SP-C/TNF{alpha} mice exhibited increased levels of TNF{alpha} in the circulation and increased endogenous TNF{alpha} expression in skeletal muscle, potentially reflecting an amplificatory response to circulating TNF{alpha}. Decreased muscle and body weights observed in SP-C/TNF{alpha} mice were indicative of muscle wasting. Further evaluation of the SP-C/TNF{alpha} mouse musculature revealed a decreased muscle regenerative capacity, evidenced by attenuated myoblast proliferation and differentiation in response to reloading of disuse-atrophied muscle, which may contribute to skeletal muscle wasting. Importantly, incubation of cultured myoblasts with TNF{alpha} also resulted in elevated TNF{alpha} mRNA levels and inhibition of myoblast differentiation. Collectively, our results demonstrate that chronic pulmonary inflammation results in muscle wasting and impaired muscle regeneration in SP-C/TNF{alpha} mice, possibly as a consequence of an amplificatory TNF{alpha} expression circuit extending from the lung to skeletal muscle.




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