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An enhanced systemic inflammatory response is a typical feature of chronic diseases, including chronic obstructive pulmonary disease (COPD), cancer, rheumatoid arthritis and chronic heart failure. The pattern and degree of systemic cytokine elevation is remarkably comparable among these conditions, despite different primary organ pathology. Interestingly, these diseases share skeletal muscle weakness and wasting as a common phenomenon in the disease course, and experimental studies using different acute and chronic disease models have clearly implicated cytokine-mediated effects, particularly of tumour necrosis factor (TNF)-α, on muscle contractility and muscle atrophy and regeneration.TNF-α is thought to act on skeletal muscle cells in an endocrine as well as autocrine/paracrine fashion, but as yet it is unclear whether this cytokine is causally related to (altered) skeletal muscle remodelling and whether its effects facilitate or interfere with muscle plasticity in COPD. One approach to unravelling the role of TNF-α in atrophy, regeneration and muscle fibre type shifting is to compare local expression of TNF-α during muscle remodelling, e.g. in conditions which are accompanied by alterations in skeletal muscle mass, structure or metabolic activity.Limited studies have investigated TNF-α expression in muscle biopsies of patients with COPD and unfortunately, no studies are yet available comparing expression levels between different muscles within the same subject. Some studies 1, 2 have demonstrated elevated muscular TNF-α expression in patients with COPD compared with healthy control subjects, but this finding was not confirmed …

Inflammation: friend or foe of muscle remodelling in COPD?