Common and Uncommon Features of Rheumatoid Arthritis and Chronic Obstructive Pulmonary Disease: Clues to a Future Therapy

Abstract

Over the last decade it has become apparent that common pathogenic mechanisms are shared between many human chronic inflammatory diseases of unrelated pathology and manifestation. These mechanisms include common inflammatory networks that control tissue destructive and repair processes and their study is of major therapeutic potential as recently demonstrated for TNFalpha. Thus, early studies in rheumatoid arthritis defined TNFalpha as a major therapeutic target, the blockade of which was subsequently proved to be of great efficacy in the clinic. This paved the way for the successful blockade of TNFalpha in various other diseases including Crohn's disease, psoriasis, spondyloarthropathies and juvenile arthritis, although no similar networks with anti-TNFalpha at their apex had previously been demonstrated. In this article, we review the current knowledge of the pathogenic mechanisms involved in rheumatoid arthritis and chronic obstructive pulmonary disease with particular emphasis on the role of inflammatory cytokines, chemokines, and tissue degrading enzymes as revealed by studies in the laboratory and the clinic. Direct comparison of these mechanisms may provide clues for a future therapy for these painful and incurable diseases.

Psoriasis and chronic obstructive pulmonary disease: a case-control study

“…T‐ and B‐cell‐mediated immunity against elastin is reported in COPD. An autoimmune process involving elastin‐bearing organs, such as blood vessels and the skin, as well as elevated titres of antinuclear antibodies, have also been reported in COPD 14,16,17,19 . COPD was therefore hypothesized to be an autoimmune disease induced by cigarette smoking 16 .…”

“…14,15 It has been suggested that COPD is an autoimmune disease with a chronic inflammatory state, 16,17 similar to rheumatoid arthritis or psoriasis. Inflammatory cytokines such as CRP, tumour necrosis factor (TNF)-a, interleukin (IL)-6 and IL-8 14,16,17 have been found to be aetiologically involved in both psoriasis and COPD. Similarly to patients with psoriasis, patients with COPD often have one or more components of the metabolic syndrome.…”

“…An autoimmune process involving elastin-bearing organs, such as blood vessels and the skin, as well as elevated titres of antinuclear antibodies, have also been reported in COPD. 14,16,17,19 COPD was therefore hypothesized to be an autoimmune disease induced by cigarette smoking. 16 The metabolic syndrome 18 and diabetes 19 have been associated with COPD.…”

Risk of Incident Chronic Obstructive Pulmonary Disease in Rheumatoid Arthritis: A Population‐Based Cohort Study

“…Although smoking is the primary risk factor for COPD, other factors seem to play a role. Several studies have established a link between COPD and inflammation . People with COPD have been found to have higher C‐reactive protein, erythrocyte sedimentation rate, fibrinogen, and tumor necrosis factor levels than the general population , as well as production of a wide range of autoantibodies .…”

Sleep depth and fatigue: Role of cellular inflammatory activation

“…We have previously found that sleep loss induces marked increases in monocyte production of IL-6 and TNF-α (Irwin et al, 2010; Irwin et al, 2006b), and such increases in the cellular expression of proinflammatory cytokines is associated with fatigue in breast cancer survivors (Collado-Hidalgo et al, 2008b). In addition, Toll-like receptors mediate innate immune responses to common pathogens, and aberrant increases of Toll-like receptor activity have been linked to inflammatory diseases such as rheumatoid arthritis (Andreakos, 2004), Crohn’s disease (Andreakos, 2004), and heart failure (Satoh et al, 2006). …”