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Airway obstruction and autoimmunity
  1. V Saravanan,
  2. C A Kelly
  1. Queen Elizabeth Hospital, Gateshead, UK; saravana_ukyahoo.co.uk

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Birring and colleagues have shown an interesting link between respiratory symptoms and autoimmunity in the form of both hypothyroidism and Crohn’s disease.1 In addition, they have previously demonstrated a link between autoimmune disease and airway obstruction in non-smokers.2 We have reported a similar association between airway obstruction and rheumatoid arthritis with a 2–3-fold increased prevalence of wheeze and physiological abnormalities in patients with rheumatoid arthritis compared with controls with osteoarthritis.3

Our group has also found correlations between the severity of airway obstruction and the extent of rheumatoid disease at both the systemic4 and articular5 levels. Our data would favour Birring’s first theory—namely, homing of activated inflammatory cells into the pulmonary compartment. We have also previously demonstrated the presence of excess lymphocytes in bronchial biopsy specimens in patients with rheumatoid arthritis, together with an increase in neutrophils in the bronchoalveolar lavage fluid (personal communication, W U Hassan). The neutrophil numbers correlated with physiological evidence of increased bronchial reactivity to methacholine and airflow obstruction, suggesting recruitment of neutrophils as the effector cell by the controlling lymphocytes. At the cytokine level, tumour necrosis factor (TNFα)—a key driver of inflammation in rheumatoid arthritis, Crohn’s disease, and hypothyroidism—has a significant role in the pathophysiology of asthma and chronic obstructive pulmonary disease (COPD).6,7

Their second hypothesis—that airway obstruction might just be a hitherto unrecognised autoimmune bronchitis—merits further investigation. COPD due to smoking itself has been suggested to be an autoimmune disease.8 A key investigation would be to study the origin of proinflammatory cells and cytokines when airway obstruction occurs in the presence of organ specific autoimmune diseases to determine whether these are produced elsewhere before “homing” into the lung or are activated and produced de novo in the lung.

We would also like to explore a third possibility—namely, the role of the lung in the aetiopathogenesis of autoimmunity. The lung is an ideal interface between the environment and the immune system. Smoking is linked to both Crohn’s disease and rheumatoid arthritis. The increased prevalence of rheumatoid factor in smokers with airway obstruction compared with smokers with normal airways9 and the presence of bronchus associated lymphoid tissue in the lung mainly in smokers10 may not be mere coincidence. Is the lung (that is, the airway) a “culprit” rather than a “target” organ in autoimmune diseases?

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