Type 2 inflammation in COPD: is it just asthma?

Abstract

COPD is a heterogeneous condition, with tobacco smoking being the main environmental risk factor. The presence of type 2 (T2) inflammation is a well-recognised feature of asthma; however, it is now apparent that a subset of COPD patients also displays evidence of T2 inflammation with respect to elevated eosinophil counts and altered gene and protein expression of several T2 inflammatory mediators. T2 inflammatory mediators represent an attractive therapeutic target in both COPD and asthma; however, the efficacy of pharmaceutical interventions varies between diseases. Furthermore, the nature of some shared clinical features also differs. We provide a narrative review of differences in the nature of T2 inflammation between COPD and asthma, which may partly explain phenotypic differences between diseases. We focus on evidence from studies of pulmonary histopathology, sputum and epithelial gene and protein expression, and response to pharmacological interventions targeted at T2 inflammation.

Figure 1

Identification of eosinophils in COPD using a) sputum and b) small airway via surgical lung resection. Eosinophils stained using a) eosin and b) major basic protein. Orange arrowheads indicate eosinophils.

Figure 2

Schematic to show differences in pathophysiology between eosinophilic COPD and asthma. ↑: increased; T2: type 2; POSTN: periostin; SERPINB2: serine peptidase inhibitor B2; IL: interleukin; RBM: reticular basement membrane.