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Thorax 57:566-568 doi:10.1136/thorax.57.7.566
  • Editorial

Is there more than one inflammatory phenotype in asthma?

  1. R A O'Donnell,
  2. A J Frew
  1. Correspondence to:
    Dr R A O'Donnell, University Medicine, Southampton General Hospital, Southampton SO16 6YD, UK;
    ROD1{at}soton.ac.uk

    Circumstantial evidence suggests an important role for neutrophilic airways inflammation in addition to eosinophilic airways inflammation in non-severe asthma.

    The existence of different clinical phenotypes of asthma is a concept that has excited considerable interest in academic, clinical, and pharmaceutical quarters. The source of this confusion goes back to the original Greek definition of asthma as a description for transient breathlessness. The ancients recognised that the symptoms of asthma could be triggered by cardiac or bronchial disease. The term “cardiac asthma” has been replaced by the physiological and pathological definitions of left ventricular failure and pulmonary oedema. Within bronchial asthma, definitions have continued to focus on physiological measurements and clinical context, including exercise induced asthma, nocturnal asthma, acute severe asthma, occupational asthma, etc. Implicit in these clinical phenotypes is the unspoken assumption that the clinical context dictates the pathophysiological mechanism. The demonstration that eosinophilic inflammation is a characteristic feature of many asthmatic airways led, during the 1990s, to the unhealthy and erroneous view that all asthma might be caused by eosinophils. Indeed, at one stage asthma was in danger of being defined for pharmaceutical purposes as eosinophilic airways inflammation. The few dissenting voices were drowned out by a series of studies showing the “anti-inflammatory” effects of anti-asthma drugs by virtue of a proxy effect on airways eosinophilic. Given the known dependence of eosinophils on T cells and cytokines such as interleukin 5 (IL-5), a further dogma arose that all asthma was orchestrated by T cells producing IL-5 and IL-4, the Th2 cytokines.

    This issue of Thorax features a hypothesis paper by Douwes et al1 that questions the assumption that Th2 driven allergic inflammation is the pathogenetic mechanism behind the majority of cases of asthma. Douwes and colleagues draw from several sources of evidence to argue that non-allergic, non-eosinophilic asthma …

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