Alveolar macrophage in equine asthma

Alveolar macrophages (AMs) are becoming increasingly recognised as key cellular players in human asthma; both in severe, steroid refractory non-Th2 driven asthma [1] and in allergic asthma, where polarisation towards a pro-inflammatory phenotype (from a largely suppressive/homeostatic phenotype) may significantly contribute towards lung pathology, especially following repeated or prolonged allergen exposures [2]. Continued efforts to unveil the mechanisms which determine their relative state of polarisation may inform the development of novel therapeutic approaches which target this “double edged” cell.

Comparative data on the potential role of AMs in equine asthma (EA) is significantly more limited. Disease associated differences (severe EA-susceptible vs healthy) in AM responsiveness (potentially reflecting differences in AM phenotype distribution) have been reported by some [3], but not by others [4]. Furthermore, manipulation of the airway monocyte/macrophage phenotype may partly explain the recently reported therapeutic benefit of airway instillation of bone marrow derived mononuclear cells in severe EA, with an associated increase in bronchoalveolar lavage fluid IL-10 [5]. Despite these proposed interpretations, in light of the sparsity of data and the contradictory results, it remains clear that further research is warranted in this area. Similarly, the role of AMs in the pathogenesis of mild to moderate EA remains undetermined; however, recent studies strongly support a compartmentalised immunosuppressive effect of training at the level of the AM [6] (and Karagianni et al, unpublished data), potentially increasing susceptibility to inhaled infectious agents. Again further work in this area is warranted.