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Eisenhut expresses a valid consideration that pertains to many of the studies investigating inflammatory mediators in respiratory syncytial virus (RSV) bronchiolitis. Many RSV immunopathogenesis studies presume a pure RSV aetiology. Co-infection (viral and/or bacterial) in severe bronchiolitis is not uncommon.1,2,3 A phagocytic (neutrophils and macrophages) and natural kill cell response is common to both viral and bacterial lower respiratory infections.4,5
Analysis of the blood differential leucocyte counts in our study group failed to discriminate between the RSV-only and bacterial co-infection groups (Mann–Whitney–Wilcoxon test: neutrophils p = 0.2; lymphocytes p = 0.2; monocytes p = 0.9), as did the C-reactive protein (p = 0.9).3 However, we only evaluated total number of leucocytes/white cells, bacterial growth density and microorganism species in the broncho-alveolar lavages, and not white cell type. Therefore we are unable to comment on potential differences in concentrations of lower respiratory tract neutrophils and alveolar macrophages between the groups.
The interaction between the phagocytic effector cells, the pathogen and endogenous immune molecules orchestrate the inflammatory response.5 Cytokine and cemokine reactions can therefore be customised by the triggering pathogen(s).6 Consequently it is vital to identify the correct perpetrator when assigning responsibility for these inflammatory effects.
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