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Thorburn et al reported on pulmonary bacterial co-infection in children with severe respiratory syncytial virus (RSV) bronchiolitis.1 The authors found that 40% of children with severe RSV infection were infected with bacteria in their lower airways. The most commonly isolated organism was Haemophilus influenzae, a Gram negative lipopolysaccharide producing organism.
Previous studies from the same paediatric intensive care unit have investigated cytokines, chemokines, and the cellular composition of specimens obtained by non-bronchoscopic bronchoalveolar lavage (BAL) in ventilated children with RSV infection using the same method as was used in this study.2,3 The investigators found a predominance of neutrophil leucocytes, increased production of interleukin (IL)-9,2 and increased levels of a number of chemokines3 compared with controls without lower respiratory tract infection.
Lipopolysaccharide, as produced by H influenzae, is a potent activator of the nuclear transcription factor NF-κB.4 NF-κB is essential in activating IL-9 production5 and in the production of an array of chemokines.4 The neutrophilia found in the airways of children with severe RSV bronchiolitis may be partly due to bacterial stimulation of the production of the neutrophil leucocyte attracting chemokine IL-8 via NF-κB activation and indirectly via IL-9 stimulating IL-8 production. Neutrophil leucocytes can contribute to IL-8 production after IL-9 stimulation of its IL-9 receptors, and McNamara et al2 have demonstrated IL-9 bound to neutrophils by immunofluorescence studies in lavage samples.
Futures studies investigating the immunopathology in the lower respiratory tract of children with RSV infection need to rule out bacterial co-infection to obtain an unbiased view of the immunopathogenesis of this disease.
Competing interests: none.