Abstract
ObjectiveBronchiectasis (BE) in children is common in some communities including Indigenous children in Australia. Relatively little is known about the nature of systemic inflammation in these children, especially the contribution of specific pro-inflammatory and cytotoxic lymphocyte subsets: T-cells, natural killer (NK) cells and NKT-like cells. We have shown that these cells produce increased cytotoxic (granzyme b and perforin) and inflammatory (IFNγ and TNFα) mediators in several adult chronic lung diseases and hypothesised that similar changes would be evident in children with BE.MethodsIntracellular cytotoxic mediators perforin and granzyme b and pro-inflammatory cytokines were measured in T cell subsets, NKT-like and NK cells from blood and bronchoalveolar samples from 12 children with BE and 10 aged-matched control children using flow cytometry.ResultsThere was a significant increase in the percentage of CD8+ T cells and T and NKT-like subsets expressing perforin/granzyme and IFNγ and TNFα in blood in BE compared with controls. There was a further increase in the percentage of pro-inflammatory cytotoxic T cells in Indigenous compared with non-Indigenous children. There was no change in any of these mediators in BAL.ConclusionsChildhood bronchiectasis is associated with increased systemic pro-inflammatory/cytotoxic lymphocytes in the peripheral blood. Future studies need to examine the extent to which elevated levels of pro-inflammatory cytotoxic cells predict future co-morbidities.
Highlights
Bronchiectasis (BE) is a progressive disease of the airways characterised by chronic infection and associated inflammation
There was a significant increase in the percentage of CD8+ T cells and T and NKT-like subsets expressing perforin/granzyme and IFNγ and TNFα in blood in BE compared with controls
There was a further increase in the percentage of pro-inflammatory cytotoxic T cells in Indigenous compared with non-Indigenous children
Summary
Bronchiectasis (BE) is a progressive disease of the airways characterised by chronic infection and associated inflammation. The potential links between long-term inflammation and co-morbidities such as the development of dysplasia and cancer [4,5], microbial infection [6] and cardiovascular disease [7] have been well described In this regard there have been reports of increases in systemic markers of inflammation during stable phases of BE in adult patients [8], and BE has been shown to be an independent risk factor for atherosclerosis [9] cardiovascular disease, which is 1.3 times more common in Indigenous people, and osteoporosis, which is 1.8 times more common in Indigenous males than their non-Indigenous counterparts [10]. The lower sociodemographic conditions experienced by Indigenous groups is likely to contribute to a higher incidence of systemic disease, including the increased rate of BE as well as increased colonisation of the lower airway with microorganisms including non-typeable Haemophilus influenzae (NTHi) and S. pneumoniae
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