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We welcome the paper by Fidler and colleagues reporting the presence of mannose-binding lectin (MBL) in infected airways.1 MBL is an important acute phase protein with pro- and anti-inflammatory immunomodulatory functions.2 The collectin family comprises surfactant protein (SP)-A, SP-D and MBL, of which the latter is mostly present in peripheral blood while the other two are mostly located in the lung.3 We agree with Fidler et al that MBL might contribute to lung host defence by acting locally at the airway surface because of its similar structure to lung collectins and its presence at a physiological level in the lung. It is possible, however, that the presence of MBL in the bronchoalveolar lavage (BAL) fluid of infected children might just be a marker of lung infection or disease severity. The data of Fidler et al clearly show a trend suggesting that MBL was more consistently detectable in acute than in chronic diseases; this may simply be a correlate of alveolar epithelial permeability. A similar study performed by our group on HIV-infected adults showed that the levels of MBL in BAL fluid were undetectable even when present in serum. The levels of SP-D in the same study were not significantly different in lung fluid from HIV-uninfected and HIV-infected individuals with a high CD4 count (>200), but were raised in HIV-infected individuals with a low CD4 count.4 We tested the hypothesis that levels of SP-D or MBL in HIV-infected individuals would be lower than in HIV-uninfected individuals, but this was not the case. The phenomenon that levels of defence factors are poorly associated with protection has also been shown with other defence factors such as antibodies.5
In conclusion, we totally agree with Fidler et al that future studies should focus on measuring the functional aspect of collectins. Functional assays will help to determine whether the presence of MBL in the lung acts as an additional host defence or whether it is just a marker of disease severity.
Footnotes
Funding This article has been written with funding from the Wellcome Trust and Commonwealth Scholarship Commission.
Competing interests None.
Provenance and Peer review Not commissioned; not externally peer reviewed.