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Macrophages are key sentinel cells of the lung, clearing inhaled particulates and micro-organisms from the airway. These cells perform this function without provoking inflammatory responses that could lead to pneumonias. Previous work suggested that the lung macrophage population was maintained by the recruitment of blood monocytes.1 However, this observation was made in transplanted lungs where macrophages had been depleted, either by hypoxia or chemotherapy. More recent work in murine models using cell fate mapping demonstrated that lung macrophages are generated early in embryonic development initially in the foetal yolk sac and slightly later in the foetal liver.2 Macrophages that arise from these sources then seed the lung, where they reside as a self-renewing population with little further recruitment from blood monocytes.
The relevance and translation of these murine findings to the ontogeny of human lung macrophages has remained unclear. The study by Eguíluz-Gracia et al3 has provided some intriguing evidence regarding the stability and longevity of the lung macrophage population. This study prospectively followed 10 gender mismatched lung transplant patients for 2 years. Transbronchial biopsies were collected at regular intervals throughout the follow-up period. The macrophage populations in these biopsies were analysed for known macrophage markers, indicators of proliferation and, importantly, in situ hybridisation for the X and Y chromosomes to differentiate between recipient and donor cells. Comparisons to normal lung tissue obtained from cancer resections, suggest that there is no significant difference in the total number of macrophages in transplanted lung tissue across the 2 years. Moreover, while there was a large amount of inter-individual variation the abundance of donor-derived macrophages was largely unchanged …
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