Influenza virus infection of human alveolar and peripheral blood-derived macrophages. Production of factors that alter fibroblast proliferation.
Influenza virus infection of the lung has been shown, in animal models as well as in isolated human case reports, to cause a long-term alveolitis characterized by increased numbers of free lung macrophages. Recruitment of peripheral blood monocytes into the interstitial spaces, with subsequent maturation into tissue macrophages, accounts for most of the observed increase in cell numbers. The current studies examined the release of soluble factors by lavage-derived alveolar macrophages from healthy volunteers, and by peripheral blood-derived macrophages from the same subjects. Cell-free supernatant fluids generated by the macrophages after in vitro exposure or sham exposure to influenza virus were tested for effects on human fibroblast proliferation. The data indicated that autologous human alveolar macrophages and peripheral blood-derived macrophages both produce fibroblast-stimulating factor(s) in response to in vitro infection. The data suggest that macrophage release of fibroblast-stimulating factor(s) may play a role in the development of end-stage fibrotic lung disease occasionally seen as a sequela of influenza pneumonia.
D000328:Adult; D002196:Capillaries; D002455:Cell Division; D002478:Cells, Cultured; D005260:Female; D005347:Fibroblasts / Q000473:pathology*; D006801:Humans; D008264:Macrophages / Q000378:metabolism*; D008297:Male; D009976:Orthomyxoviridae Infections / Q000097:blood / Q000473:pathology*; D011650:Pulmonary Alveoli / Q000473:pathology*