Open AccessAlveolar macrophages from subjects infected with HIV‐1 express macrophage inflammatory protein‐1α (MIP‐1α): contribution to the CD8 + alveolitis
Author(s) -
DENIS M.,
GHADIRIAN E.
Publication year - 1994
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1994.tb06540.x
Subject(s) - pulmonary alveolus , immunology , bronchoalveolar lavage , cd8 , alveolar macrophage , macrophage , cytokine , macrophage inflammatory protein , lipopolysaccharide , biology , medicine , lung , in vitro , immune system , interleukin , biochemistry
SUMMARY We examined the synthesis and release of MIP‐1α in alveolar macrophages obtained from normal subjects or subjects infected with HIV‐1, at different stages of the disease. HIV‐1‐infected subjects in groups II, III and IV all had significant interstitial pneumonitis, featuring a significant infiltration of CD8 + lymphocytes in the bronchoalveolar lavage. Alveolar macrophages from HIV‐1‐infected subjects were shown to express significant levels of MIP‐1α via immunohistochemistry, both spontaneously and in response to lipopolysaccharide (LPS), whereas cells from normal subjects expressed very low levels of the cytokine. Supernatants of alveolar macrophages from HIV‐1‐infected subjects exerted strong chemotactic activity for purified activated blood CD8 + T lymphocytes, which was strongly inhibited by neutralizing MIP‐1α. Studies of patients with HIV‐1 infection at different stages of the disease showed that MIP‐1α secretion increased as viral infection developed, There was a significant positive correlation between MIP‐1α secretion and the CD8 + alveolitis in HIV‐1‐infected subjects. Infection of alveolar macrophages in vitro with three distinct strains of HIV‐1 which replicated profusely in macrophages did not induce the expression of MIP‐1α. Collectively, these data suggest that HIV‐1 infection in vivo induces MIP‐1α expression and release in alveolar macrophages, and this appears to contribute significantly to the alveolar lymphocytosis seen in HIV‐1‐infected subjects.