Premium
Primary human alveolar epithelial cells can elicit the transendothelial migration of CD14 + monocytes and CD3 + lymphocytes
Author(s) -
Eghtesad M.,
Jackson H. E.,
Cunningham A. C.
Publication year - 2001
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.2001.01172.x
Subject(s) - monocyte , cd14 , immunology , tumor necrosis factor alpha , microbiology and biotechnology , biology , chemotaxis , cytokine , lymphocyte , chemistry , immune system , biochemistry , receptor
Summary The ability of freshly isolated primary human alveolar epithelial cells (type II pneumocytes) to induce leucocyte migration across an endothelial monolayer was investigated. Three‐way factorial analysis of variance ( anova ) demonstrated that resting alveolar endothelial cells (AEC) could produce detectable quantities of monocyte chemoattractant protein 1 (MCP‐1), which was upregulated in response to tumour necrosis factor‐α (TNF‐α) in a dose‐ and time‐dependent fashion. Interferon‐γ (IFN‐γ) had no significant effect on this process. TNF‐α and IFN‐γ both induced AEC to provoke migration of CD14 + monocytes and CD3 + lymphocytes across endothelium. IFN‐γ and TNF‐α synergized in their ability to induce production of T lymphocyte, but not monocyte, chemoattractants from AEC. Leucocyte transendothelial migration was inhibited by anti‐MCP‐1 neutralizing antibody and by heparin, a polyanionic glycosaminoglycan (GAG). These data suggest that human AEC play a role in the multiple mechanisms that facilitate monocyte and T lymphocyte migration into the alveolar compartment of the lung under homeostasis and inflammatory conditions. One of these mechanisms is mediated via constitutive MCP‐1 production by alveolar epithelial cells, which is upregulated by TNF‐α.