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Am. J. Respir. Cell Mol. Biol., Volume 24, Number 4, April, 2001 442-451

Human Lung Tissue Macrophages, but not Alveolar Macrophages, Express Matrix Metalloproteinases after Direct Contact with Activated T Lymphocytes

Sylvie Ferrari-Lacraz, Laurent P. Nicod, Rachel Chicheportiche, Howard G. Welgus, and Jean-Michel Dayer

Divisions of Immunology and Allergy (Hans Wilsdorf Laboratory), and Respiratory Diseases, Department of Internal Medicine, University Hospital, Geneva, Switzerland; and Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri

Human alveolar macrophages (AM) and lung tissue macrophages (LTM) have a distinct localization in the cellular environment. We studied their response to direct contact with activated T lymphocytes in terms of the production of interstitial collagenase (MMP-1), 92-kD gelatinase (MMP-9), and of TIMP-1, one of the counter-regulatory tissue inhibitors of metalloproteinases. Either AM obtained by bronchoalveolar lavage or LTM obtained by mincing and digestion of lung tissue were exposed for 48 h to plasma membranes of T lymphocytes previously activated with phorbol myristate acetate and phytohemagglutinin for 24 h. Membranes of activated T cells strongly induced the production of MMP-1, MMP-9, and TIMP-1 exclusively in LTM but not in AM, whereas membranes from unstimulated T cells failed to induce the release of MMPs. Both populations of mononuclear phagocytes spontaneously released only small amounts of MMPs and TIMP-1. Similar results were obtained when MMP and TIMP-1 expression was analyzed at pretranslational and biosynthetic levels, respectively. Blockade experiments with cytokine antagonists revealed the involvement of T-cell membrane-associated interleukin-1 and tumor necrosis factor-alpha in MMP production by LTM upon contact with T cells. These data suggest that the ability of lung macrophages to produce MMPs after direct contact with activated T cells is related to the difference in phenotype of mononuclear phagocytes and cell localization. In addition, these observations indicate that cell-cell contact represents an important biological mechanism in potentiating the inflammatory response of mononuclear phagocytes in the lungs.

Abbreviations: alveolar macrophages, AM; complementary DNA, cDNA; enzyme-linked immunosorbent assay, ELISA; fluorescein isothiocyanate, FITC; glyceraldehyde-3-phosphate dehydrogenase, GAPDH; human leukocyte-associated antigen-DR, HLA-DR; immunoglobulin, Ig; interleukin, IL; interleukin-1 receptor antagonist, IL1RA; lung tissue macrophages, LTM; matrix metalloproteinase, MMP; interstitial collagenase, MMP-1; 92-kD gelatinase, MMP-9; matrilysin, MMP-7; messenger RNA, mRNA; peripheral blood T lymphocytes, PBTL; phosphate-buffered saline, PBS; phytohemagglutinin, PHA; phorbol myristate acetate, PMA; standard error of the mean, SEM; T helper, Th; tissue inhibitor of metalloproteinases, TIMP; T-cell membranes, Tmb; tumor necrosis factor, TNF; stimulated membranes of T cells, Tsmb; unstimulated membranes of T cells, Tumb.




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