AJP - Lung Cellular and Molecular Physiology, Vol 268, Issue 5 856-L861, Copyright © 1995 by American Physiological Society
Stimulus and cell-specific expression of C-X-C and C-C chemokines by pulmonary stromal cell populations
N. W. Lukacs, S. L. Kunkel, R. Allen, H. L. Evanoff, C. L. Shaklee, J. S. Sherman, M. D. Burdick and R. M. Strieter
Department of Pathology and Internal Medicine, University of Michigan Medical School, Ann Arbor 48109-0602, USA.
Chronic inflammatory responses in the lung rely on the continual
recruitment of leukocytes to the site of inflammation. Recent data have
demonstrated a possible role for stromal cell-derived chemokines in
leukocyte recruitment. In the present study we examined the production of
interleukin (IL)-8 and ENA-78, members of the C-X-C family of chemokines,
and macrophage inflammatory protein (MIP)-1 alpha and MIP-1 beta, members
of the C-C chemokine family, from pulmonary smooth muscle and endothelial
cells. The production of IL-8 and ENA-78 was induced by early response
cytokines, IL-1 and tumor necrosis factor (TNF), but not by
immune-associated cytokines, IL-4, IL-10, or interferon (IFN)-gamma. In
contrast, the production of MIP-1 alpha and MIP-1 beta by pulmonary
vascular smooth muscle cells increased when stimulated by immune-associated
cytokines as well as with IL-1 beta and TNF. The level of MIP-1 alpha
production induced in smooth muscle cells by the immune-associated
cytokines, IL-4, IFN-gamma, and IL-10 ranged from 0 to 340 pg/ml. The
production of MIP-1 beta in response to the immune-associated cytokines
IL-4, IFN-gamma, and IL-10 in smooth muscle cells ranged from 260 to 940
pg/ml. Human pulmonary artery endothelial cells did not generate MIP-1
alpha or MIP-1 beta in response to graded doses of any of the cytokines.
These data demonstrate differential induction of C-X-C and C-C chemokines
from nonimmune stromal cell populations.(ABSTRACT TRUNCATED AT 250 WORDS)
