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Department of Pathology, University of Michigan Medical School, Ann Arbor, MI 48109
Although alveolar epithelial cells (AEC) form an important barrier
for host defenses in the lung, there is limited information about ways
in which AEC can directly participate in the lung inflammatory
response. In the current studies, primary cultures of rat AEC (RAEC)
have been shown to specifically bind recombinant rat C5a at high
affinity and in a saturable manner. This binding was enhanced in a
time-dependent manner by pre-exposure of RAEC to LPS, IL-6, or TNF-
,
the increased binding of C5a being associated with increased levels of
mRNA for the C5a receptor (C5aR). Exposure of RAEC to C5a also caused
increased expression of mRNA for C5aR. As compared with exposure
of RAEC to LPS or to C5a alone, exposure to the combination caused
enhanced production of TNF-, macrophage inflammatory protein-2, and
cytokine-induced neutrophil chemoattractant-1, as well as increased
intracellular levels of IL-1
. These data indicate that RAEC, when
activated, have enhanced binding of C5a in association with increased
mRNA for C5aR. The functional outcome is enhanced release of
proinflammatory mediators. These data underscore the phlogistic
potential of RAEC and the ability of C5a to enhance the phlogistic
responses of RAEC.
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