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Differences in LPS‐Induced Activation of Bronchial Epithelial Cells (BEAS‐2B) and Type II‐Like Pneumocytes (A‐549)
Author(s) -
SCHULZ C.,
FARKAS L.,
WOLF K.,
KRÄTZEL K.,
EISSNER G.,
PFEIFER M.
Publication year - 2002
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.2002.01137.x
Subject(s) - lipopolysaccharide , microbiology and biotechnology , cd14 , receptor , tlr4 , stimulation , cytokine , alveolar epithelium , chemistry , biology , immunology , interleukin 8 , signal transduction , epithelium , immune system , endocrinology , biochemistry , genetics
Lipopolysaccharide (LPS) as a major component of the outer membrane of gram‐negative bacteria stimulates various cells to initiate a signalling cascade which ultimately leads to cell activation and expression of immunoregulatory or inflammatory cytokines. The human respiratory epithelium is an important environmental interface, but differences in LPS‐induced cell activation between bronchial and alveolar epithelial cells have not yet been investigated in detail. First, the expression of Toll‐like receptors (TLRs), as pattern‐recognition receptors, was investigated for the bronchial epithelial cells and type II‐like pneumocytes, demonstrating that they fulfil the prerequisites for LPS signalling. Thereafter, the effects of LPS, soluble CD14 (sCD14) and LPS‐binding protein (LBP) on the release of interleukin‐6 (IL‐6) and IL‐8 were studied. In the presence of LPS, sCD14 induced a significant and concentration‐dependent cytokine release in type II‐like pneumocytes, whereas the response of bronchial epithelial cells to sCD14 stimulation was low, implicating sCD14‐independent activation mechanisms. Furthermore, LBP revealed inhibitory effects on the activation of alveolar epithelial cells, which may represent a novel local defence mechanism during gram‐negative infection. We conclude that distinct pathways exist for LPS‐induced activation of bronchial and alveolar epithelial cells.