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Mycobacterial Mammalian Cell Entry Protein 1A (Mce1A)‐Mediated Adherence Enhances the Chemokine Production by A549 Alveolar Epithelial Cells
Author(s) -
Kohwiwattanagun Juthaporn,
Kawamura Ikuo,
Fujimura Takao,
Mitsuyama Masao
Publication year - 2007
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.2007.tb03897.x
Subject(s) - chemokine , a549 cell , biology , microbiology and biotechnology , interleukin 8 , immunology , cell , cytokine , inflammation , biochemistry
Mycobacterial mammalian cell entry protein 1A (Mce1A) is involved in the uptake of bacteria in non‐phagocytic cells and also possibly in granuloma formation. However, it has not been clarified whether the interaction between mycobacterial Mce1A and epithelial cell induces chemokine and cytokine production which is required for granuloma formation. To this end, we infected A549 alveolar epithelial cells in vitro with E. coli expressing Mce1A on the cell surface and examined the resultant chemokine/cytokine production. Mce1A promoted bacterial adherence and internalization of E. coli into A549 cells, and these recombinant bacteria induced high levels of MCP‐1 and IL‐8 production, compared to E. coli harboring the plasmid vector alone. Chemokine production was enhanced by the internalization of recombinant E. coli expressing Mce1A because cytochalasin D treatment partially inhibited MCP‐1 and IL‐8 production. However, Mce1A‐coated latex beads did not induce the chemokine production. These results suggest that although Mce1A does not induce production of chemokines, it may promote chemokine induction by augmenting the interaction between bacteria and epithelial cells.