Burkholderia pseudomallei stimulates low interleukin‐8 production in the human lung epithelial cell line A549
Author(s) -
UTAISINCHAROEN P.,
ANUNTAGOOL N.,
ARJCHAROEN S.,
LENGWEHASATIT I.,
LIMPOSUWAN K.,
CHAISURIYA P.,
SIRISINHA S.
Publication year - 2004
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2004.02601.x
Subject(s) - burkholderia pseudomallei , melioidosis , microbiology and biotechnology , biology , a549 cell , immunology , cell culture , chemokine , bacteria , immune system , genetics
SUMMARY Melioidosis is a life‐threatening disease caused by Burkholderia pseudomallei . The lung is the most commonly affected organ, resulting in abscess formation in patients with chronic melioidosis. Previous study has shown that B. pseudomallei was able to invade and multiply in epithelial cells. In the present study, we have demonstrated that B. pseudomallei is able to stimulate interleukin 8 (IL‐8) production from the human alveolar lung epithelium cell line A549. However, the level of IL‐8 production was significantly lower than when the cells were infected with other Gram‐negative bacteria such as Salmonella enterica serovar Typhi ( S. typhi ) which were used for comparison. The degree of I κ B α degradation in the B. pseudomallei ‐infected cells was lower than that of the S. typhi ‐infected cells, suggesting that B. pseudomallei is also a poorer cell activator. Inhibition of B. pseudomallei invasion by cytochalasin D did not interfere with either IL‐8 production or I κ B α degradation, indicating that bacterial uptake is not required for the production of this chemokine. Thus, it appears that the signalling initiated by the interaction of B. pseudomallei with the epithelial cell surface is sufficient for epithelial cell activation.
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