title: Burkholderia pseudomallei stimulates low interleukin-8 production in the human lung epithelial cell line A549.
abstract: 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 IkappaBalpha 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 IkappaBalpha 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.
authors.affiliation: Department of Microbiology, Faculty of Science, Mahidol University, Bangkok, Thailand. scput@mahidol.ac.th
authors.forename: P
authors.initials: P
authors.lastname: Utaisincharoen
authors.forename: N
authors.initials: N
authors.lastname: Anuntagool
authors.forename: S
authors.initials: S
authors.lastname: Arjcharoen
authors.forename: I
authors.initials: I
authors.lastname: Lengwehasatit
authors.forename: K
authors.initials: K
authors.lastname: Limposuwan
authors.forename: P
authors.initials: P
authors.lastname: Chaisuriya
authors.forename: S
authors.initials: S
authors.lastname: Sirisinha
mesh_terms: D016957:Burkholderia pseudomallei / Q000187:drug effects / Q000276:immunology; D002460:Cell Line; D003513:Cycloheximide / Q000494:pharmacology; D015638:Cytochalasin D / Q000494:pharmacology; D016207:Cytokines / Q000276:immunology; D004847:Epithelial Cells / Q000187:drug effects / Q000276:immunology; D006801:Humans; D020672:I-kappa B Proteins / Q000378:metabolism; D016209:Interleukin-8 / Q000096:biosynthesis* / Q000276:immunology; D008554:Melioidosis / Q000276:immunology*; D000072000:NF-KappaB Inhibitor alpha; D019384:Nucleic Acid Synthesis Inhibitors / Q000494:pharmacology; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D011650:Pulmonary Alveoli / Q000166:cytology / Q000187:drug effects / Q000276:immunology; D012333:RNA, Messenger / Q000032:analysis; D012480:Salmonella Infections / Q000276:immunology; D012485:Salmonella typhi / Q000276:immunology
chemical_list: D016207:Cytokines; D020672:I-kappa B Proteins; D016209:Interleukin-8; C000606204:NFKBIA protein, human; D019384:Nucleic Acid Synthesis Inhibitors; D011500:Protein Synthesis Inhibitors; D012333:RNA, Messenger; D000072000:NF-KappaB Inhibitor alpha; D015638:Cytochalasin D; D003513:Cycloheximide