Differential regulation of CCL-11/eotaxin-1 and CXCL-8/IL-8 by gram-positive and gram-negative bacteria in human airway smooth muscle cells.
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Issa, Razao, Sorrentino, Rosalinda, Sukkar, Maria B, Sriskandan, Shiranee, Chung, Kian Fan and Mitchell, Jane A (2008) Differential regulation of CCL-11/eotaxin-1 and CXCL-8/IL-8 by gram-positive and gram-negative bacteria in human airway smooth muscle cells. Respiratory Research, 9. p. 30. ISSN 1465-993X
Abstract
BACKGROUND: Bacterial infections are a cause of exacerbation of airway disease. Airway smooth muscle cells (ASMC) are a source of inflammatory cytokines/chemokines that may propagate local airway inflammatory responses. We hypothesize that bacteria and bacterial products could induce cytokine/chemokine release from ASMC. METHODS: Human ASMC were grown in culture and treated with whole bacteria or pathogen associated molecular patterns (PAMPs) for 24 or 48 h. The release of eotaxin-1, CXCL-8 or GMCSF was measured by ELISA. RESULTS: Gram-negative E. coli or gram-positive S. aureus increased the release of CXCL-8, as did IL-1beta, LPS, FSL-1 and Pam3CSK4, whereas FK565, MODLys18 or Poly I:C did not. E. coli inhibited eotaxin-1 release under control conditions and after stimulation with IL-1beta. S. aureus tended to inhibit eotaxin-1 release stimulated with IL-1beta. E. coli or LPS, but not S. aureus, induced the release of GMCSF. CONCLUSION: Gram-positive or gram-negative bacteria activate human ASMC to release CXCL-8. By contrast gram-negative bacteria inhibited the release of eotaxin-1 from human ASMCs. E. coli, but not S. aureus induced GMCSF release from cells. Our findings that ASMC can respond directly to gram-negative and gram-positive bacteria by releasing the neutrophil selective chemokine, CXCL-8, is consistent with what we know about the role of neutrophil recruitment in bacterial infections in the lung. Our findings that bacteria inhibit the release of the eosinophil selective chemokine, eotaxin-1 may help to explain the mechanisms by which bacterial immunotherapy reduces allergic inflammation in the lung.
| Item Type: | Article |
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| Additional Information: | author can archive post-print (ie final draft post-refereeing); Publisher's version/PDF may be used |
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| Date Deposited: | 14 Dec 2009 13:52 |
| Last Modified: | 14 Dec 2009 13:52 |
| URI: | https://oak.novartis.com/id/eprint/855 |