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BMC. Anti-inflammatory effects of antibacterials on human bronchial epithelial cells
Anti-inflammatory effects of antibacterials on human bronchial epithelial cells (BMC, abstract, edited)
Anti-inflammatory effects of antibacterials on human bronchial epithelial cells
Gregor S Zimmermann, Claus Neurohr, Heidrun Villena-Hermoza, Rudolf Hatz and Juergen Behr
Respiratory Research 2009, 10:89
doi:10.1186/1465-9921-10-89
Published: 29 September 2009
Abstract (provisional)
Background
Human Bronchial epithelial cells (hu-BEC) have been claimed to play a significant role in the pathogenesis of chronic inflammatory airway diseases like COPD. In this context IL-8 and GM-CSF have been shown to be key cytokines. Some antibiotics which are routinely used to treat lower respiratory tract infections have been shown to exert additional immunomodulatory or anti-inflammatory effects. We investigated whether these effects can also be detected in hu-BEC.
Methods
Hu-BEC obtained from patients undergoing lung resections were transferred to air-liquid-interface (ALI) culture. These cultures were incubated with cefuroxime (CXM, 10-62.5 mg/l), azithromycin (AZM, 0.1-1.5 mg/l), levofloxacin (LVX, 1-8 mg/l) and moxifloxacin (MXF, 1-16 mg/l). The spontaneous and TNF-alpha (10 ng/ml) induced expression and release of IL-8 and GM-CSF were measured using PCR and ELISA in the absence or presence of these antibiotics.
Results
The spontaneous IL-8 and GM-CSF release was significantly reduced with MXF (8 mg/l) by 37+/- 20% and 45+/- 31%, respectively (both p<0.01). IL-8 release in TNF-alpha stimulated hu-BEC decreased by 16+/- 8% (p<0.05) with AZM (1.5 mg/l). With MXF a concentration dependent decrease of IL-8 release was noted up to 39+/- 7% (p<0.05). GM-CSF release from TNF-alpha stimulated hu-BEC was maximally decreased by 35+/- 24% (p<0.01) with MXF (4 mg/l).
Conclusions
Using ALI cultures of hu-BEC we observed differential effects of antibiotics on spontaneous and TNF-alpha induced cytokine release. Our data suggest that MXF and AZM, beyond bactericidal effects, may attenuate the inflammatory process mediated by hu-BEC.
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<cite cite="http://respiratory-research.com/content/10/1/89/abstract">Abstract | Anti-inflammatory effects of antibacterials on human bronchial epithelial cells</cite>
Gregor S Zimmermann, Claus Neurohr, Heidrun Villena-Hermoza, Rudolf Hatz and Juergen Behr
Respiratory Research 2009, 10:89
doi:10.1186/1465-9921-10-89
Published: 29 September 2009
Abstract (provisional)
Background
Human Bronchial epithelial cells (hu-BEC) have been claimed to play a significant role in the pathogenesis of chronic inflammatory airway diseases like COPD. In this context IL-8 and GM-CSF have been shown to be key cytokines. Some antibiotics which are routinely used to treat lower respiratory tract infections have been shown to exert additional immunomodulatory or anti-inflammatory effects. We investigated whether these effects can also be detected in hu-BEC.
Methods
Hu-BEC obtained from patients undergoing lung resections were transferred to air-liquid-interface (ALI) culture. These cultures were incubated with cefuroxime (CXM, 10-62.5 mg/l), azithromycin (AZM, 0.1-1.5 mg/l), levofloxacin (LVX, 1-8 mg/l) and moxifloxacin (MXF, 1-16 mg/l). The spontaneous and TNF-alpha (10 ng/ml) induced expression and release of IL-8 and GM-CSF were measured using PCR and ELISA in the absence or presence of these antibiotics.
Results
The spontaneous IL-8 and GM-CSF release was significantly reduced with MXF (8 mg/l) by 37+/- 20% and 45+/- 31%, respectively (both p<0.01). IL-8 release in TNF-alpha stimulated hu-BEC decreased by 16+/- 8% (p<0.05) with AZM (1.5 mg/l). With MXF a concentration dependent decrease of IL-8 release was noted up to 39+/- 7% (p<0.05). GM-CSF release from TNF-alpha stimulated hu-BEC was maximally decreased by 35+/- 24% (p<0.01) with MXF (4 mg/l).
Conclusions
Using ALI cultures of hu-BEC we observed differential effects of antibiotics on spontaneous and TNF-alpha induced cytokine release. Our data suggest that MXF and AZM, beyond bactericidal effects, may attenuate the inflammatory process mediated by hu-BEC.
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