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-1β, 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-1β. S. aureus tended to
inhibit eotaxin-1 release stimulated with IL-1β. 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.