Aims
Exacerbation of innate immune responses can contribute to development of acute lung injury. Multiple cell populations, including the bronchiolar epithelium, coordinate these inflammatory responses. Clara cells, non-ciliated epithelial cells, are located in the distal airways in humans and conducting airways in mice. These cells actively participate in innate immune responses but their precise contributions remain poorly defined.
Background/aims
Exacerbation of innate immune responses can contribute to development of acute lung injury. Multiple cell populations, including the bronchiolar epithelium, coordinate these inflammatory responses. Clara cells, non-ciliated epithelial cells, are located in the distal airways in humans and conducting airways in mice. These cells actively participate in innate immune responses but their precise contributions remain poorly defined.
Conclusions
While the role for Clara cells in the regulation of host defense and the progression of acute lung injury needs further characterization, our data suggests the importance of this unique cell population in the pathogenesis of LPS-induced acute lung injury.
Methods
To test the hypothesis that E. coli lipopolysaccaride (LPS) treatment stimulates production of pro-inflammatory mediators in mouse transformed Clara cells (MTCC), MTCC were treated with E. coli lipopolysaccaride (LPS).
Results
LPS increased COX-2 expression and stimulated production of prostaglandins, including prostaglandin E(2) (PGE(2)). Enhanced mitogen activated protein kinase (MAPK) activation, nuclear factor-κB (NFκB) activation, and chemokine production were observed in MTCC in response to LPS treatment. Conclusions: While the role for Clara cells in the regulation of host defense and the progression of acute lung injury needs further characterization, our data suggests the importance of this unique cell population in the pathogenesis of LPS-induced acute lung injury.