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Published ahead of print on October 20, 2005, doi:10.1165/rcmb.2005-0205OC

Am. J. Respir. Cell Mol. Biol., Volume 34, Number 2, February 2006, 158-166

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Submitted on June 1, 2005
Revised on October 19, 2005

Alveolar Epithelial Cells Secrete Chemokines in Response to IL-1{beta} and LPS but not to Ozone

Rizwan Manzer1, Jieru Wang1, Kahoru Nishina1, Glen McConville1, and Robert J Mason1*

1 Department of Medicine, National Jewish Medical and Research Center, Denver, CO, USA

* To whom correspondence should be addressed. E-mail: masonb{at}njc.org.

Ozone exposure produces acute inflammation and neutrophil influx in the distal lung. Alveolar epithelial cells cover a very large surface area, secrete chemokines, and may initiate or modify the inflammatory response. However, the effect of ozone on chemokine production by these cells has not been defined. Isolated rat type II cells were cultured in different conditions to express the morphologic appearance and biochemical markers for the type I and the type II cell phenotypes. These cells were exposed to ozone at an air/liquid interface. The type I-like cells were more susceptible to injury than the type II cells and showed signs of injury at exposure levels of 100 ppb ozone for 60 min. Both phenotypes showed evidence of lipid peroxidation after ozone exposure as measured by 8-isoprostane production, but neither phenotype secreted increased amounts of MIP-2 (CXCL3), CINC-1 (CXCL1) or MCP-1 (CCL2) in response to ozone. Both cell phenotypes secreted MIP-2 and MCP-1 in response to IL-1{beta} or lipopolysaccharide (LPS), but there was no priming or synergy with ozone. It is likely that the inflammatory response to ozone in the alveolar compartment is not due to the direct effect of ozone on epithelial cells.




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