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Published ahead of print on March 18, 2005, doi:10.1165/rcmb.2005-0063OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 6, June 2005, 531-539

A more recent version of this article appeared on June 1, 2005
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Submitted on February 14, 2005
Revised on March 18, 2005

Induction of CXCL5 During Inflammation in the Rodent Lung Involves Activation of Alveolar Epithelium

Samithamby Jeyaseelan1*, Rizwan Manzer2, Scott K Young3, Masahiro Yamamoto4, Shizuo Akira4, Robert J Mason5, and G. Scott Worthen1

1 Division of Respiratory Infections, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado, USA; Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences, Denver, Colorado, USA, 2 Division of Pulmonary Diseases, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado, USA, 3 Division of Respiratory Infections, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado, USA, 4 Department of Host Defense, Osaka University, Research Institute for Microbial Diseases, Osaka, Japan, 5 Division of Pulmonary Diseases, Department of Medicine, National Jewish Medical and Research Center, Denver, Colorado, USA; Division of Pulmonary Sciences and Critical Care Medicine, University of Colorado Health Sciences, Denver, Colorado, USA

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

The lung is continuously exposed to bacteria and their products, and has developed a complex defense mechanism, including neutrophil recruitment. In rodents, KC and MIP-2 are the major chemokines for neutrophil recruitment into the lung. We have previously described a role for C-X-C chemokine (CXCL5), in neutrophil trafficking during lung inflammation in mice induced by LPS. The aims of the present study were to identify the cellular origin of CXCL5 and to determine the signaling cascades that regulate its expression in the lung during LPS-induced inflammation and in isolated LPS-stimulated CXCL5 expressing cells. Our immunohistochemical analysis indicates that alveolar epithelial type II (AEII) cells are the predominant source of CXCL5 in the rodent lung. These in vivo observations were confirmed with primary AEII cells. In addition, our data indicate that the TLR4 signaling cascade involving TLR4, MyD88 and TIRAP is required to induce CXCL5 expression in the lung. Furthermore, p38 and JNK kinases are involved in lung CXCL5 expression. Similarly, TLR4, and p38 and JNK kinases are associated with LPS-induced CXCL5 expression in AEII cells. These novel observations demonstrate that activation of AEII cells via TLR4-dependent signaling is important for the production of CXCL5 in the lung exposed to LPS.




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