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Published ahead of print on March 3, 2005, doi:10.1165/rcmb.2004-0300OC

Am. J. Respir. Cell Mol. Biol., Volume 32, Number 6, June 2005, 490-497

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Submitted on September 23, 2004
Revised on September 22, 2004

Pneumocystis {beta}-Glucans Stimulate Epithelial Cell Chemokine Generation Through NF-{kappa}B Mechanisms

Scott E Evans1, Peter Y Hahn1, Frances McCann2, Theodore J Kottom1, Zvezdana Vuk Pavlovic1, and Andrew H Limper3*

1 Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA, 2 Department of Immunology, Mayo Clinic College of Medicine, Rochester, MN, USA, 3 Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, Mayo Clinic College of Medicine, Rochester, MN, USA; Department of Biochemistry and Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, USA

* To whom correspondence should be addressed. E-mail: limper.andrew{at}mayo.edu.

Exuberant inflammatory responses are associated with respiratory failure during Pneumocystis pneumonia. Alveolar epithelial cells (AECs) promote Pneumocystis attachment and proliferation, but also contribute prominently to host cytokine-mediated inflammation during pneumonia. Recent investigations indicate that AECs produce macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-{alpha} (TNF-{alpha}) following challenge with Pneumocystis carinii (P. carinii). NF-{kappa}B is a ubiquitous transcription factor critical for regulation of proinflammatory cytokine expression. Herein, we assess rat AEC NF-{kappa}B responses to challenge with a P. carinii {beta}-glucan cell wall component (PCBG). Prominent nuclear translocation of p65 NF-{kappa}B was demonstrated following PCBG challenge. NF-{kappa}B activation was in part mediated through Protein Kinase C (PKC) signaling pathways. PCBG challenge of AECs was also shown to induce MIP-2 and TNF-{alpha} mRNA production, a response which was ameliorated by NF-{kappa}B inhibition. MIP-2 protein expression was also dramatically increased by PCBG challenge, in a manner that was significantly attenuated by both PKC and NF-{kappa}B inhibition. The data further demonstrate that AEC chemokine responses were not be mediated by the recently described dectin-1 receptor, but instead involved participation of cell surface lactosylceramide. These data support a significant role for AECs in host responses during Pneumocystis pneumonia, and further indicate that {beta}-glucan induces inflammatory cytokine production through NF-{kappa}B dependent mechanisms.




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