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Recent investigations indicate that AECs produce macrophage inflammatory protein-2 (MIP-2) and tumor necrosis factor-\u03b1 (TNF-\u03b1) following challenge with Pneumocystis carinii. Nuclear factor-\u03baB (NF-\u03baB) is a ubiquitous transcription factor critical for regulation of proinflammatory cytokine expression. Herein, we assess rat AEC NF-\u03baB responses to challenge with a P. carinii \u03b2-glucan cell wall component (PCBG). Prominent nuclear translocation of p65 NF-\u03baB was demonstrated following PCBG challenge. NF-\u03baB 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-\u03b1 mRNA production, a response that was ameliorated by NF-\u03baB inhibition. MIP-2 protein expression was also dramatically increased by PCBG challenge, in a manner that was significantly attenuated by both PKC and NF-\u03baB inhibition. The data further demonstrate that AEC chemokine responses were not 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 \u03b2-glucan induces inflammatory cytokine production through NF-\u03baB\u2013dependent mechanisms.<\/jats:p>","DOI":"10.1165\/rcmb.2004-0300oc","type":"journal-article","created":{"date-parts":[[2005,3,3]],"date-time":"2005-03-03T20:35:01Z","timestamp":1109882101000},"page":"490-497","source":"Crossref","is-referenced-by-count":97,"title":["<i>Pneumocystis<\/i>\n                    Cell Wall \u03b2-Glucans Stimulate Alveolar Epithelial Cell Chemokine Generation through Nuclear Factor-\u03baB\u2013Dependent Mechanisms"],"prefix":"10.1093","volume":"32","author":[{"given":"Scott E.","family":"Evans","sequence":"first","affiliation":[{"name":"Thoracic Diseases Research Unit, Division of Pulmonary, Critical Care and Internal Medicine, Department of Medicine; Department of Immunology; and Department of Biochemistry and Molecular Biology, Mayo Clinic College of 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