It mediates both heterophilic (ALCAM-CD6) and homophilic (ALCAM-ALCAM) cell-cell interactions [72]. Its down-regulation in expression would affect the movement and thus phagocytic function of AMs. The cell death-inducing DFF45-like effector (CIDE) family proteins include CIDEA, CIDEB, and CIDEC. These proteins are important regulators of energy homeostasis and are closely linked to the development of metabolic LY2835219 mw disorders including obesity, diabetes, and liver steatosis. CIDEA may initiate apoptosis by disrupting a complex consisting of the 40-kDa caspase-3-activated nuclease (DFF40/CAD) and its 45-kDa inhibitor (DFF45/ICAD) [73]. Its down-regulation can be viewed as the attempt of AMs to fight for survival
by decreasing CIDEA-mediated apoptosis. Conclusions Our data provide the first comprehensive description of the response of AMs to Pneumocystis infection using microarray and revealed a wide variety of genes and cellular functions that are affected by dexamethasone or Pneumocystis infection. Dexamethasone will continue to be used for immunosuppression if the rat PCP model is to be used for study of Pneumocystis infection.
Knowing what dexamethasone will do to the cells will give investigators a better insight in studying the effect of Pneumocystis infection on gene expression and function of AMs. This study also revealed many defects of AMs that may occur AZD8186 concentration during Pneumocystis infection, as many genes whose expressions are affected by the infection. Investigation of these genes will allow us to better understand the mechanisms of pathogenesis of PCP. Acknowledgements This study was supported by grants from the National Institutes of Health (RO1 HL65170 and RO1 AI062259). We thank the Center for Medical Genomics at Indiana University School of Medicine for assistance in Affymetrix
GeneChip analysis. Electronic supplementary material Additional file 1: Table S1. Rat alveolar macrophage genes up-regulated by dexamethasone. Table S2. Rat alveolar macrophage genes down-regulated by dexamethasone. Table S3. Rat alveolar macrophage genes up-regulated by Pneumocystis infection. Table S4. Rat alveolar macrophage genes down-regulated PLEK2 by Pneumocystis infection. (PDF 211 KB) References 1. Sepkowitz KA: Opportunistic infections in patients with and patients without Acquired Immunodeficiency Syndrome. Clin Infect Dis 2002,34(8):1098–1107.PubMedCrossRef 2. Tellez I, Barragán M, Franco-Paredes C, Petraro P, Nelson K, Del Rio C: Pneumocystis jiroveci pneumonia in patients with AIDS in the inner city: a persistent and deadly opportunistic infection. Am J Med Sci 2008,335(3):192–197.PubMedCrossRef 3. Mocroft A, Sabin CA, Youle M, Madge S, Tyrer M, Devereux H, Deayton J, Dykhoff A, Lipman MC, Phillips AN, et al.: Changes in AIDS-defining illnesses in a London Clinic, 1987–1998. J Acquir selleck chemicals llc Immune Defic Syndr 1999,21(5):401–407.PubMedCrossRef 4. Matsumoto Y, Matsuda S, Tegoshi T: Yeast glucan in the cyst wall of Pneumocystis carinii .