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Department of Microbiology, Immunology and Pathology, Mycobacteria Research Laboratories, Colorado State University, Fort Collins, CO 80523
Members of the CSF cytokine family play important roles in macrophage recruitment and activation. However, the role of M-CSF in pulmonary infection with Mycobacterium tuberculosis is not clear. In this study, we show the lungs of mice infected with M. tuberculosis displayed a progressive decrease in M-CSF in contrast to increasing levels of GM-CSF. Restoring pulmonary M-CSF levels during infection resulted in a significant decrease in the presence of foamy macrophages and increased expression of CCR7 and MHC class II, specifically on alveolar macrophages. In response to M-CSF, alveolar macrophages also increased their T cell-stimulating capacity and expression of DEC-205. These studies show that the levels of expression of M-CSF and GM-CSF participate in the progression of macrophages into foamy cells and that these cytokines are important factors in the differentiation and regulation of expression of dendritic cell-associated markers on alveolar macrophages. In addition, these studies demonstrate that M-CSF may have a role in the adaptive immune response to infection with M. tuberculosis.
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1 This work was supported by National Institutes of Health Grant AI44072.
2 Current address: Departamento de Histologia y Anatomia Patologica Comparadas, Universidad de Murcia, 30071 Murcia, Spain.
3 Address correspondence and reprint requests to Dr. Mercedes Gonzalez-Juarrero, Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523. E-mail address: malba{at}mail.colostate.edu
4 Abbreviations used in this paper: TB, tuberculosis; AM, alveolar macrophage; DC, dendritic cell; BAL, bronchoalveolar lavage; cRPMI, complete RPMI.
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