Granulomas, the pathologic hallmarks of tuberculosis, are composed of tightly numerous immune cells that respond to a variety of persistent stimuli during pathogen-host interaction. The granuloma is essential for host containment of mycobacterial infection, however, the mechanism of host and pathogen determinants to recruit immune cells at the site of inflammation and the formation of granulomas remains elusive until now. Macrophage migration inhibitory factor (MIF), a cytokine produced by many cell types, modulates cellular and humoral immune responses and promote lymphocytes migration to the site of infection. In this study, we evaluate the expression of MIF in tuberculous granulomas by three different models of diseases: mouse, human tissues and zebrafish. The overall results demonstrated that the expression of MIF positive signals markedly increased in the tissues which have been infected with mycobacterium, whereas a few presence of MIF in the PBS-treated animals (means the control group). In the mycobacterial-infected animals, the MIF positives distributed extensively within the granuloma especially in the multinucleated giant cells. Thus, three independent lines of evidence support the hypothesis that MIF may be an important player in aggregate immune cells to the granuloma microenvironments in these animal models of tuberculosis.
Copyright © 2012 Elsevier Inc. All rights reserved.