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Title:   Author  item
                                            Waters, Wadeitem
                                            Palmer, Mitchellitem
                                            Nonnecke, Brianitem
                                            Waters, Theresaitem
                                            Whipple, Diana
  Submitted to: Meeting Abstract
                                    Publication Type: Abstract Only
                                    Publication Acceptance Date: 5/6/2003
                                    Publication  Date: N/A
                                    Citation: N/AInterpretive Summary:
                                Technical Abstract: Mycobacterium bovis infection of cattle represents a natural host/pathogen interaction and, in addition to its economic and zoonotic impact, represents a model for human tuberculosis. To determine effects of M. bovis infection on adhesion molecule expression, peripheral blood mononuclear cells from M. bovis-infected cattle were stimulated with M. bovis PPD or pokeweed mitogen (PWM) and evaluated concurrently for proliferation and activation marker expression. Stimulation with PPD or PWM increased CD25 and CD44 mfi and decreased CD62L mfi on CD4+ cells from infected animals.  CD62L mfi on PPD- and PWM-stimulated gd TCR+ and CD8+ cells was also reduced when compared to that of non-stimulated gd TCR+ and CD8+ cells. Using a dye tracking assay, it was determined that proliferating cells, regardless of lymphocyte subset, exhibited increased expression of CD25 and CD44 and decreased expression of CD62L when compared to that of cells that had not proliferated. In contrast to proliferation, activation-induced apoptosis of CD4+ cells resulted in a significant down regulation of CD44 expression. Lymphocytes obtained from lungs of M. bovis-infected cattle also had reduced expression of CD44 when compared to lymphocytes from lungs of non-infected cattle. These alterations in surface molecule expression upon activation likely impact trafficking to sites of inflammation and the functional capacity of these cells within tuberculous granulomas.


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