Abstract
Mice lacking the multidrug resistance protein 1 have a transiently impaired immune response during tuberculosis.
Verbon A, Leemans JC, Weijer S, Florquin S, Van Der Poll T.
Department of Infectious Diseases, Tropical Medicine and AIDS, Laboratory of Experimental Internal Medicine and Department of Pathology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. A.Verboon@amc.uva.nl
A T helper (Th) 1 immune response is important for host defense against tuberculosis. The multidrug resistance protein (Mrp) 1 is constitutively present at low levels on Th2 lymphocytes, and is expressed on Th1 lymphocytes upon activation. To determine the role of Mrp1 in the pathogenesis of tuberculosis, Mrp1 deficient (-/-) and normal wild type mice were intranasally infected with Mycobacterium tuberculosis. At 2 weeks after infection, Mrp1(-/-) mice had reduced levels of the Th1 cytokine interferon-gamma and an impaired granuloma formation in their lungs. At 5 weeks postinfection, M. tuberculosis outgrowth was enhanced in lungs and livers of Mrp1(-/-) mice. A more prolonged observation of these mice, up to 4 months, revealed no differences in survival or mycobacterial outgrowth. These data suggest that Mrp1 plays an early but dispensable role in the protective immune response to pulmonary tuberculosis.
Verbon A, Leemans JC, Weijer S, Florquin S, Van Der Poll T.
Department of Infectious Diseases, Tropical Medicine and AIDS, Laboratory of Experimental Internal Medicine and Department of Pathology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands. A.Verboon@amc.uva.nl
A T helper (Th) 1 immune response is important for host defense against tuberculosis. The multidrug resistance protein (Mrp) 1 is constitutively present at low levels on Th2 lymphocytes, and is expressed on Th1 lymphocytes upon activation. To determine the role of Mrp1 in the pathogenesis of tuberculosis, Mrp1 deficient (-/-) and normal wild type mice were intranasally infected with Mycobacterium tuberculosis. At 2 weeks after infection, Mrp1(-/-) mice had reduced levels of the Th1 cytokine interferon-gamma and an impaired granuloma formation in their lungs. At 5 weeks postinfection, M. tuberculosis outgrowth was enhanced in lungs and livers of Mrp1(-/-) mice. A more prolonged observation of these mice, up to 4 months, revealed no differences in survival or mycobacterial outgrowth. These data suggest that Mrp1 plays an early but dispensable role in the protective immune response to pulmonary tuberculosis.
| Original language | English |
|---|---|
| Pages (from-to) | 32-36 |
| Number of pages | 5 |
| Journal | Clinical Infectious Diseases |
| Volume | 130 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 1 Jan 2002 |