TY - JOUR
T1 - CD4+ cells play a limited role in murine lung infection with Mycobacterium kansasii
AU - Wieland, Catharina W.
AU - Florquin, Sandrine
AU - Pater, Jennie M.
AU - Weijer, Sebastiaan
AU - van der Poll, Tom
PY - 2006
Y1 - 2006
N2 - Mycobacterium kansasii has emerged as an important nontuberculous mycobacterium that can cause severe infection in the immunocompromised host, especially in human immunodeficiency virus-infected patients. However, little is known about the pathogenesis of this infection. Because patients suffering from M. kansasii infection are severely compromised in their cellular immune response, we studied the course of infection in CD4+ cell knockout (KO) mice. Wild-type (WT) mice and CD4+ KO mice were infected with 10(5) cfu of M. kansasii. Although previously shown to be susceptible to Mycobacterium tuberculosis infection, CD4+ KO mice demonstrated no impairment in clearing infection with M. kansasii when compared with WT animals, despite reduced pulmonary inflammation (reduced granuloma formation and lymphocyte infiltration in the lungs). Pulmonary IFN-gamma levels and M. kansasii-induced IFN-gamma production by splenocytes from infected animals were reduced in CD4+ KO mice, confirming that these mice were defective in the M. kansasii-specific T helper cell type 1 immune response. Furthermore, mice deficient for IFN-gamma, IL-12p35, IL-12p40, or IL-18 also displayed a normal host defense against pulmonary infection with M. kansasii. These data suggest that CD4+ cells, IFN-gamma, and an intact T helper cell type 1 response play a limited role in protective immunity against pulmonary M. kansasii infection
AB - Mycobacterium kansasii has emerged as an important nontuberculous mycobacterium that can cause severe infection in the immunocompromised host, especially in human immunodeficiency virus-infected patients. However, little is known about the pathogenesis of this infection. Because patients suffering from M. kansasii infection are severely compromised in their cellular immune response, we studied the course of infection in CD4+ cell knockout (KO) mice. Wild-type (WT) mice and CD4+ KO mice were infected with 10(5) cfu of M. kansasii. Although previously shown to be susceptible to Mycobacterium tuberculosis infection, CD4+ KO mice demonstrated no impairment in clearing infection with M. kansasii when compared with WT animals, despite reduced pulmonary inflammation (reduced granuloma formation and lymphocyte infiltration in the lungs). Pulmonary IFN-gamma levels and M. kansasii-induced IFN-gamma production by splenocytes from infected animals were reduced in CD4+ KO mice, confirming that these mice were defective in the M. kansasii-specific T helper cell type 1 immune response. Furthermore, mice deficient for IFN-gamma, IL-12p35, IL-12p40, or IL-18 also displayed a normal host defense against pulmonary infection with M. kansasii. These data suggest that CD4+ cells, IFN-gamma, and an intact T helper cell type 1 response play a limited role in protective immunity against pulmonary M. kansasii infection
U2 - https://doi.org/10.1165/rcmb.2005-0198OC
DO - https://doi.org/10.1165/rcmb.2005-0198OC
M3 - Article
C2 - 16195537
SN - 1044-1549
VL - 34
SP - 167
EP - 173
JO - American journal of respiratory cell and molecular biology
JF - American journal of respiratory cell and molecular biology
IS - 2
ER -