TY - JOUR
T1 - Alterations of the mucosal immune system due to Cryptosporidium parvum infection in normal mice
AU - Huang, Dennis S.
AU - Lopez, Maria C.
AU - Wang, James Y.
AU - Martinez, Franciscia
AU - Watson, Ronald R.
N1 - Funding Information:
We especially thank Esther Kerr and Helen Russell for the technical assistance in the preparation of the paraf®n-embedded sections, Jan MacMillen for preparation of the cryostat sections, and Andrea Hebert for staining the cryostat sections. D. S. Huang, M. C. Lopez, and J. Y. Wang contributed equally to the work presented here. This work was supported by NIH Research Grant AA09037.
PY - 1996/11/1
Y1 - 1996/11/1
N2 - The mechanism with which the immune system of an immunocompetent host responds to Cryptosporidium parvum infection is still poorly understood. We have therefore investigated the immune response of adult immunocompetent C57BL/6 mice at Days 6 and 10 to postinfection during a self-limiting C. parvum infection. We evaluated the immune changes at the levels of intestinal intraepithelium and lamina propria as well as mesenteric lymph nodes. At Day 6 postinfection, there was a decrease in the production of IFN-γ, IL-5, IL-6, and IL-10 by in vitro mitogen-stimulated intraepithelial lymphocytes. Moreover, an increase in the number of γδ-TCR+, CD8+, and cytoplasmic IgE+ cells in intestinal lamina propria was found. Concomitantly, a significant decrease in the number of cytoplasmic IgA+ and IgG+ cells was observed. These phenotypic changes may be associated with the cytokine-producing profile (decreased IL-4, IFNγ, and IL-10) by lamina propria lymphocytes. At Days 6 and 10 postinfection cytoplasmic IgA+ and IgG+ cell numbers remained. Nevertheless, the production of IL-5 and IL-10 by intraepithelial lymphocytes was higher than the noninfected control values; these changes may be associated with the decreased CD4+ cell numbers. In mesenteric lymphocytes IgG and IgA production in vitro was elevated while no changes were observed in cytokine production except for a significant decrease in IL-5. In conclusion, our results demonstrate that an immunocompetent defense mechanism leading to a successful recovery from C. parvum infection involved changes of T(H1-) or T(H2)-type cytokine production as well as alterations of the lymphocyte subpopulation at mucosal-associated lymphoid tissues.
AB - The mechanism with which the immune system of an immunocompetent host responds to Cryptosporidium parvum infection is still poorly understood. We have therefore investigated the immune response of adult immunocompetent C57BL/6 mice at Days 6 and 10 to postinfection during a self-limiting C. parvum infection. We evaluated the immune changes at the levels of intestinal intraepithelium and lamina propria as well as mesenteric lymph nodes. At Day 6 postinfection, there was a decrease in the production of IFN-γ, IL-5, IL-6, and IL-10 by in vitro mitogen-stimulated intraepithelial lymphocytes. Moreover, an increase in the number of γδ-TCR+, CD8+, and cytoplasmic IgE+ cells in intestinal lamina propria was found. Concomitantly, a significant decrease in the number of cytoplasmic IgA+ and IgG+ cells was observed. These phenotypic changes may be associated with the cytokine-producing profile (decreased IL-4, IFNγ, and IL-10) by lamina propria lymphocytes. At Days 6 and 10 postinfection cytoplasmic IgA+ and IgG+ cell numbers remained. Nevertheless, the production of IL-5 and IL-10 by intraepithelial lymphocytes was higher than the noninfected control values; these changes may be associated with the decreased CD4+ cell numbers. In mesenteric lymphocytes IgG and IgA production in vitro was elevated while no changes were observed in cytokine production except for a significant decrease in IL-5. In conclusion, our results demonstrate that an immunocompetent defense mechanism leading to a successful recovery from C. parvum infection involved changes of T(H1-) or T(H2)-type cytokine production as well as alterations of the lymphocyte subpopulation at mucosal-associated lymphoid tissues.
UR - http://www.scopus.com/inward/record.url?scp=0030296273&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0030296273&partnerID=8YFLogxK
U2 - 10.1006/cimm.1996.0265
DO - 10.1006/cimm.1996.0265
M3 - Article
C2 - 8912874
AN - SCOPUS:0030296273
SN - 0008-8749
VL - 173
SP - 176
EP - 182
JO - Cellular Immunology
JF - Cellular Immunology
IS - 2
ER -