title: Induced susceptibility of host is associated with an impaired antioxidant system following infection with Cryptosporidium parvum in Se-deficient mice.
abstract: BACKGROUND
  Susceptibility or resistance to infection with Cryptosporidium parvum (C.parvum) correlates with Selenium (Se) deficiency in response to infection. Both adult Se-adequate and Se-deficient mouse models of cryptosporidiosis were used to study the cell-mediated immune response during the course of C. parvum infection.
  
  
  RESULTS
  Blood samples from mouse models were used for Se status. The concentration of MDA, SOD, GPx and CAT in blood has revealed that lower Se level exist in Se-deficient mice. Mesenteric lymph node (MLN) lymphocytes from both mouse models were proliferated after ex vivo re-stimulation with C. parvum sporozoite antigen. The study of the cytokine profiles from the supernatant of proliferated MLN cells revealed that Se-adequate mice produced higher levels of Th1 (IFN-gamma and IL-2) and moderate amounts of Th2 (IL-4) cytokines throughout the course of infection. Whereas, MLN cells from Se-deficient mice produced lower levels of IFN-gamma, IL-2 and IL-4 cytokines. The counts of total white cell and CD3, CD4, CD8 cell in Se-adequate were higher than that in Se-deficient mice.
  
  
  CONCLUSIONS
  These results suggest that Cell immunity is affected by Se status after infection with C. parvum from kinetic changes of different white cells and cytokine. In conclusion, induced susceptibility of host is associated with an impaired antioxidant system following infection with C. parvum in C57BL/6 Selenium deficient mice.
authors.affiliation: National Research Center For Wildlife Born Diseases, Key Laboratory of Animal Ecology and Conservation Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, People's Republic of China.
authors.forename: Chengmin
authors.initials: C
authors.lastname: Wang
authors.forename: Yanyun
authors.initials: Y
authors.lastname: Wu
authors.forename: Jianhua
authors.initials: J
authors.lastname: Qin
authors.forename: Haoxue
authors.initials: H
authors.lastname: Sun
authors.forename: Hongxuan
authors.initials: H
authors.lastname: He
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000276:immunology; D000975:Antioxidants / Q000378:metabolism*; D002374:Catalase / Q000097:blood; D003457:Cryptosporidiosis / Q000276:immunology* / Q000469:parasitology; D016785:Cryptosporidium parvum / Q000302:isolation & purification*; D016207:Cytokines / Q000096:biosynthesis; D004198:Disease Susceptibility; D005979:Glutathione Peroxidase / Q000097:blood; D007111:Immunity, Cellular; D007958:Leukocyte Count; D008315:Malondialdehyde / Q000097:blood; D051379:Mice; D008810:Mice, Inbred C57BL; D012643:Selenium / Q000172:deficiency*; D013482:Superoxide Dismutase / Q000097:blood
chemical_list: D015703:Antigens, CD; D000975:Antioxidants; D016207:Cytokines; D008315:Malondialdehyde; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D012643:Selenium