Divergent chemokine, cytokine and beta-defensin responses to gastric candidiasis in immunocompetent C57BL/6 and BALB/c mice.
Previous studies of animal models of candidiasis have produced conflicting results concerning the cytokines and host defence mechanisms that are most relevant for protection against Candida infections. In this study, the host defence mechanisms evoked by two different immunocompetent murine strains following oral colonization with Candida albicans were assessed. beta-Defensin (mBD1, mBD3 and mBD4), chemokine (MIP-2 and KC) and cytokine (TNF-alpha, IFN-gamma, IL-4, IL-10, IL-12 and IL-15) gene expression in germ-free (gf) and C. albicans-infected (gastric) C57BL/6 and BALB/c mice was contrasted. Gf C57BL/6 and BALB/c mice expressed significantly different basal levels of mBD3, mBD4, TNF-alpha and IL-12 in gastric tissues; however, gf C57BL/6 and BALB/c mice were equally susceptible to intestinal colonization with C. albicans and had similar fungal burdens in gastric tissues 4 weeks after oral challenge. C57BL/6 mice responded to colonization and gastric candidiasis with increased expression of mBD1, mBD3, mBD4, TNF-alpha, MIP-2, KC and IL-12. Conversely, a much more specific and attenuated response was observed in Candida-infected gastric tissues from BALB/c mice. Therefore, different strains of mice that were equally susceptible to gastric candidiasis after oral challenge had divergent cytokine, chemokine and beta-defensin responses. This suggests that conflicting data as to the relevance of cytokines and other host factors in murine resistance to candidiasis may be explained, at least in part, by the strain of mouse studied.
Schofield
David A
DA
Department of Microbiology and Immunology1 and Department of Stomatology2, Medical University of South Carolina, 173 Ashley Avenue, Charleston, SC 29403, USA.
Westwater
Caroline
C
Department of Microbiology and Immunology1 and Department of Stomatology2, Medical University of South Carolina, 173 Ashley Avenue, Charleston, SC 29403, USA.
Balish
Edward
E
Department of Microbiology and Immunology1 and Department of Stomatology2, Medical University of South Carolina, 173 Ashley Avenue, Charleston, SC 29403, USA.
D000818:Animals; D002176:Candida albicans / Q000254:growth & development / Q000276:immunology*; D002177:Candidiasis / Q000276:immunology* / Q000382:microbiology; D018925:Chemokines / Q000235:genetics / Q000276:immunology*; D016207:Cytokines / Q000235:genetics / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D015870:Gene Expression; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000032:analysis; D013272:Stomach Diseases / Q000276:immunology* / Q000382:microbiology; D023083:beta-Defensins / Q000235:genetics / Q000276:immunology*
D018925:Chemokines; D016207:Cytokines; D012333:RNA, Messenger; D023083:beta-Defensins