Chlamydia trachomatis infection does not enhance local cellular immunity against concurrent Candida vaginal infection.
Although Th1-type cell-mediated immunity (CMI) is the predominant host defense mechanism against mucosal Candida albicans infection, CMI against a vaginal C. albicans infection in mice is limited at the vaginal mucosa despite a strong Candida-specific Th1-type response in the draining lymph nodes. In contrast, Th1-type CMI is highly effective against an experimental Chlamydia trachomatis genital tract infection. This study demonstrated through two independent designs that a concurrent Candida and Chlamydia infection could not accelerate or modulate the anti-Candida CMI response. Together, these results suggest that host responses to these genital tract infections are independent and not influenced by the presence of the other.
Kelly
K A
KA
Department of Pathology and Laboratory Medicine, UCLA Medical Center, Los Angeles, California, USA.
Gray
H L
HL
Walker
J C
JC
Rank
R G
RG
Wormley
F L
FL
Fidel
P L
PL
D000818:Animals; D018791:CD4 Lymphocyte Count; D002181:Candidiasis, Vulvovaginal / Q000276:immunology*; D002690:Chlamydia Infections / Q000276:immunology*; D002692:Chlamydia trachomatis; D005260:Female; D008213:Lymphocyte Activation; D051379:Mice; D008807:Mice, Inbred BALB C; D018417:Th1 Cells / Q000276:immunology