In the present study we verified the hypothesis that a perturbation of the anticandidal T helper (Th) cell function in mucosal tissues might be associated with gastrointestinal (GI) colonization by C.albicans. To this purpose, DBA/2 female mice H-2d), known to be highly susceptible to inoculation candidiasis, were GI colonized by an oral-intragastric inoculation with viable C.albicans cells. Two weeks after infection, at the time when the number of viable yeast cells were highest in the stomach and absent in visceral organs such as kidneys, local and systemic parameters of T helper immunity were evaluated in terms of: a) pattern of IFN-gamma and IL-5 producing cells in T cell populations isolated from Payer's Patches (PP), mesenteric lymph nodes (MLN) and spleen cells (SC); b) isotype of immunoglobulins produced by PP cells in vitro and c) resistance of GI colonized mice to a lethal systemic infection. The results can be summarized as follows: a) GI colonization of DBA/2 mice resulted in an impaired production of IL-5 and IgA antibodies by PP cells in vitro, the effect being mainly due to the decreased number of IL-5-producing T cells in vivo; b) concurrently, the IFN-gamma production by PP cells was decreased, even though to a smaller extent; c) in contrast, the number of IFN-gamma-producing T cells in vivo increased in MLN and SC from colonized mice which showed high levels of serum IFN-gamma; d) colonized mice developed a strong DTH response to Candida antigens and were more resistant to a lethal systemic infection than uninfected controls. Taken together, these results suggest that, analogous to what observed in systemic infection, differential activation of T CD4+ subsets may occur in mice with mucosal candidiasis.

*Candidiasis/IMMUNOLOGY *Gastric Mucosa/IMMUNOLOGY *Stomach Diseases/IMMUNOLOGY

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