Galectins expressed differently in genetically susceptible C57BL/6 and resistant BALB/c mice during acute ocularToxoplasma gondiiinfection

Abstract

SUMMARYOcular toxoplasmosis (OT) caused byToxoplasma gondiiis a major cause of infectious uveitis, however little is known about its immunopathological mechanism. Susceptible C57BL/6 (B6) and resistant BALB/c mice were intravitreally infected with 500 tachyzoites of the RH strain ofT. gondii. B6 mice showed more severe ocular pathology and higher parasite loads in the eyes. The levels of galectin (Gal)-9 and its receptors (Tim-3 and CD137), interferon (IFN)-γ, IL-6 and IL-10 were significantly higher in the eyes of B6 mice than those of BALB/c mice; however, the levels of IFN-αand -βwere significantly decreased in the eyes and CLNs of B6 mice but significantly increased in BALB/c mice after infection. After blockage of galectin–receptor interactions byα-lactose, neither ocular immunopathology nor parasite loads were different from those of infected BALB/c mice withoutα-lactose treatment. Although the expressions of Gal-9/receptor were significantly increased in B6 mice and Gal-1 and -3 were upregulated in both strains of mice upon ocularT. gondiiinfection, blockage of galectins did not change the ocular pathogenesis of genetic resistant BALB/c mice. However, IFN-αand -βwere differently expressed in B6 and BALB/c mice, suggesting that type I IFNs may play a protective role in experimental OT.