Low dose of Concanavalin-A enhances innate immune response and prevents liver injury in mice infected withCandida albicans

Abstract

The mechanisms through which Candida albicans is recognized by immune cells and how it triggers host defence are not completely understood. In this study, we evaluated the effect of Concanavalin-A on the clearance of C. albicans by infected mice and their production of proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha). Subgroups of 5 animals were pretreated with Con-A (250 mug mL(-1) PBS) and after 96 h were infected intraperitoneally with 10(7) cells of C. albicans CR15 (an isolate from a HIV+ person); 30 min, 2, 6, 24 or 72 h after infection the mice were sacrificed. Phagocytosis of C. albicans by peritoneal macrophages increased 30 min after infection in mice pretreated with Con-A. The liver presented the greatest number of CFUs, and this number was reduced by pretreatment with Con-A. Control animals infected with C. albicans presented a significant increase in plasmatic alanine aminotransferase, which was not observed in mice treated with Con-A. Two hours after infection the production of TNF-alpha in the liver of mice pretreated with Con-A was significantly increased. These results suggest that a single dose of Con-A caused a beneficial modulating action of the inflammatory response during infection with C. albicans.

Protective effect of Artin M from extract of Artocarpus integrifolia seeds by Th1 and Th17 immune response on the course of infection by Candida albicans

“…Dysfunction in cell-mediated immunity by low IFN-γ production has been also verified in patients with mucocutaneous candidiasis [7]. Therefore, strategies that cause an increase in Th1 immune response and increased phagocytic functions have been used in experimental models [8][9][10].…”

Artin M enhances TNF-α production and phagocytosis of Candida albicans mediated by dectin-1 and mannose receptors

“…Previously, our group observed that containment of dimorphism was correlated with an increase in TNF-α levels, as described for concanavalin-A-activated macrophages in phagocytic assays [12]. TNF-α is a cytokine produced by macrophages that increases respiratory burst and antifungal activities [4,10,12,24,25,28].…”

“…Therefore, treatment with cytokines that present immunoregulatory activity has been studied, particularly those that promote the activation of neutrophils and macrophages. Studies involving experimental animal models have shown that Th1 cells play an important role in regulating the immune response to Candida albicans infection by secreting cytokines that modulate the activity of immune effector cells [3][4][5][6]. Cytokines produced by Th1 cells activate phagocytes to the fungicidal state, whereas those produced by Th2 cells exacerbate the disease, because they deactivate fungicidal effector cells [7][8][9].…”

Interações entre Candida albicans e hospedeiro

“…As células do padrão T helper 1 (TH1), T helper 2 (TH2), T helper 17 (TH17) e T regulatórias (Tregs) com funções efetoras diferentes estão relacionadas com manifestações clínicas de diferentes graus de severidade ou superação da infecção ou ainda comensalismo (ROMANI; KAUFMANN, 1998;ROMANI, 2004;KOGUCHI;KAWAKAMI, 2002;HUFFNAGLE;DEEPE, 2003;CONCHON-COSTA et al, 2007;GAZIRI, 2008;FELIPE et al, 2008).…”

“…Tais polissacarídeos e glicoconjugados são reconhecidos por várias lectinas que podem atuar independentemente ou em associação com receptores tipo Toll ou ainda com outros receptores de sinalização (CONCHON-COSTA et al, 2006;GAZIRI, 2008). Os receptores dectina-1 podem reconhecer o ligante independente ou associado a receptores tipo Toll-2 para conferir responsividade a β-glucanas microbianas GANTNER;SIMMONS;UNDERHILL, 2005;LOYOLA et al, 2007;ROSAS et al, 2008).…”