Prado, Morgana K. B.
[1, 2, 3]
Souza, Camila O. S.
Gardinassi, Luiz G.
Zoccal, Karina F.
de Paula-Silva, Francisco W. G.
Peti, Ana P. F.
Sorgi, Carlos A.
Meirelles, Alyne F. G.
Ramos, Simone G.
Alves-Filho, Jose C.
Faccioli, Lucia H.
Número total de Autores: 12
Afiliação do(s) autor(es):
 Univ Sao Paulo, Dept Anal Clin Toxicol & Bromatol, Fac Ciencias Farmaceut Ribeirao Preto, BR-14040903 Ribeirao Preto, SP - Brazil
 Univ Fed Goias, Inst Patol Trop & Saude Publ, BR-74605050 Goiania, Go - Brazil
 Univ Sao Paulo, Programa Posgrad Imunol Basica & Aplicada, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP - Brazil
 Ctr Univ Barao de Maua, BR-14090180 Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Dept Patol & Med Legal, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP - Brazil
 Univ Sao Paulo, Dept Farmacol, Fac Med Ribeirao Preto, BR-14049900 Ribeirao Preto, SP - Brazil
Número total de Afiliações: 6
Tipo de documento:
Citações Web of Science:
Histoplasma capsulatum is the agent of histoplasmosis, one of the most frequent mycoses in the world. The infection initiates with fungal spore inhalation, transformation into yeasts in the lungs and establishment of a granulomatous disease, which is characterized by a Th1 response. The production of Th1 signature cytokines, such as IFN-gamma, is crucial for yeast clearance from the lungs, and to prevent dissemination. Recently, it was demonstrated that IL-17, a Th17 signature cytokine, is also important for fungal control, particularly in the absence of Th1 response. IL-22 is another cytokine with multiple functions on host response and disease progression. However, little is known about the role of IL-22 during histoplasmosis. In this study, we demonstrated that absence of IL-22 affected the clearance of yeasts from the lungs and increased the spreading to the spleen. In addition, IL-22 deficient mice (Il22(-/-)) succumbed to infection, which correlated with reductions in the numbers of CD4(+) IFN-gamma(+) T cells, reduced IFN-gamma levels, and diminished nitric oxide synthase type 2 (NOS2) expression in the lungs. Importantly, treatment with rIFN-gamma mitigated the susceptibility of Il22(-/-) mice to H. capsulatum infection. These data indicate that IL-22 is crucial for IFN-gamma/NO production and resistance to experimental histoplasmosis. (AU)