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2017 ; 8
(ä): 949
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Th17-Inducing Cytokines IL-6 and IL-23 Are Crucial for Granuloma Formation during
Experimental Paracoccidioidomycosis
#MMPMID28871251
Tristão FSM
; Rocha FA
; Carlos D
; Ketelut-Carneiro N
; Souza COS
; Milanezi CM
; Silva JS
Front Immunol
2017[]; 8
(ä): 949
PMID28871251
show ga
Paracoccidioidomycosis (PCM), a chronic granulomatous disease caused by the
thermally dimorphic fungus Paracoccidioides brasiliensis and Paracoccidioides
lutzii, has the highest mortality rate among systemic mycosis. The T helper
1-mediated immunity is primarily responsible for acquired resistance during P.
brasiliensis infection, while susceptibility is associated with Th2 occurrence.
Th17 is a population of T CD4(+) cells that, among several chemokines and
cytokines, produces IL-17A and requires the presence of IL-1, IL-6, and TGF-? for
differentiation in mice and IL-23 for its maintenance. Th17 has been described as
an arm of the immune system that enhances host protection against several
bacterial and fungal infections, as Pneumocystis carinii and Candida albicans. In
this study, we aimed to evaluate the Th17 immune response and the role of
Th17-associated cytokines (IL-6, IL-23, and IL-17A) during experimental PCM.
First, we observed that P. brasiliensis infection [virulent yeast strain 18 of P.
brasiliensis (Pb18)] increased the IL-17A production in vitro and all the
evaluated Th17-associated cytokines in the lung tissue from C57BL/6 wild-type
mice. In addition, the deficiency of IL-6, IL-23, or IL-17 receptor A (IL-17RA)
impaired the compact granuloma formation and conferred susceptibility during
infection, associated with reduced tumor necrosis factor-?, IFN-?, and inducible
nitric oxide synthase enzyme expression. Our data suggest that IL-6 production by
bone marrow-derived macrophages (BMDMs) is important to promote the Th17
differentiation during Pb18 infection. In accordance, the adoptive transfer of
BMDMs from C57BL/6 to infected IL-6(-/-) or IL-17RA(-/-) mice reduced the fungal
burden in the lungs compared to nontransferred mice and reestablished the
pulmonary granuloma formation. Taken together, these results suggest that
Th17-associated cytokines are involved in the modulation of immune response and
granuloma formation during experimental PCM.