Interleukin-9 in Immunopathology of Trypanosoma cruzi Experimental Infection
Chagas' disease is a parasitosis caused by , which affects approximately 8 million people worldwide. The balance between pro- and anti-inflammatory cytokines produced during immunological responses contributes to disease prognosis and progression. Parasite tissue persistence can induce chronic...
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| Published in: | Frontiers in cellular and infection microbiology Vol. 11; p. 756521 |
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| Main Authors: | , , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
Switzerland
Frontiers Media S.A
15-10-2021
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| Subjects: | |
| Online Access: | Get full text |
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| Summary: | Chagas' disease is a parasitosis caused by
, which affects approximately 8 million people worldwide. The balance between pro- and anti-inflammatory cytokines produced during immunological responses contributes to disease prognosis and progression. Parasite tissue persistence can induce chronic inflammatory stimuli, which can cause long-term tissue injury and fibrosis. Chronic Chagas' patients exhibit increased levels of interleukin (IL)-9, an important cytokine in the regulation of inflammatory and fibrogenic processes. Data on the role of IL-9 in other pathologies are sometimes contradictory, and few studies have explored this cytokine's influence in Chagas' disease pathology. Hence, the aim of this study was to evaluate the role of IL-9 in the progression of
infection
and
.
infection demonstrated that IL-9 reduced the number of infected cells and decreased the multiplication of intracellular amastigotes in both C2C12 myoblasts and bone marrow-derived macrophages. In myoblasts, the increased production of nitric oxide (NO) was essential for reduced parasite multiplication, whereas macrophage responses resulted in increased IL-6 and reduced TGF-β levels, indicating that parasite growth restriction mechanisms induced by IL-9 were cell-type specific. Experimental infection of BALB/c mice with
trypomastigotes of the Y strain implicated a major role of IL-9 during the chronic phase, as increased Th9 and Tc9 cells were detected among splenocytes; higher levels of IL-9 in these cell populations and increased cardiac IL-9 levels were detected compared to those of uninfected mice. Moreover, rIL9 treatment decreased serum IL-12, IL-6, and IL-10 levels and cardiac TNF-α levels, possibly attempting to control the inflammatory response. IL-9 neutralization increased cardiac fibrosis, synthesis of collagens I and III, and mastocyte recruitment in BALB/c heart tissue during the chronic phase. In conclusion, our data showed that IL-9 reduced the invasion and multiplication of
, in both myoblasts and macrophages, favoring disease control through cell-specific mechanisms.
, IL-9 was elevated during experimental chronic infection in BALB/c mice, and this cytokine played a protective role in the immunopathological response during this phase by controlling cardiac fibrosis and proinflammatory cytokine production. |
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| Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 This article was submitted to Parasite and Host, a section of the journal Frontiers in Cellular and Infection Microbiology Reviewed by: Renato Augusto DaMatta, State University of the North Fluminense Darcy Ribeiro, Brazil; Bellisa Freitas Barbosa, Federal University of Uberlandia, Brazil Edited by: Andréa Teixeira-Carvalho, René Rachou Institute (Fiocruz), Brazil |
| ISSN: | 2235-2988 2235-2988 |
| DOI: | 10.3389/fcimb.2021.756521 |