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논문 기본 정보

자료유형
학술저널
저자정보
José Luis Muñoz-Carrillo (Autonomous University of Zacatecas) José Luis Muñoz-López (Mexican Social Security Institute) José Jesús Muñoz-Escobedo (Autonomous University of Zacatecas) Claudia Maldonado-Tapia (Autonomous University of Zacatecas) Oscar Gutiérrez-Coronado (University of Guadalajara) Juan Francisco Contreras-Cordero (Autonomous University of Nuevo Leon) María Alejandra Moreno-García (Autonomous University of Zacatecas)
저널정보
대한기생충학열대의학회 Parasites, Hosts and Diseases The Korean Journal of Parasitology Vol.55 No.6
발행연도
2017.12
수록면
587 - 599 (13page)

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초록· 키워드

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The immune response against Trichinella spiralis at the intestinal level depends on the CD4+ T cells, which can both suppress or promote the inflammatory response through the synthesis of diverse cytokines. During the intestinal phase, the immune response is mixed (Th1/Th2) with the initial predominance of the Th1 response and the subsequent domination of Th2 response, which favor the development of intestinal pathology. In this context, the glucocorticoids (GC) are the pharmacotherapy for the intestinal inflammatory response in trichinellosis. However, its therapeutic use is limited, since studies have shown that treatment with GC suppresses the host immune system, favoring T. spiralis infection. In the search for novel pharmacological strategies that inhibit the Th1 immune response (proinflammatory) and assist the host against T. spiralis infection, recent studies showed that resiniferatoxin (RTX) had anti-inflammatory activity, which decreased the serum levels of IL-12, INF-γ, IL-1β, TNF-α, NO, and PGE₂ as well the number of eosinophils in the blood, associated with decreased intestinal pathology and muscle parasite burden. These researches demonstrate that RTX is capable to inhibit the production of Th1 cytokines, contributing to the defense against T. spiralis infection, which places it as a new potential drug modulator of the immune response.

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Abstract
INTRODUCTION
LIFE CYCLE OF T. SPIRALIS
IMMUNE RESPONSES TO T. SPIRALIS INFECTION
ANTI-INFLAMMATORY TREATMENT
CONCLUSIONS
REFERENCES

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