e-Article
Role of Th17 Cytokines in the Liver's Immune Response during Fatal Yellow Fever: Triggering Cell Damage Mechanisms.
Document Type
Article
Author
Carvalho, Marcos Luiz Gaia; Falcão, Luiz Fábio Magno; da Costa Lopes, Jeferson; Mendes, Caio Cesar Henriques; Olímpio, Fábio Alves; Miranda, Vanessa do Socorro Cabral; Santos, Lais Carneiro dos; de Moraes, Daniel Dias Pinheiro; Bertonsin Filho, Marcos Virgilio; da Costa, Luccas Delgado; da Silva Azevedo, Raimunda do Socorro; Cruz, Ana Cecília Ribeiro; Galúcio, Vanessa Costa Alves; Martins, Lívia Caricio; Duarte, Maria Irma Seixas; Martins Filho, Arnaldo Jorge; Sousa, Jorge Rodrigues de; Vasconcelos, Pedro Fernando da Costa; Quaresma, Juarez Antônio Simões
Source
Subject
*YELLOW fever
*IMMUNE response
*LIVER
*HEMORRHAGIC diseases
*VIRUS diseases
*DEAD
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Language
ISSN
2073-4409
Abstract
Yellow fever (YF) is an infectious and acute viral haemorrhagic disease that triggers a cascade of host immune responses. We investigated the Th17 cytokine profile in the liver tissue of patients with fatal YF. Liver tissue samples were collected from 26 deceased patients, including 21 YF-positive and 5 flavivirus-negative patients, with preserved hepatic parenchyma architecture, who died of other causes. Histopathological and immunohistochemical analysis were performed on the liver samples to evaluate the Th17 profiles (ROR-γ, STAT3, IL-6, TGF-β, IL-17A, and IL-23). Substantial differences were found in the expression levels of these markers between the patients with fatal YF and controls. A predominant expression of Th17 cytokine markers was observed in the midzonal region of the YF cases, the most affected area in the liver acinus, compared with the controls. Histopathological changes in the hepatic parenchyma revealed cellular damage characterised mainly by the presence of inflammatory cell infiltrates, Councilman bodies (apoptotic cells), micro/macrovesicular steatosis, and lytic and coagulative necrosis. Hence, Th17 cytokines play a pivotal role in the immunopathogenesis of YF and contribute markedly to triggering cell damage in patients with fatal disease outcomes. [ABSTRACT FROM AUTHOR]