Predominance of Th1 Immune Response in Pleural Effusion of Patients with Tuberculosis among Other Exudative Etiologies.

Autor: da Cunha Lisboa V; Laboratory of Immunopathology, Medical Science Faculty, Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil., Ribeiro-Alves M; Laboratory of Clinical Research on STD/AIDS, National Institute of Infectology Evandro Chagas, Oswaldo Cruz Institute, Rio de Janeiro, Rio de Janeiro, Brazil., da Silva Corrêa R; Laboratory of Immunopathology, Medical Science Faculty, Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil., Ramos Lopes I; Laboratory of Immunopathology, Medical Science Faculty, Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil., Mafort TT; Department of Pulmonary and Tisiology Care, Pedro Ernesto University Hospital/Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil., Santos AP; Department of Pulmonary and Tisiology Care, Pedro Ernesto University Hospital/Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil., Porto Amadeu T; Laboratory of Immunopathology, Medical Science Faculty, Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil., Rufino R; Department of Pulmonary and Tisiology Care, Pedro Ernesto University Hospital/Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil., Silva Rodrigues L; Laboratory of Immunopathology, Medical Science Faculty, Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil lrodrigues.uerj@gmail.com.
Jazyk: angličtina
Zdroj: Journal of clinical microbiology [J Clin Microbiol] 2019 Dec 23; Vol. 58 (1). Date of Electronic Publication: 2019 Dec 23 (Print Publication: 2019).
DOI: 10.1128/JCM.00927-19
Abstrakt: Pleural tuberculosis (PlTB), a common form of extrapulmonary TB, remains a challenge in the diagnosis among many causes of pleural effusion. We recently reported that the combinatorial analysis of interferon gamma (IFN-γ), IFN-γ-inducible protein 10 (IP-10), and adenosine deaminase (ADA) from the pleural microenvironment was useful to distinguish pleural effusion caused by TB (microbiologically confirmed or not) among other etiologies. In this cross-sectional cohort study, a set of inflammatory mediators was quantified in blood and pleural fluid (PF) from exudative pleural effusion cases, including PlTB ( n  = 27) and non-PlTB (nTB) ( n  = 25) patients. The levels of interleukin-2 (IL-2), IL-4, IL-6, IL-10, IL-17A, IFN-γ, tumor necrosis factor (TNF), IP-10, transforming growth factor β1 (TGF-β), and ADA were determined using cytometric bead assay, enzyme-linked immunosorbent assay (ELISA), or biochemical tests. IFN-γ, IP-10, TNF, TGF-β, and ADA quantified in PF showed significantly higher concentrations in PlTB patients than in nTB patients. When blood and PF were compared, significantly higher concentrations of IL-6 and IL-10 in PF were identified in both groups. TGF-β, solely, showed significantly increased levels in PF and blood from PlTB patients when both clinical specimens were compared to those from nTB patients. Principal-component analysis (PCA) revealed a T helper type 1 (Th1) pattern attributed mainly to higher levels of IP-10, IFN-γ, TGF-β, and TNF in the pleural cavity, which was distinct between PlTB and nTB. In conclusion, our findings showed a predominantly cellular immune response in PF from TB cases, rather than other causes of exudative effusion commonly considered in the differential diagnosis of PlTB.
(Copyright © 2019 American Society for Microbiology.)
Databáze: MEDLINE
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