RT Journal Article
SR Electronic
T1 The discriminant pattern of pleural fluid inflammatory mediators between tuberculosis and other causes of exudative pleural effusion
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 667360
DO 10.1101/667360
A1 Vinícius da Cunha Lisboa
A1 Raquel da Silva Corrêa
A1 Marcelo Ribeiro-Alves
A1 Isabelle Ramos Lopes
A1 Thiago Thomaz Mafort
A1 Ana Paula Gomes dos Santos
A1 Thaís Porto Amadeu
A1 Rogério Lopes Rufino Alves
A1 Luciana Silva Rodrigues
YR 2019
UL http://biorxiv.org/content/early/2019/06/11/667360.abstract
AB Pleural tuberculosis (PlTB), a form of extrapulmonary TB, remains as 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 or not confirmed cases) among other etiologies. In this prospective cohort study, a set of inflammatory mediators was quantified in blood and pleural fluid (PF) from exudative pleural effusion cases, including PlTB (n = 22) and non-PlTB (NTB; n= 17) patients. The levels of IL-2, IL-4, IL-6, IL-10, IL-17A, IFN-γ, TNF, IP-10, TGF-β1, and ADA were measured and a principal component analysis was applied in order to identify the mediators who contributed most for the variance in data. IFN-γ, IP-10, TNF, TGF-β, and ADA quantified in PF showed significantly higher concentrations in PlTB patients when compared to NTB ones. When blood and PF were compared, we have identified significantly higher concentrations of IL-6 and IL-10 in PF, in both groups. TGF-β, solely, showed significantly increased levels in PF and blood from PlTB when both clinical specimens were compared to NTB patients. Principal components analysis from PF revealed that the ADA, IP-10, TGF-β, and IFN-γ contributed most for the discriminatory capacity between TPlB and NTB. Our findings showed that important inflammatory mediators in PF may discriminate TB cases from other causes of exudative effusion, the main diseases considered in the differential diagnosis of PlTB.