Correa, R. d. S. | Search bioRxiv

bioRxiv2024

Proteomic And Transcriptomic Host Biomarkers For Detection Of Pleural Tuberculosis

Current diagnosis of pleural tuberculosis (PLTB) is based on highly invasive procedures. Therefore, blood-based host biomarkers could represent a low-invasive diagnostic alternative. Plasma and pleural effusion, as well as blood-and pleural fluid mononuclear cells (PBMCs and PFMCs), were sampled from patients with PLTB and other pleural diseases (OPLDs). In pleural effusion, ApoA1, C1q, CRP, IL-6, IFN-{gamma}, IP-10, MIG, S100A12, SAA1/A2, and serpin-A3 were significantly higher in PLTB compared to OPLD, whereas only SAA1/A2 showed discriminatory potential in plasma. Increased mRNA levels were observed in PFMCs of PLTB for CD8A, GBP5, SLAMF7, CXCL10, IL2, GNLY, IL23A, PDCD1 and BCMA, whereas HMOX1, CD163, DUSP3, IGF1, GUSB and MARCO were decreased. In PBMCs of PLTB, only CCL22 expression was decreased. GBP5 was significantly higher expressed in PLTB for both cell types. This study shows the potential of transcriptomic and proteomic host biomarkers to differentiate PLTB from OPLDs also when applying low-invasive methods.

microbiology↗

bioRxiv2019

The discriminant pattern of pleural fluid inflammatory mediators between tuberculosis and other causes of exudative pleural effusion

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-{gamma}), IFN-{gamma}-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-{gamma}, TNF, IP-10, TGF-{beta}1, 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-{gamma}, IP-10, TNF, TGF-{beta}, 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-{beta}, 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-{beta}, and IFN-{gamma} 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.

immunology↗