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Rodrigues, L. S.

Publications and source records attributed to Rodrigues, L. S..

2 recordsLinked to original sources

HERV-K and HERV-W transcriptional activity in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome

Chronic Fatigue Syndrome / Myalgic Encephalomyelitis (CFS / MS) is an incapacitating chronic disease that dramatically compromise the life quality. The CFS/ME pathogenesis is multifactorial, and it is believed that immunological, metabolic and environmental factors play a role. It is well documented an increased activity of Human endogenous retroviruses (HERVs) from different families in autoimmune and neurological diseases, making these elements good candidates for biomarkers or even triggers for such diseases. Here the expression of Endogenous retroviruses K and W (HERV-K and HERV-W) was determined in blood from moderately and severely affected ME/CFS patients. HERV-K was overexpressed only in moderately affected individuals and HERV-W showed no difference. This is the first report about HERV-K differential expression in moderate ME/CFS.

molecular biology

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