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Tuberculosis (TB) is a major cause of illness and public health concern, especially in resource-limited countries. This study analyzed the characteristics related to anti-TB drug resistance. Moreover, we examined the evidence-based indications for the treatment of active TB in Angola. This study evaluated the medical records of 176 patients screened for TB from January to September 2016 in Luanda, the capital city of Angola. Approximately 66.5% of the patients were newly diagnosed with active TB. The residence area showed a significant relationship with TB (P = 0.025), whereas age group (P = 0.272), gender (P = 0.853), and HIV status (P = 0.284) did not showed any relationship with TB. Overall, 72.4% of TB patients had resistance to at least one of the anti-TB drugs. The risk of anti-TB drug resistance was higher in males (odds ratio [OR]: 1.22; 95% confidence interval [CI]: 0.42–3.58, P = 0.685] and in TB-HIV coinfected patients [OR: 1.39; (95% CI: 0.26–7.28), P = 0.700], whereas it was lower in patients aged 30 years or older (OR: 0.56; 95% CI: 0.18–1.69) P = 0.303) and in patients living in urbanized areas (OR: 0.74; 95% CI: 0.17–3.25; P = 0.685). Our findings showed that drug-resistant TB is emerging in Angola. Further studies on factors related to anti-TB drug resistance are urgently needed to ascertain the magnitude of the problem and to proffer strategies toward TB control in Angola.

Background Despite the guidelines provided by the World Health Organization for the treatment of malaria, treatment failure occurs in many hospitalized patients. Objective Evaluate whether blood cell count parameters may serve as predictors for malaria treatment. Methodology A cross-sectional study with a quantitative approach. Results Of the 219 patients, 21.5% showed failure to antimalarial treatment, Patient with 21 and 40 years (72.6%), male (53.4%), from peri-urban area (47.5%), with high parasitemia (59.8%), treated with Arthemeter (90.9%) and the mortality were 5.9%. Significant associations were observed between occupation, level of parasitemia and outcome with resistance to antimalarial treatment (p Conclusion The importance of blood cell count parameters in monitoring malaria therapy necessitates the urgent need to re-evaluate Artemether-based therapy. Future studies involving more participants in different settings are needed to provide further evidence.

Beta-defensins 2 and 3 (BD2 and BD3) are inducible peptides present at the sites of infection, and they are well characterized for their antimicrobial activities and immune-regulatory functions. However, no study has thoroughly investigated their immunomodulatory effects on macrophage-mediated immune responses against Pseudomonas aeruginosa (PA). Here, we use THP-1 and RAW264.7 cell lines and demonstrate that BD2 and BD3 suppressed macrophage autophagy but enhanced the engulfment of PA and Zymosan bioparticles as well as the formation of phagolysosomes, using immunofluorescence staining and confocal microscopy. Plate count assay showed that macrophage-mediated phagocytosis and intracellular killing of PA were promoted by BD2 and BD3. Furthermore, microarray and real-time PCR showed that the expression of two genes, early growth response gene-1 (EGR1) and c-FOS, was attenuated by BD2 and BD3. Western blot revealed that BD2 and BD3 inhibited the expression and nuclear translocation of EGR1 and c-FOS. Knockdown of EGR1 and c-FOS by siRNA transfection suppressed macrophage autophagy before and after PA infection; while overexpression of these two transcription factors enhanced autophagy but reversed the role of BD2 and BD3 on macrophage-mediated PA eradication. Together, these results demonstrate a novel immune defense activity of BD2 and BD3, which promotes clearance of PA by inhibiting macrophage autophagy through downregulation of EGR1 and c-FOS.

Triggering receptor expressed on myeloid cells 1 (TREM-1) is a receptor mainly expressed on myeloid cells, and it plays an important role in modulating immune response against infectious agents. The function of TREM-1 on nonmyeloid cells such as Vδ2 T cells has not been characterized, and their role in pulmonary tuberculosis (TB) remains unclear. To assess the expression of TREM-1 on blood Vδ2 T cells from pulmonary TB patients and investigate its mechanism of induction, we exploited flow cytometry analysis to study the expression of TREM-1 on Vδ2 T cells from active pulmonary TB patients and control subjects. In this study we demonstrate that TREM-1 (TREM-1

Summary Objective We validated the accuracy of host selected signature gene set using unstimulated whole blood (WB), and peripheral blood mononuclear cells (PBMC) in the diagnosis of tuberculosis (TB). Methods The unstimulated WB and PBMC from 1417 individuals with active pulmonary TB patients, other lung diseases and healthy participants were analyzed using real time polymerase chain reaction (RT-PCR). Results The WB cohort test demonstrates that the combination of GBP5 and KLF2 can differentiate active TB versus HC with sensitivity and specificity of 77.8% and 87.1%, respectively; but most importantly active TB versus OD with sensitivity and specificity of 96.1% and 85.2%, respectively. Again during treatment course, the TB score of GBP5 and KLF2 , analytes secretion and clinical parameters were found to be associated in disease progression. In the PBMC cohort test, we found that the only and best discriminatory combination was GBP5 , DUSP3 and KLF2 inthe active TB versus HC with a sensitivity and specificity of 76.4% and 85.9%, respectively. Conclusions Our study reveals that GBP5 and KLF2 may be useful as a diagnostic tool for active TB, also the two-gene set may serve as surrogate biomarkers for monitoring TB therapy.

Mycobacterium tuberculosis infection of the central nervous system is thought to be initiated once the bacilli have breached the blood brain barrier and are phagocytosed, primarily by microglial cells. In this study, the interactions of M. tuberculosis with neurons in vitro and in vivo were investigated. The data obtained demonstrate that neurons can act as host cells for M. tuberculosis . M. tuberculosis bacilli were internalized by murine neuronal cultured cells in a time-dependent manner after exposure, with superior uptake by HT22 cells compared to Neuro-2a cells (17.7% versus 9.8%). Internalization of M. tuberculosis bacilli by human SK-N-SH cultured neurons suggested the clinical relevance of the findings. Moreover, primary murine hippocampus-derived neuronal cultures could similarly internalize M. tuberculosis . Internalized M. tuberculosis bacilli represented a productive infection with retention of bacterial viability and replicative potential, increasing 2- to 4-fold within 48 h. M. tuberculosis bacillus infection of neurons was confirmed in vivo in the brains of C57BL/6 mice after intracerebral challenge. This study, therefore, demonstrates neurons as potential new target cells for M. tuberculosis within the central nervous system.