BackgroundMulti-drug resistance (MDR) has been a cause of concern for tuberculosis (TB) control in both developed and developing countries. This study described the characteristics and risk factors associated with MDR-TB among 287 cases and 291 controls in Henan province, China.MethodsA hospital-based case-control study was conducted between June 2012 and December 2013. The study subjects were selected using multistage probability sampling. Multivariate conditional logistic regression models were used to determine the risk factors associated with MDR-TB.ResultsThe following risk factors for MDR-TB were identified: previous TB treatment (AOR = 4.51, 95 % CI: 3.55–5.56), male sex (AOR = 1.09, 95 % CI: 0.24–1.88), high school or lower education degree (AOR = 1.87, 95 % CI: 1.27–2.69), unemployment (AOR = 1.30, 95 % CI: 0.78–2.52), long distance of residence from the health facility (AOR = 6.66,95 % CI: 5.92–7.72), smoking (AOR = 2.07, 95 % CI: 1.66–3.19), poor knowledge regarding MDR-TB (AOR = 2.06, 95 % CI: 1.66–2.92), traveling by foot to reach the health facility (AOR = 1.85, 95 % CI: 1.12–3.09), estimated amount of time to reach the health facility was greater than 3 h (AOR = 1.42, 95 % CI: 0.51–2.35), social stigma (AOR = 1.17, 95 % CI: 0.27–2.03), having an opportunistic infection (AOR = 1.45, 95 % CI: 0.58–2.4), more than 3 TB foci in the lungs (AOR = 1.98, 95 % CI: 1.49–3.25), total time of first treatment was more than 8 months (AOR = 1.39, 95 % CI: 0.65–2.54), adverse effects of anti-TB medication (AOR = 2.39, 95 % CI: 1.40–3.26), and more than 3 prior episodes of anti-TB treatment (AOR = 1.83, 95 % CI: 1.26–2.80).ConclusionThe identified risk factors should be given priority in TB control programs. Additionally, there is a compelling need for better management and control of MDR-TB, particularly through increasing laboratory capacity, regular screening, enhancing drug sensitivity testing, novel MDR-TB drug regimens, and adherence to medication.

ABSTRACT. We conducted a case-control study in a Chinese population to examine the correlations between interleukin (IL)-17 gene polymorphisms and tuberculosis (TB) development. The study population included 336 TB subjects and 351 control subjects who were enrolled between June 2012 and June 2014. Genotyping analyses of IL-17A rs2275913 and rs3748067 and IL-17F rs763780 were analyzed using polymerase chain reaction-restriction fragment length of polymorphism. The genotype distributions of IL-17 rs2275913 were found to be in Hardy-Weinberg equilibrium in the controls, while the IL-17 rs3748067 and rs763780 were not. Based on unconditional logistic regression, individuals carrying the AA genotype and GA + AA genotype of rs2275913 were more likely to have a significantly increased risk of TB compared to subjects with the GG genotype. The ORs (95%CI) for the AA genotype and GA + AA genotype were 2.20 (1.35-3.60) and 1.52 (1.11-2.09), respectively. The CC genotype and TC + CC genotype of rs763780 were associated with increased risk of TB when compared with the TT genotype. The ORs (95%CI) for the CC genotype and TC + CC genotype were 1.99 (1.05-3.87) and 1.58 (1.07-2.33), respectively. In conclusion, rs763780 may play a critical role in the etiology of TB.

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The Mycobacterium tuberculosis 19-kDa lipoprotein (P19) is both cell wall-associated and secreted and is a candidate virulence factor that could cause the apoptosis of human macrophages infected with M. tuberculosis. P19 induces TLR2 activation, resulting in the upregulation of death receptors and ligands, followed by a death-receptor signaling cascade. The mechanisms by which P19 induces macrophage apoptosis are not fully characterized. Curcumin, a natural polyphenol, exhibits a variety of pharmacological effects such as antioxidant, anti-inflammatory and antitumor properties. In the present study, we investigated the effect of curcumin on P19-induced apoptosis in human macrophage cells and the underlying mechanisms. The results showed that both P19 and curcumin inhibit the growth of macrophages in a dose- and time-dependent manner. A low dose of curcumin (10 or 20 µM) attenuated both the macrophage cell growth inhibition and the increase in the expression of IL-6 and TNF-α induced by P19. Curcumin also decreased the phosphorylation of JNK and p38 that were induced by P19. However, JNK but not p38 inhibitors reversed the effect of P19 on the growth inhibition of macrophages. These data suggest that curcumin may protect macrophages from P19-induced cell apoptosis via a TLR2-mediated JNK-dependent pathway.