A Part of Intracellular Life of Mycobacterium

D. Bisht, L. Meena
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引用次数: 1

Abstract

Tuberculosis pathogenesis is the major cause of high morbidity and mortality in the current scenario. Major aspects supports this prevalence, the most significant is the mycobacterium’s ability to modulate host immune system [1]. Also the resistivity it shows towards many antituberculosis drugs which support its infectivity leading the world towards prevalence of more harmful forms of tuberculosis like XDR and MDR. According to WHO reports 2015, approximately 4000 people are killed each day due to this disease which clearly demonstrates us the need to work towards eradicating it [2]. During its interaction with the host cell mycobacteria adopts many strategies to circumvent host immune system which it initialises with the adhesion molecules which interacts with their specified receptors and with this they help mycobacteria to interact with their host cell [3]. Recent studies have shown with these extracellular receptors there are many signalling molecules which are enhanced intracellularly during adhesion and pathogenesis. Hence, we can elaborate their mechanism in host pathogenesis so that we can be more evident about Mycobacterium’s strategy to circumvent host cell. Adhesion molecule expression forms a backbone of cell to cell communication in granuloma formation. Leukocyte adhesion molecules like ICAM and other stimulatory and costimulatory molecules show increased or decreased level of expressions in host pathogenesis [4]. In a study of tuberculous pleuritus patients soluble vascular cell adhesion molecules sVCAM, sICAM [5] were evaluated which can be helpful in diagnosis of the disease. Being much conclusive about them can further help us to be brief about these significant molecules and target them to open new avenues to invent more significant and reasonable antituberculosis drugs to eradicate the pandemic.
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分枝杆菌胞内生活的一部分
结核病的发病机制是目前高发病率和高死亡率的主要原因。主要方面支持这种流行,最重要的是分枝杆菌调节宿主免疫系统的能力。此外,它对许多抗结核药物表现出抵抗力,这些药物支持其传染性,导致世界流行更有害的结核病形式,如广泛耐药和耐多药耐药。根据世卫组织2015年的报告,每天约有4000人死于这种疾病,这清楚地表明我们需要努力根除这种疾病。在与宿主细胞相互作用的过程中,分枝杆菌采用多种策略来规避宿主免疫系统,它通过与特定受体相互作用的粘附分子来初始化宿主免疫系统,并通过这种粘附分子帮助分枝杆菌与宿主细胞[3]相互作用。最近的研究表明,这些细胞外受体中有许多信号分子在细胞内粘附和发病过程中被增强。因此,我们可以详细阐述它们在宿主发病中的机制,从而更清楚地了解分枝杆菌绕过宿主细胞的策略。黏附分子的表达是肉芽肿形成过程中细胞间通讯的主干。白细胞粘附分子如ICAM和其他刺激和共刺激分子在宿主发病[4]中表达水平升高或降低。本研究对结核性胸膜炎患者的可溶性血管细胞黏附分子sVCAM、sICAM[5]进行了测定,有助于该病的诊断。对它们有更多的结论可以进一步帮助我们简要了解这些重要分子,并针对它们开辟新的途径,发明更重要、更合理的抗结核药物,以根除这种流行病。
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