Proteomic changes in Mycobacterium tuberculosis H37Rv under hyperglycemic conditions favour its growth through altered expression of Tgs3(Rv3234c) and supportive proteins (Rv0547c, AcrA1 and Mpa)

Kundu, Jyoti; Verma, Arpana; Verma, Indu; Bhadada, Sanjay; Sharma, Sonal

doi:10.1016/j.tube.2019.03.006

Cited by 4 publications

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“…Persistent hyperglycemia is the predominant cause of most of the complications observed in diabetes and is responsible for increased susceptibility to various infections including tuberculosis. Our earlier observations have demonstrated alterations in the proteomic profile of M. tuberculosis exposed to concurrent high glucose and tuberculosis conditions [ 12 ] suggesting a crosstalk between host and pathogen. In this context, we tried to analyse the interaction between intracellular mycobacteria and host macrophages under copathogenesis conditions of tuberculosis and high glucose concentration prevalent in diabetics.…”

Section: Discussionmentioning

confidence: 99%

Molecular mechanism of interaction of Mycobacterium tuberculosis with host macrophages under high glucose conditions

Kundu¹,

Verma²,

Verma³

et al. 2021

Biochemistry and Biophysics Reports

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Mycobacterium tuberculosis has the potential to escape various cellular defense mechanisms for its survival which include various oxidative stress responses, inhibition of phagosome-lysosomes fusion and alterations in cell death mechanisms of host macrophages that are crucial for its infectivity and dissemination. Diabetic patients are more susceptible to developing tuberculosis because of impairement of innate immunity and prevailing higher glucose levels. Our earlier observations have demonstrated alterations in the protein profile of M. tuberculosis exposed to concurrent high glucose and tuberculosis conditions suggesting a crosstalk between host and pathogen under high glucose conditions. Since high glucose environment plays crucial role in the interaction of mycobacterium with host macrophages which provide a niche for the survival of M. tuberculosis , it is important to understand various interactive mechanisms under such conditions. Initial phagocytosis and containment of M. tuberculosis by macrophages, mode of macrophage cell death, respiratory burst responses, Mycobacterium and lysosomal co-localization were studied in M. tuberculosis H37Rv infected cells in the presence of varied concentrations of glucose in order to mimic diabetes like conditions. It was observed that initial attachment, phagocytosis and later containment were less effective under high glucose conditions in comparison to normal glucose. Mycobacterium infected cells showed more necrosis than apoptosis as cell death mechanism during the course of infection under high glucose concentrations. Co-localization and respiratory burst assay also indicated evasion strategies adopted by M. tuberculosis under such conditions. This study by using THP1 macrophage model of tuberculosis and high glucose conditions showed immune evasion strategies adapted during co-pathogenesis of tuberculosis and diabetes.

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