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We have reported that the cholesterol-induced activation of VapC12 ribonuclease is critical for disease persistence in TB. In this study, we observed that relative to the wild type, mice infected with \u0394<jats:italic>vapC12<\/jats:italic> induced a pro-inflammatory response, had a higher pathogen load, and responded better to the anti-TB treatment. In a high-dose infection model, all the mice infected with \u0394<jats:italic>vapC12<\/jats:italic> succumbed early to the disease. Finally, we reported that the above phenotype of \u0394<jats:italic>vapC12<\/jats:italic> was dependent on the presence of the TLR4 receptor. Overall, the data suggests that failure of a timely resolution of the early inflammation by the \u0394<jats:italic>vapC12<\/jats:italic> infected mice led to hyperinflammation, altered T-cell response and high bacterial load. 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