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. 2022 Feb 25;13:842858. doi: 10.3389/fimmu.2022.842858

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Copyright © 2022 Yang, Ouyang, Lu, Harypursat and Chen

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The role of HO-1 in MTB infection. Free heme is highly cytotoxic via the production of free radicals. Accordingly, when HO-1 is activated moderately, HO-1 exerts a cytoprotective effect by neutralizing ROS. Conversely, the large amounts of excessive free heme released during the late stages of tuberculosis overwhelms the cytoprotective effects of HO-1, thereby contributing to oxidative stress and excessive ROS production. The over-activation of HO-1 becomes detrimental due to the excessive labile Fe²⁺, along with ROS overload, leading to oxidative-cell death (ferroptosis), which contributes to the spread of infection. MTB, Mycobacterium tuberculosis; HO-1, heme oxygenase-1; ROS, reactive oxygen species; Fe, free iron.