Myeloid Sirtuin 2 Expression Does Not Impact Long-Term <i>Mycobacterium tuberculosis</i> Control

<div><p>Sirtuins (Sirts) regulate several cellular mechanisms through deacetylation of several transcription factors and enzymes. Recently, Sirt2 was shown to prevent the development of inflammatory processes and its expression favors acute <i>Listeria monocytogenes</i> infection. The impact of this molecule in the context of chronic infections remains unknown. We found that specific Sirt2 deletion in the myeloid lineage transiently increased <i>Mycobacterium tuberculosis</i> load in the lungs and liver of conditional mice. Sirt2 did not affect long-term infection since no significant differences were observed in the bacterial burden at days 60 and 120 post-infection. The initial increase in <i>M</i>. <i>tuberculosis</i> growth was not due to differences in inflammatory cell infiltrates in the lung, myeloid or CD4⁺ T cells. The transcription levels of IFN-γ, IL-17, TNF, IL-6 and NOS2 were also not affected in the lungs by Sirt2-myeloid specific deletion. Overall, our results demonstrate that Sirt2 expression has a transitory effect in <i>M</i>. <i>tuberculosis</i> infection. Thus, modulation of Sirt2 activity <i>in vivo</i> is not expected to affect chronic infection with <i>M</i>. <i>tuberculosis</i>.</p>