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Curcumin controls MTB infection in model

Researchers in this study showed an ability to control Mycobacterium tuberculosis in a macrophage infection model using curcumin, according to recent research.

“In summary, we have shown that curcumin can augment the ability of human macrophages to control Mycobacterium tuberculosis (MTB) infection,” Xiyuan Bai, PhD, from the Department of Medicine at the Denver Veterans Affairs Medical Center in Denver, Colorado, and colleagues wrote in their study. “While the results are promising, in vivo studies using a practical approach to achieve therapeutic tissue levels of curcumin are needed to advance our findings to one that is more clinically relevant.”

Bai and colleagues used an in vitro human macrophage infection model to assess the effect of curcumin on MTB, according to the abstract. Researchers administered 10 μM, 30 μM and 50 μM of curcumin or 0.05% of dimethyl sulfoxide (DMSO) to human promonocytic cell line THP-1 for 1 hour before infecting the cells with MTB H37Rv.

They found that curcumin did not affect phagocytosis among the various samples; however, there was an inhibition of MTB growth by 4 days in the cells with 10 μM curcumin, and a significant decrease in MTB recovered at 2 days and 4 days post-infection in the 30 μM and 50 μM curcumin groups.

“Based on these findings, we next examined the effects of curcumin in MTB–infected primary human alveolar macrophages,” Bai and colleagues wrote. “As seen with the THP-1 cells, 50 μM of curcumin significantly reduced the number of viable intracellular MTB recovered after 4 days of infection.”

To determine the association between capase-3–dependent classical apoptosis and curcumin  as an anti-MTB agent, Bai and colleagues also infected THP-1 cells with and without a capase-3 inhibitor (Z-DEVD-fmk).

“As previously seen, curcumin significantly increased the number of apoptotic cells and reduced the number of recovered colony forming units; however, pharmacologic inhibition of caspase-3 significantly abrogated both of these effects,” the researchers wrote. “There were no significant differences between 10 and 20 μM of z-DEVD-fmk in regard to either apoptosis or colony forming units.”

The researchers noted that curcumin also induced autophagy in MTB-infected cells, and mediated MTB cellular functions partly through nuclear factor-kappa B (NFκB) activation, according to the abstract.

“THP-1 cells were infected with MTB for 30 min and 3 h and p65 NFκB binding to its consensus oligonucleotide quantified,” Bai and colleagues wrote. “MTB induced NFκB p65 binding at both time points, and curcumin significantly inhibited this activation.” – by Jeff Craven

Disclosure: The researchers report no relevant financial disclosures.