August 6, 2025

Dexamethasone inhibits Mycobacterium tuberculosis-induced glycolysis but preserves antimicrobial function in primary human macrophages

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Dexamethasone significantly inhibits glycolysis in both airway and monocyte-derived macrophages.
The drug reduced cytokine secretion levels, such as IL-1β and TNF, linked to inflammation.
Macrophages showed improved survival against Mycobacterium tuberculosis infection after dexamethasone treatment.
Findings suggest potential for using glucocorticoids in tuberculosis therapy without compromising immune defense.

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Implication

Dexamethasone reduces glycolysis in human macrophages while enhancing antimicrobial function against Mycobacterium tuberculosis, indicating therapeutic potential.

Cite This Study

Thong et al. (2025) studied this question.

synapsesocial.com/papers/689a0f99e6551bb0af8d1642 https://doi.org/10.21203/rs.3.rs-7129594/v1

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Implication

Dexamethasone reduces glycolysis in human macrophages while enhancing antimicrobial function against Mycobacterium tuberculosis, indicating therapeutic potential.

Dexamethasone inhibits Mycobacterium tuberculosis-induced glycolysis but preserves antimicrobial function in primary human macrophages

Key Points

Discussion

Implication

Cite This Study

Dexamethasone inhibits Mycobacterium tuberculosis-induced glycolysis but preserves antimicrobial function in primary human macrophages

Key Points

Discussion

Implication

Cite This Study

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