Mitochondrial transplantation redirects rather than suppresses the inflammatory response in primary human monocytes

Mitochondrial transplantation into primary human CD14 monocytes shifts LPS-driven inflammatory mediator release, lowering TNF- to 0.06-fold and CXCL10/IP-10 to 0.25-fold.

• Why it matters: Monocytes decide inflammatory versus resolving fates after leaving blood, and their inflammatory function is tightly linked to mitochondrial metabolism, creating a window to reprogram circulating cells.
• What they did: Freshly isolated, respiration-competent mitochondria from HEK293T cells were transplanted into primary human CD14 monocytes; uptake reached 88% labeled mitochondria in viable cells within 3 h, and mitochondrial function showed a respiratory control ratio of 8.7 and coupling efficiency of 78.9%.
• The result: Transplanted monocytes reduced the pro-inflammatory intermediate subset, increased CD14 2.11-fold and HLA-DR 1.31-fold, decreased CD163, and in most donors increased IL-10 3.33-fold after LPS stimulation.

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