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Review
. 2022 Dec 18;11(24):4113.
doi: 10.3390/cells11244113.

Mitochondria Drive Immune Responses in Critical Disease

Shilpa Tiwari-Heckler  1 , Simon C Robson  2   3 , Maria Serena Longhi  2
Affiliations
Review

Mitochondria Drive Immune Responses in Critical Disease

Shilpa Tiwari-Heckler et al. Cells. .

Abstract

Mitochondria engage in multiple cellular and extracellular signaling pathways ranging from metabolic control, antiviral and antibacterial host defense to the modulation of inflammatory responses following cellular damage and stress. The remarkable contributions of these organelles to innate and adaptive immunity, shape cell phenotype and modulate their functions during infection, after trauma and in the setting of inflammatory disease. We review the latest knowledge of mitochondrial biology and then discuss how these organelles may impact immune cells to drive aberrant immune responses in critical disease.

Keywords: adaptive immunity; critical illness; immunometabolism; immunosuppression; inflammation; innate immunity; mitochondria; mitochondrial danger-associated-molecular-pattern; trauma.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Mitochondria modulate innate and adaptive immune responses and impact clinical course of critically ill patients. Trauma-induced injury elicit rapid immune responses mediated by released mitochondria after cellular damage. Circulating mtDNA and mitochondrial derived N-formyl peptides are sensed by TLR9 and FPR1. ATP-producing mitochondria boost CD39, PD-1 and Tim-3 levels in CD8 T cells, favoring immune exhaustion. These immunological changes might increase the susceptibility to secondary infection and systemic inflammation in critically ill patients after traumatic insult.
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