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Updated: Mar 12, 2026

Real-Time Measurement of the Mitochondrial Bioenergetic Profile of Neutrophils
Published on: June 2, 2023
Mitochondria as a centrally positioned hub in the innate immune response
Rajat Sandhir1, Avishek Halder1, Aditya Sunkaria1
1Department of Biochemistry, Panjab University, Chandigarh, India.
Abstract:
Mitochondria are vital organelles involved in numerous cellular functions ranging from energy metabolism to cell survival. Emerging evidence suggests that mitochondria provide a platform for signaling pathways involved in innate immune response. Mitochondrial ROS (mtROS) production, mitochondrial DNA (mtDNA) release, mitochondrial antiviral signaling protein (MAVS) are key triggers in the activation of innate immune response following variety of stress signals that include infection, tissue damage and metabolic dysregulation. The process is mediated through pattern recognition receptors (PRRs) that consist of retinoic acid inducible gene like receptors (RLRs), c-type lectin receptors (CLRs), toll type receptors (TLRs) and nuclear oligomerization-domain like receptors (NLRs). These signals converge to form a multiprotein complex called inflammasome that leads to caspase-1 activation to promote processing of precursor cytokines (pro-IL1β and pro-IL-18) to active cytokines (IL-1β and IL-18). It appears that mitochondria induced inflammasome activation contributes to inflammatory process in many diverse disorders. Therefore, strategies aimed at modulating mitochondria mediated inflammasome activation might be beneficial in many pathophysiological conditions. This article is part of a Special Issue entitled: Oxidative Stress and Mitochondrial Quality in Diabetes/Obesity and Critical Illness Spectrum of Diseases - edited by P. Hemachandra Reddy.
Insights
Mitochondria play a key role in the innate immune response by triggering inflammasome activation through mechanisms like mitochondrial ROS production and mtDNA release. Modulating these mitochondrial pathways may offer therapeutic benefits for various inflammatory conditions.
Area of Science:
- Cellular Biology
- Immunology
- Mitochondrial Biology
Background:
- Mitochondria are essential for cellular functions, including energy metabolism and survival.
- Emerging evidence highlights mitochondria's role as a signaling platform in innate immunity.
- Mitochondrial dysfunction is implicated in various stress responses and diseases.
Purpose of the Study:
- To review the role of mitochondria in activating innate immune signaling pathways.
- To explore the mechanisms by which mitochondria trigger inflammasome activation.
- To discuss the potential of targeting mitochondria-mediated inflammasome activation for therapeutic interventions.
Main Methods:
- Review of current literature on mitochondrial signaling in innate immunity.
- Discussion of key mitochondrial components involved in immune activation (mtROS, mtDNA, MAVS).
- Explanation of pattern recognition receptor (PRR) pathways leading to inflammasome assembly.
Main Results:
- Mitochondrial ROS (mtROS) production, mitochondrial DNA (mtDNA) release, and MAVS are critical initiators of innate immune responses.
- PRRs, including RLRs, CLRs, TLRs, and NLRs, mediate these mitochondrial signals.
- Mitochondria-induced inflammasome activation leads to caspase-1 activation and subsequent cytokine maturation (IL-1β, IL-18).
Conclusions:
- Mitochondria are central players in the innate immune response, particularly in inflammasome activation.
- Mitochondrial dysfunction and subsequent inflammatory processes are implicated in diverse pathophysiological conditions.
- Targeting mitochondria-mediated inflammasome activation presents a promising therapeutic strategy for inflammatory disorders.
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