Within the field of immunology, mitochondria transcend their traditional roles as mere energy producers and emerge as pivotal facilitators of host immunity against pathogenic infections. Their involvement extends from regulating cellular energy states to dictatorial roles in innate and adaptive immune responses. During infections, mitochondria undergo structural and functional modifications indicating their critical roles in host defense mechanisms. Pathogens, including varied viruses and bacteria, actively manipulate mitochondrial functions to subvert immune detection and maximize their survival odds. Conversely, the host's defense mechanisms capitalize on the dynamic versatility of mitochondrial structures to adapt and maintain cellular balance under such stress.

Immune cells rely on six major cellular metabolic pathways- glycolysis, tricarboxylic acid (TCA) cycle, fatty acid oxidation (FAO) and synthesis, pentose phosphate pathway, and amino acid metabolism. Notably, the TCA cycle and FAO occur within the mitochondria, positioning these organelles as critical regulators of metabolic reprogramming in innate and adaptive immune cells to adjust their functions according to the micro-environment cues and immune demands, as seen during macrophage polarization. Mitochondria influence metabolic shifts in B- and T-cells as they transition from quiescent to active states, indispensable for effective adaptive immune responses. The metabolic shifts enable mitochondria to transition from catabolic to anabolic roles, facilitating macromolecule synthesis to meet the demands of immune cell activation and differentiation under pathophysiological conditions.

Mitochondria play a crucial role in immune signaling pathways by releasing danger-associated molecular patterns (DAMPs), like reactive oxygen species (mtROS), ATP, and mitochondrial DNA(mtDNA), which activate pathogen recognition receptors (PRRs) and initiate immune signaling pathways. This positions them as a link between cellular metabolism and immune signaling, allowing tailored immune responses. Their involvement in anterograde and retrograde signaling highlights essential cytosolic-mitochondria cross-talk for maintaining homeostasis under pathogenic stress.

This research topic aims to dissect and understand the intricate role of mitochondria within the sphere of host immunity during pathogenic incursions. The objective is to highlight how mitochondrial structure and functions interplay with immune mechanisms to control and dictate disease outcomes. It focuses on understanding how microbes influence mitochondrial structure and function, and how the host leverages mitochondrial mechanisms for effective immune responses. The exploration extends to examining how mitochondrial metabolic shifts and signaling pathways.

To gather further insights, we welcome contributions exploring various aspects of mitochondrial and immune cell interactions during infections. The following themes are particularly of interest:
- Metabolic reprogramming of innate and adaptive immune cells in response to pathogenic scenarios.
- Role of anterograde and retrograde-signaling in host-pathogen interaction.
- Impact of mitochondrial network dynamics on immune cell function during pathogenic stress.
- Pathogen strategies in manipulating mitochondria to evade immune surveillance.
- The impact of altered mitochondrial metabolic profiles and mitochondrial network dynamics on the development and progression of pathogenic diseases.
- Impact of mitochondrial DAMPs in autoimmune disorders and strategies to modulate their release to
prevent autoimmunity.
- Novel therapeutic strategies targeting mitochondria within immune-metabolic pathways for disease prevention and treatment.

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Frontiers in Cellular and Infection Microbiology

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