Regulation of Host Innate Immunity During Pathogens Infection
A special issue of Pathogens (ISSN 2076-0817). This special issue belongs to the section "Immunological Responses and Immune Defense Mechanisms".
Deadline for manuscript submissions: 31 August 2026 | Viewed by 41
Special Issue Editor
Special Issue Information
Dear Colleagues,
Bacterial pathogens exploit and subvert innate immune circuits, making regulated cell death a decisive determinant of infection outcome. Pattern-recognition receptors (TLRs, NLRs, RLRs, and cGAS–STING) detect extracellular and cytosolic cues and thereby coordinate antimicrobial programs while gating apoptosis, pyroptosis, necroptosis, ferroptosis, and emerging PANoptosis. Across Gram-negative and Gram-positive infections, inflammasome activation (e.g., NLRP3, NLRC4, AIM2) drives caspase-1–dependent gasdermin D cleavage, IL-1β/IL-18 release, and pyroptotic lysis that can both restrict bacterial replication and propagate tissue injury. Parallel axes—caspase-8-tuned apoptosis and RIPK1/3–MLKL necroptosis—serve as fail-safe backups when pathogens block one route, while lipid peroxidation-driven ferroptosis shapes bacterial fitness in iron-rich niches. Timing and magnitude matter: premature lytic death fuels pathology; delayed death enables intracellular persistence.
Bacteria deploy effectors and toxins to rewrite this choreography—modulating ubiquitination, ion flux, mitochondrial stress, and interferon signaling—to influence fate decisions. Host metabolic tone (glycolysis, itaconate, NADPH/ROS) and organ-specific cues further calibrate death thresholds and cytokine milieus. These multilayered controls highlight actionable opportunities for host-directed therapy: small molecules that temper priming or pore formation, inhibitors or activators targeting gasdermins, RIPK1/3–MLKL checkpoints or lipid peroxidation pathways, and GPCR/ion-channel ligands that reset danger signaling without blunting bacterial clearance.
This Special Issue will spotlight (i) pathogen-specific logic of death pathway selection; (ii) cross-talk among pyroptosis, apoptosis, and necroptosis (PANoptosis); (iii) metabolic and interferon control of death timing.
Dr. Xin Ran
Guest Editor
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Keywords
- pathogens
- bacterial pathogens
- pattern-recognition receptors
- innate immune circuits
- gram-negative and gram-positive infections
- inflammasome activation
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