The inflammatory response is a complex and highly regulated process. A simplified framework for discussing inflammatory response is outlined below. Each of the three phases involve a series of coordinated events and interactions between various immune cells, signaling molecules, and tissue components.
- Initiation:
- Recognition of Pathogens or Damage:
- Immune cells detect PAMPs or DAMPs through PRRs (e.g., TLRs, NLRs).
- Activation of PRRs triggers the release of inflammatory mediators.
- Recognition of Pathogens or Damage:
- Effector Mechanisms:
- Vasodilation and Increased Permeability:
- Cytokines, chemokines, lipid mediators, and histamine release leads to vasodilation and increased permeability of blood vessels.
- Recruitment of Immune Cells:
- Chemokines attract neutrophils and monocytes to the site of inflammation.
- Phagocytosis and Inflammatory Mediator Production:
- Neutrophils, monocytes, DCs, and macrophages phagocytose pathogens, releasing cytokines and chemokines.
- Vasodilation and Increased Permeability:
- Resolution:
- Anti-inflammatory Signals and Termination of Inflammation:
- Production of anti-inflammatory cytokines (e.g., IL-10) counters pro-inflammatory signals.
- Negative feedback loops inhibit inflammatory pathways.
- Tissue Repair and Return to Homeostasis:
- Activation of fibroblasts contributes to tissue repair.
- Clearance of apoptotic immune cells and debris by macrophages.
- Restoration of tissue function and return to homeostasis.
- Anti-inflammatory Signals and Termination of Inflammation:
Next Topic: Details Related to the Effector Phase of Inflammation
Source: ChatGPT response prompted and edited by Joel Graff.
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