Скачать или смотреть Factors that lead to the Termination of Acute inflammatory Response

The acute inflammatory response is terminated through several mechanisms:

1. Resolution of inflammation: Inflammatory mediators are degraded, and anti-inflammatory cytokines are produced.

2. Clearance of inflammatory stimuli: Removal of the initial trigger, such as bacteria or damaged tissue.

3. Exhaustion of immune cells: Activated immune cells undergo apoptosis (programmed cell death) or become tolerized.

4. Regulatory immune cells: Tregs (regulatory T cells) and other immune suppressive cells dampen the inflammatory response.

5. Anti-inflammatory cytokines: Cytokines like IL-10, TGF-β, and IL-22 counteract pro-inflammatory effects.

6. Lipid mediators: Specialized pro-resolving mediators (SPMs) promote resolution and tissue repair.

7. Hormonal regulation: Glucocorticoids and other hormones can suppress inflammation.

8. Cellular senescence: Activated immune cells become senescent and cease to produce pro-inflammatory cytokines.

9. Apoptosis: Immune cells undergo programmed cell death, reducing inflammation.

10. Tissue repair: Injured tissue is repaired, reducing the need for inflammation.

These factors work together to terminate the acute inflammatory response, restoring tissue homeostasis and preventing chronic inflammation.

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