Mediators of inflammation and the inflammatory process - 2.5

Mediators of Inflammation

• Tissue injury can be caused by physical, chemical agents, or pathogens.
• Extravasation: Immune cells are recruited to the injury site rapidly.
• Inflammation process:
  • Damage triggers mast cells to release histamine.
  • Histamine causes blood vessel dilation and leakage.
  • Complement proteins attract phagocytes (white blood cells).
  • Plasma and phagocytes move from blood vessels into infected tissue.
  • Histamine and complement signaling decrease, phagocytes are no longer attracted.
  • Phagocytes engulf bacteria and dead cells.
  • Growth factors stimulate skin cell division for wound healing.

Mediators of Inflammation - Plasma Derived

• Clotting system
• Kinin system
• Fibrinolytic system (plasmins)
• Complement system

Mediators of Inflammation - Cell Derived

• Auxiliary cells: Basophils, mast cells, platelets, lymphocytes, monocytes, and kinins
• Kinins: Enzymes that cause vasodilation, vascular permeability, and pain.
• Enzymatic proteins: Bradykinin and lysyl-bradykinin (result in production of vasodilators)
• Vasoactive peptide: Venous dilation, increased vascular permeability.
• Activated by Hageman factor (XIIa): Plasmin cascade initiation
• Plasmins: enzymes from damaged tissues activating plasminogen into plasmin, contributing to tissue remodeling and angiogenesis.
• Basophils, Mast cells, platelets: Activated by C3a and C5a (innate) and IgE (adaptive).
  • Rapid release of histamine and serotonin (degranulation).
  • Slow release of leukotrienes and prostaglandins.
  • Activated by antigen-antibody (AB) complexes.

Mediators of Inflammation - Pain

• Mast cells and basophils release mediators (PAF, histamine, serotonin, prostaglandins, leukotrienes).
• Act on C fibers leading to poorly localized pain (dull, aching).

Arachidonic Acid Pathway

• Arachidonic acid (AA) is crucial for prostaglandin and leukotriene formation
• Phospholipases release AA from cell membranes.
• Cyclooxygenase (COX) enzymes convert AA to prostaglandins (PGs):
  • PGI2: vasodilation, inhibits platelet aggregation
  • TXA2: vasoconstriction, promotes platelet aggregation
  • PGD2, PGE2: vasodilation, increased vascular permeability
• Lipoxygenase enzymes convert AA into leukotrienes (LTs):
  • Types of leukotrienes (LTA4, LTB4, LTC4, LTD4, LTE4): bronchospasm, increased vascular permeability (inflammation).
• Steroids inhibit the pathway by interfering with phospholipase activity.

Acute and Chronic Inflammation

• If the insult persists, immune cells accumulate.
• Inflammation response becomes dysregulated.
• Repair response is inhibited.

Summary Table (Page 5)

• Table lists the mediators of inflammation, their actions, and associated mechanisms(actions and mediators)

Explore the key mediators of inflammation in this quiz. Understand the roles of both plasma-derived and cell-derived mediators in the inflammatory response. This quiz covers mechanisms such as histamine release, the clotting system, and the involvement of various immune cells.