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What is inflammation?

Inflammation is the response of vascularized tissue to the contagious agent or infectious agent and damaged tissues.

  • It brings molecules and cells of the host defense from the systemic circulation to the site of injury.
  • To eliminate the offending agents.

Protective role:

  • Series to get rid of the initial cause of cell injury (microbes, toxins agents) and consequences of injury (necrotic cells/ tissues)
  • The wound would never hell up if there would be no inflammation. 

Double-edged sword:

  • Some may cause tissue destruction, for example, immune-mediated disorders. 

Sequential steps:

  • The offending agent recognized by host cells and molecules
  • Plasma proteins and Leukocytes recruited from circulation to the site of the offending agent
  • Leukocytes and proteins activated to eliminate (remove) offending substance
  • The reaction is controlled (regulation) and terminated 
  • Damaged tissue repaired (resolution) 

Causes of inflammation

  • Physical agents
    • Heat, radiation, mechanical trauma
  • Chemical agents
    • Organic and inorganic poisons
  • Infectious agents
    • Bacteria, viruses, parasites, fungus, and microbial toxins
  • Immunological agents
    • Hypersensitivity reactions
  • Deficiency of nutrients 
  • Tissue necrosis 
  • Foreign bodies 

Recognitions of microbes and damaged cells:

  • Cellular receptors for microbes:
    • Family of Toll-like receptors (TLRs)
    • Located in plasma membranes and endosomes, & detect extracellular and ingested microbes.
    • Recognition stimulates the productions and expression of cytokines.
    • Cytokines cause lymphocyte activation and even more potent immune responses.
  • Sensors of cell damage:
    • All cells have cytosolic receptors that recognize molecules altered due to cell damage and called damage-associated molecular patterns (DAMPs)
    • Uric acid, ATP, reduced intracellular K+ concentration, DNA.
    • Receptors with DAMPs activate cytosolic complex inflammasome, which induces the production of IL-1.
    • IL-1 recruits lymphocytes to induce inflammation.
  • Circulating plasma proteins:
    • Recognize microbes and promote the destruction 
  1. Complement produces mediators of inflammation.
  2. Circulating protein called mannose-binding lectin:
    1. Recognizes microbial sugars and
    2. Circulating protein called mannose-binding lectin:
      1. Recognizes microbial sugars and 
      2. Promotes microbe ingestion and activation of complement
    3. Collectins bind to microbes and promote phagocytosis.

Types of inflammation

  • Acute Inflammation
  • Chronic inflammation

Acute inflammation

  • Transient process: initial, rapid response to infections and tissue damage.
  • Occurs within minutes of injury abrupt origin.
  • Last for hours or days
  • Is short duration 
  • Represents early body reaction 
  • Usually is followed by the repair-a process by which tissue is restored to its original state as far as possible.
  • Hallmarks (main characteristics) 
  • Edema and emigration of neutrophils (polymorphonuclear leukocytes)
  • When offender agents are eliminated or removed. And subsides & residual injury repaired.
  • It fails to clear the stimulus, progresses to chronic inflammation. 

Cardinal signs of inflammation

  • Rubor (redness)
  • Calor (heat)
  • Dolor (pain)
  • A tumor (swelling)
  • Function laesa (loss of function) 

The upper four are proposed by Celsus in the 1st century AD whereas added later by Rudolf Virchow.

  • Rubor (redness): Due to vasodilatation (caused by histamine, NO, etc.)
  • A tumor (swelling): Due to increased vascularity, edema.
  • Calor (Heat): Due to increased blood supply.
  • Dolor (Pain): Due to compression of free nerve endings and action of prostaglandin.
  • Functio Laesa (loss of function): Due to local pain and tissue destruction.

Chronic inflammations

It may follow acute inflammation or arise de novo as chronic from the beginning.

It is of longer duration and associated with more tissue destruction. 

The hallmarks of chronic inflammation:

  • presence of lymphocytes and macrophages
  • the proliferation of blood vessels and fibrosis.  

Chemical mediators

  • The chemical mediators have induced inflammations.
  • Presence of injury is sensed by:
    • various cell types
    • Secrete mediators to induces and regulate inflammation
  • Mediators also produced from plasma proteins
  • Mediators also activate recruited leukocytes, enhancing the ability to eliminate offending agents.

Excessive VS defective inflammations

  • Excessive inflammation
    • life-threatening hypersensitivity reactions to drugs, differents toxins, and insect bites.
  • Too little inflammation:
    • leads to increased susceptibility to infections
    • often caused by a reduced number of leukocytes as in bone marrow suppression
  • Both are responsible for serious illnesses.

Inflammations PDF FILE

Notesmed

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