PHARMACOLOGY Chapter15

Chapter 15: Introduction to the Immune Response and Inflammation Body's Defenses

• Barrier defenses

• Cellular defenses

• Inflammatory response

• Immune response

Barrier Defenses

• Skin: First line of defense, protects internal tissues and organs.

• Mucous membranes: Line areas exposed to external influences without skin protection.

• Gastric acid: Destroys ingested pathogens post-removal from the respiratory tract.

• Major histocompatibility complex (MHC): Distinguishes between self-cells and foreign cells.

Cellular Defenses

• Mononuclear phagocyte system (MPS): Includes leukocytes:

  • Lymphocytes: T cells, B cells, natural killer cells

  • Myelocytes: neutrophils, basophils, eosinophils, monocytes, macrophages

• Involves lymphoid tissue and various chemical mediators.

Types of White Blood Cells (Leukocytes)

• Produced by the body to fight infection.

Lymphoid Tissues

• Lymph nodes

• Spleen

• Thymus gland

• Bone marrow

• Lymphoid tissue throughout the respiratory and gastrointestinal (GI) tracts.

The Inflammatory Response #1

• Hageman factor involvement.

• Kinin system includes:

  • Bradykinin

  • Arachidonic acid leading to:

    • Prostaglandins

    • Cyclooxygenase

    • Leukotrienes

    • Thromboxanes

The Inflammatory Response #2

• Exposure of plasma to injured cells initiates activation of Hageman factor.

• Cascade of:

  • Prekallikrein

  • Kallikrein

  • Kininogen to Bradykinin leading to:

    • Tissue injury

    • Release of arachidonic acid leading to

    • Leukotrienes (LTs)

    • Prostaglandins (PGs)

    • Chemotaxis of leukocytes

    • Activation of neutrophils leading to phagocytosis.

• Symptoms of inflammation:

  • Dolor (pain)

  • Tumor (swelling)

  • Rubor (redness)

  • Calor (heat)

The Inflammatory Response #3

• Histamine release: Causes vasodilation and alters capillary permeability.

• Neutrophils and chemical agents enter the injured area.

The Inflammatory Response #4

• Chemotaxis activated by arachidonic acid.

• Aggressive action of neutrophils and macrophages.

• Acute inflammation lasts minutes to a few days (protective).

• Chronic inflammation can last years (potentially harmful).

Clinical Presentation of the Inflammatory Response

• Calor: Caused by increased blood flow.

• Tumor: Caused by fluid leakage into tissues.

• Rubor: Related to enhanced blood flow due to vasodilation.

• Dolor: Pain caused by activation of pain fibers.

Immune Response

• Specific invasion triggers an immune response.

• Lymphocytes developed in bone marrow (T & B lymphocytes).

• Other lymphocytes include natural killer cells.

T Cells

• Effector or cytotoxic T cells: Aggressively target non-self cells.

• Helper T cells: Stimulate other lymphocytes (B cells).

• Suppressor T cells: Slow down reactions to conserve energy.

The Role of the B Cell

• Identify specific proteins (antigens).

• Provide humoral immunity.

• Transform into plasma cells that produce antibodies.

Complement Proteins

• React in a cascade to form a barrier around antigen-antibody complex.

• Can destroy antigens through alterations in the membrane.

• Induce chemotaxis and release histamine.

Antibody Formation

• Takes several days for B cells to produce antibodies.

• Memory cells formed for future rapid responses against antigens.

• Antibodies released as immunoglobulins:

  • IgM, IgG, IgA, IgE, IgD.

Other Mediators in the Immune Response

• Interferons: Prevent viral replication.

• Interleukins: Chemicals secreted by leukocytes.

• Thymus gland: Releases hormones for T cell maturation.

• Tumor necrosis factor (TNF): Released by macrophages, inhibits tumor growth.

Interrelationship of Immune and Inflammatory Responses

• Work together to maintain homeostasis.

• Hageman factor and histamine promote neutrophil activity.

• Helper T cells stimulate B cells and effector T cells.

• Both B and T cells rely on effective inflammation.

Pathophysiology Involving the Immune System

• Neoplasms

• Viral invasions

• Autoimmune diseases

• Transplant rejection.