immune system: from textbook PT1

Overview of Body's Defenses

  • The body constantly faces threats from harmful entities such as bacteria, viruses, parasites, chemicals, mutated body cells, and foreign cells.

  • Protection is critical from pre-birth to the end of life.

Defense Mechanisms

Types of Defense Mechanisms

The body has developed a range of protective measures categorized as:

  1. Non-specific (innate) defense mechanisms

    • Present at birth.

    • First line of defense.

    • Comprises cells, chemicals, and physical barriers.

  2. Specific defense mechanisms (immunity)

    • Second line of defense activated by the innate immune system or presence of microbes.

    • Involves specialized cells and antibodies that target specific pathogens.

    • Adaptability and immunological memory provide long-term immunity.

Key Immune Cells

  • T-lymphocytes (T-cells)

  • B-lymphocytes (B-cells)

Non-Specific (Innate) Defense Mechanisms

Learning Outcomes

After studying this section, you should be able to:

  • Identify main non-specific defense cells.

  • Describe features and functions of the inflammatory response.

  • Explain the process of phagocytosis.

  • List main antimicrobial substances in the body.

Categories of Non-Specific Defense Mechanisms

  1. Epithelial Barriers

    • Intact skin and mucous membranes provide physical barriers.

    • Contains commensal bacteria that inhibit pathogenic organisms.

    • Sebum and sweat possess antibacterial and antifungal properties.

    • Epithelial membranes (respiratory, genitourinary, digestive) contain antimicrobial secretions, antibodies, and sticky mucus.

    • Nose hairs filter particles and cilia in the respiratory tract expel pathogens.

    • Urine flow minimizes risk of urinary tract infections; vaginal secretions are acidic to deter microbial growth.

  2. Phagocytes and Phagocytosis

    • Phagocytosis is a process where cells like neutrophils and macrophages engulf and digest pathogens and debris.

    • Neutrophils are short-lived and destroy themselves during phagocytosis; they migrate to infection sites via chemotaxis.

    • Macrophages have longer lifespans, and after phagocytosis, present antigens to activate T-cells.

    • Impact on inflammation and healing processes.

  3. Antimicrobial Chemicals

    • Hydrochloric Acid: Found in gastric juice; pH between 1-2 kills swallowed microbes.

    • Lysozyme: Found in tears and secretions; destroys bacterial cell walls.

    • Antibodies: Proteins that bind to antigens, distributed throughout body fluids.

    • Saliva: Contains antibodies and enzymes that help prevent dental decay.

  4. Interferons

    • Released by infected cells to warn neighboring cells and activate immune responses against viral replication.

  5. Complement System

    • Consists of ~20 proteins activated by antigens-antibody complexes.

    • Functions include targeting bacteria, promoting phagocytosis, and recruiting phagocytic cells to infection sites.

Inflammatory Response

  • Physiological response to tissue damage aimed at protection and repair.

Cardinal Signs of Inflammation

  1. Redness

  2. Heat

  3. Swelling

  4. Pain

  • Recognized by the suffix '-itis' in terms such as appendicitis (inflammation of the appendix).

Causes of Inflammation

  • Tissue damage from various stimuli including temperature extremes, foreign bodies, corrosive chemicals, and immune reactions.

  • Triggers the acute inflammatory response, which can lead to healing or chronic inflammation if not resolved.

Acute Inflammation

  • Short duration (days to weeks) and can vary from mild to severe.

  • Beneficial for removing harmful agents.

  • Events involved include:

    • Increased blood flow

    • Tissue fluid accumulation

    • Leukocyte migration

    • Pain and analytics causing pus formation.

Migration of Leukocytes

  • Neutrophils are the primary leukocytes in acute inflammation, followed by macrophages which persist longer.

  • Process of chemotaxis where leukocytes are attracted to sites of inflammation via toxins and released chemicals.

Systemic Effects

  • Release of mediators into blood can lead to systemic indicators of inflammation including fever and elevated leukocyte counts.

Fever

  • Temporary increase in body temperature set by the hypothalamus during infection/inflammation enhances immune functions while inhibiting microorganism growth.

Pain

  • Caused by nerve compression from swelling and increased sensitivity due to inflammatory mediators. Helps protect the damaged area.

Suppuration (Pus Formation)

  • Collection of dead cells, microbes, and exudate in tissues, potentially leading to the formation of abscesses.

Outcomes of Acute Inflammation

  1. Resolution: Complete healing without significant scarring.

  2. Chronic Inflammation: Occurs when acute inflammation does not resolve completely, typically with persistent irritation or infection.

Chronic Inflammation

  • Involves different cells (primarily lymphocytes), often leads to continued tissue damage and fibrosis. Granulomas may form in response to persistent infections. For example, Mycobacterium tuberculosis can survive within cells leading to chronic inflammation.