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Questions and Answers
What is the first phase of phagocytosis?
Which phase involves the phagocyte merging with a lysosome?
What type of cell releases histamine during inflammation?
Which of the following mediators causes vasodilation and increased vascular permeability?
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Which inflammation symptom is characterized by heat?
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What occurs during the adherence phase of phagocytosis?
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What is pus primarily composed of?
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What is the role of C3b in complement activation?
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Which type of immunity is characterized by its non-specific nature?
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What is the role of epithelial tight junctions in the respiratory tract?
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Which of the following is NOT an external innate immune defense?
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What is the primary function of interferons in the immune system?
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Which type of cell produces mucus in the respiratory tract?
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What is the function of natural killer (NK) cells in the immune system?
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How fast can a bacterial population double under optimal conditions every 20 minutes?
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Which antimicrobial substance is produced in sweat?
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Study Notes
Phagocytosis
- Phagocytosis is a process involving neutrophils and macrophages to engulf and destroy foreign substances and microbes.
- Phagocytosis involves five phases: chemotaxis, adherence, ingestion, digestion, and killing.
- Chemotaxis: microbe attracts phagocytes towards itself.
- Adherence: phagocyte attaches to the microbe.
- Ingestion: phagocyte engulfs the microbe, forming a phagosome.
- Digestion: the phagosome merges with a lysosome, releasing enzymes and breaking down the microbe.
- Killing: the microbe is destroyed.
Wound Repair in the Skin
- Damaged tissue releases chemical signals that attract macrophages.
- Macrophages release chemical signals that initiate blood clotting.
- A new blood clot forms, and phagocytosis occurs.
- The wound is eventually repaired.
Mediators of Vasodilation and Increased Vascular Permeability
- Histamine: released from mast cells activated by complement proteins (C3a and C5a).
- Bradykinin: a vasoactive peptide.
- Prostaglandins: also affect nerve endings and cause pain.
- Leukotrienes (LTC4): induce vasodilation and increased vascular permeability.
Inflammation
- The stages of inflammation include vasodilation, increased vascular permeability, phagocyte emigration, and tissue repair.
- The symptoms of inflammation are rubor (redness), calor (heat), tumor (swelling), and dolor (pain).
- Phagocyte migration involves the movement of phagocytes from the blood to the site of tissue injury.
Pus
- Macrophages engulf bacteria, damaged tissue, and worn out neutrophils, eventually leading to the formation of pus.
- Pus is a pocket of dead phagocytes and damaged tissue that occurs at most sites of inflammation and persists until the bacteria is cleared.
- Pus can drain externally or internally, for example in patients with massive lung infection.
Complement Activation
- Complement activation enhances phagocytosis by coating with C3b (opsonisation).
- Complement activation increases blood vessel permeability and chemotactic attraction of phagocytes.
Immunology
- The immune system can be divided into two categories: innate immunity and adaptive immunity.
- Innate immunity is a natural immune response that prevents or limits infection and is non-specific.
- Adaptive immunity is an acquired response that eradicates infection and is highly specific.
Infection
- Bacteria can be as small as 1.8 µm in diameter and 7 µm long.
- Viruses can be as small as 20-300 nm.
- Parasites can range from 15-35 cm (Ascaris) to 30 m (Tapeworm).
Mucus Membranes in the Respiratory Tract and Gut
- Epithelial tight junctions prevent infection.
- Mucus is produced by goblet cells in the epithelium and by mucus glands in the lower respiratory tract.
- Cilia in the lower respiratory tract move the mucus up toward the larynx.
- Epithelial cells produce antimicrobial peptides (defensins) and lysozyme.
Internal Innate Immune Defences
- Interferons: antiviral proteins that inhibit replication of viruses in cells nearby, and limit the spread of the virus.
- Complement proteins: when activated promote bacterial cytolysis, phagocytosis, and inflammation.
- Iron binding proteins: inhibit the growth of iron-dependent bacteria.
- Antimicrobial peptides (AMPs): such as dermicidin in sweat, defensins produced by epithelial cells, neutrophils, and macrophages.
External Defenses
- The skin provides a physical barrier to infection.
- Antimicrobial fatty acids in sebum from sebaceous glands.
- Extracellular antimicrobial lipids; ceramide and sphingosine.
- Acid pH of sweat (lactic acid).
- Antimicrobial peptides eg dermicidin in sweat from eccrine glands.
- The flow of tears, urine, saliva, perspiration, vaginal secretions, to prevent microbe adhesion to epithelial surfaces.
- Lysozyme (muramidase) in tears, saliva, and mucus.
- Defecation (diarrhea) and vomiting to expel microbes.
- Highly acidic gastric acid secretions (pH 1.2-3.0) destroy bacteria and toxins.
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Description
Learn about the phases of phagocytosis, including chemotaxis, adherence, ingestion, digestion, and killing, as well as the role of macrophages in wound repair in the skin.
