Phagocytosis and Wound Repair in the Skin

Study Notes

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.

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.

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.

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 enhances phagocytosis by coating with C3b (opsonisation).
Complement activation increases blood vessel permeability and chemotactic attraction of phagocytes.

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.

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.

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.

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.