Summary
Highlights
Upon injury, such as a cut, pathogens can infiltrate the body. Bacteria express Pathogen-Associated Molecular Patterns (PAMPs), which are recognized by immune cells like mast cells and macrophages in the tissue. This recognition triggers the release of histamine from mast cells.
Inflammation is defined as the sum of host defenses against infectious or noxious stimuli. Its main goals are to bring immune cells to the affected area, destroy invaders, and initiate repair. Clinically, inflammation is indicated by the suffix "-itis," such as in dermatitis (skin inflammation) or arthritis (joint inflammation).
The video illustrates inflammation using a diagram of the skin, submucosa, blood vessels, and lymphatic vessels. It highlights that lymphatic vessels connect to lymph nodes, containing naive B and T cells. Blood vessels contain various cells like erythrocytes, monocytes, and neutrophils, as well as inflammatory mediators.
There are two main types of inflammatory mediators: plasma inflammatory mediators (e.g., coagulation proteins, kinins) produced by the liver and activated by inflammation, and cell-derived inflammatory mediators. Mast cells, located in tissues, contain histamine granules and are crucial for initiating inflammation by releasing histamine.
Secreted histamine causes vasodilation (widening of blood vessels) and increased vascular permeability (endothelial cells contract, creating gaps). This allows more blood flow and facilitates the migration of immune cells from the blood vessels into the inflamed tissue, a process known as diapedesis.
Macrophages, recognizing PAMPs, secrete cytokines, which are also inflammatory mediators. Key cytokines include TNF-alpha (tumor necrosis factor alpha) and interleukin 1. These cytokines have both local and systemic effects.
Locally, cytokines cause vasodilation and increased vascular permeability, promoting immune cell immigration into the inflamed tissue (e.g., neutrophils and monocytes, which become macrophages upon entering tissue). Cytokines also initiate tissue repair by stimulating fibroblast activity. Systemic effects include fever and leukocytosis (increased white blood cell count).