Lecture Notes on Inflammation

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All organisms respond to local injury.

The inflammatory process is the reaction of blood vessel, which brings about an accumulation of fluid and white blood cell in the extravascular tissue.

Inflammation and repair go hand in hand.

Inflammation is a protective response:

• Rid organism of cause of injury (microbe, toxin)
• Rid the organism of consequences of injury (necrotic cells)

• Without wounds would never heal

Inflammation and repair can be harmful thus leading to:

• Hypersensitivity
• Unnecessary scarring

Inflammatory response occurs in vascularized connective tissue.

Intravascular Cells important to inflammation are:

• Neutrophils
• Eosinophils
• Basphils
• Lymphocytes
• Monocytes

Cells outside the vessels which are important are"

• Fibrocytes
• Mast cells (basophil)
• Macrophage (monocyte)

Inflammation is divided into acute and chronic

• Acute is of short duration, primary cell is the neutrophil, characterized by exudation of fluid and plasma proteins.
• Chronic is longer, main cells are lymphocytes and macrophages, proliferation of blood vessels, fibrosis and necrosis.

Vascular and cellular responses of both acute and chronic are mediated by chemical factors derived from cells and plasma and triggered by the inflammatory stimulus. Necrotic cells, themselves, release these chemical. These are called chemical mediators of inflammation. Inflammation stops when the injurious stimulus is removed.

Acute inflammation has three major components:

• Alteration in vessels leading to increased blood flow to the area.
• Structural changes in microvessels that allow plasma protein and WBCs to leave the circulation.
• Emigration of WBCs from vessels so they can accumulate at the site of injury.

Vasodilatation occurs resulting in increased blood flow to the area. New capillary beds open up. (HEAT AND REDNESS).

This is followed by slowing of the circulation that is brought about by increased permeability. Fluid moves into the extravascular space, the blood becomes thicker and thus moves more slowly. At this point the blood is more viscous; there are a higher concentration of RBCs in the vessels. We call this stasis.

When stasis occurs the WBCs start to move toward the periphery of the vessel. This is call margination or pavementing.

The hallmark of acute inflammation is increased vascular permeability leading to edema.

How does excess fluid get out of the vessels?

• Endothelial gaps. Gaps are do to endothelial contraction mediated by histamine, bradykinin, leukotrienes, substance P and others.
• Direct endothelial injury by burns, lytic bacterial infections.
• Delayed prolonged leakage beginning after a delay of 2 to 12 hours. Usually caused by thermal injury, radiation and certain bacterial toxins. An example is a late occurring sunburn.
• Leukocyte-mediated endothelial injury. Seem mostly in the kidneys and lungs and is related to a hypersensitivity reaction.
• Leakage from new blood vessels which have lots of receptors for chemical mediators.

Cellular Events

• Margination, cells have to adhere to vessels. There are adhesion receptors and chemical mediators that allow this to happen. There are genetic disorders where people can not make adequate adhesion factors; these people can not mount a normal inflammatory response.
• Transmigration
• Migration, leukocytes emigrate to the site of injury by a process called chemotaxis. Chemotactic factors can be both endogenous and exogenous. Bacterial products are the most common exogenous factors. Endogenous agents include components of compliment, leukotrienes and cytokines. Chemotactic factors stimulate locomotion.

Phagocytosis is the ability of the WBC to recognize the pathogen, form an attachment, engulf it and kill it. Various chemical mediators are important in this function. Bacterial killing is accomplished mostly by an oxygen-dependent mechanism. Killing can also occur by the release of granules from the lysosomes.