Inflammation Basics and Acute Response

Inflammation: Basics

• Inflammation is a non-specific response of the body to local injury. It's an immune response to many things.
• It is also part of the body's secondary defense system, the skin being the first response.
• It can have devastating effects, such as rheumatoid arthritis.
• It is caused by various agents:
  • Physical: trauma, ischemia, temperature extremes
  • Chemical: strong acids, bases, venom
  • Biological: bacteria, fungi, etc.
• Inflammation can be acute or chronic.
  • Acute inflammation is self-limiting and a good thing.
  • Chronic inflammation is self-perpetuating and bad since it keeps coming back causing harm.

Acute Inflammation – Vascular Response

• Acute inflammation starts almost instantly after injury.
• It involves vasodilation of arterioles and venules which increases blood flow to the area.
• The increased blood flow causes redness and warmth.
• Increased permeability of capillaries leads to fluid leakage into the tissue causing swelling.
• Pain and impaired function occur as a result of tissue swelling and release of chemical mediators.

Vascular Response

• Fluid moving into tissues can be beneficial because:
  • It dilutes the harmful agent.
  • It carries plasma proteins and leukocytes to the injury site.
  • It carries away bacterial toxins, dead cells, and debris to the lymphatic system.
  • It brings clotting factors that prevent the spread of microorganisms.

Types of Inflammation

• Depending on injury severity, inflammation can be:
  • Immediate transient response (minor injury)
  • Immediate sustained response (more serious injury)
  • Delayed response (injuries like sunburn).
• Inflammation can also be systemic (widespread) as well as local, which may include:
  • Fever due to infections
  • Leukocytosis (high white blood cell count in blood)
  • Increased circulating plasma proteins (risk of clotting)

Acute Inflammation – Cellular Response – Mast Cells

• Mast cells are found in connective tissues throughout the body, however, are most abundant in the dermis of skin and mucosas of GI and respiratory tracts.
• Mast cells contain granules with histamine and chemotactic factors (and basophils).
• Degranulation (release of chemicals) occurs due to physical injury (like massage), chemical agents, or immune responses.

Acute Inflammation – Cellular Response – Histamine

• Histamine causes dilation of blood vessels and increased permeability.
• Mast cells also release chemotactic factors attracting neutrophils and eosinophils to the injured area.
• It causes pain and swelling.

Acute Inflammation – Cellular Response – Neutrophils

• Neutrophils are the first to arrive (white blood cells/phagocytes) at the site of an injury.
• They clean up debris and dead cells.

Acute Inflammation – Cellular Response – Monocytes/Macrophages

• Monocytes are white blood cells, and the ones at the injury site a little later.
• Monocytes mature into macrophages, which last longer than neutrophils.
• Macrophages destroy injurious agents via phagocytosis (cellular eating) which helps with specific immunity. They also help resolve the inflammation.

Acute Inflammation – Cellular Response – Natural Killer (NK) Cells

• Natural Killer (NK) cells patrol the blood and lymph.
• They are able to kill cancer cells and virus-infected cells.
• They use non-specific mechanisms, identifying the lack of "self" cell surface receptors and recognizing carbohydrates for killing.
• Perforins are the chemicals used.

Acute Inflammation – Cellular Response – Platelets

• Platelets are cytoplasmic fragments in the bloodstream.
• They are involved in clotting and releasing chemical mediators involved in inflammation.

Response of White Blood Cells

• The response includes WBCs, primarily neutrophils and monocytes.
• The sequence of events involves: margination, diapedesis, chemotaxis, and phagocytosis.
• Margination: WBCs slow down, adhere to capillary walls.
• Diapedesis: WBCs move through capillary walls.
• Chemotaxis: WBCs move towards the injury site due to chemical signals.
• Phagocytosis: WBCs engulf and destroy bacteria or debris.

Margination

• Leukocytes slow their migration, sticking to endothelial cells via adhesion molecules.
• Release of chemical mediators (kinins, histamine, leukotrienes, cytokines) encourages adhesion molecules expression.
• Endothelial cells also express adhesion molecules.

Emigration (Diapedesis)

• Leukocytes extend projections through the permeable capillary walls to enter tissue.
• Movement happens after adhering to endothelial cells.

Chemotaxis

• Leukocytes move toward the injury site via chemical signals.
• Chemotactic agents include cytokines, bacterial debris, and complement fragments.

Phagocytosis

• Cells (macrophages and neutrophils) engulf and destroy bacteria, cellular debris, and other foreign materials.

Phagocytosis Stages

• Adherence: phagocyte binds to the target.
• Engulfment: pseudopods surround the target, creating a phagosome.
• Phagolysosome formation: fusion of phagosome with lysosome.
• Intracellular killing: lysosomal enzymes destroy material.
• Exocytosis: residual material is expelled.

Explore the essential concepts of inflammation, including its definitions, causes, and effects on the body. This quiz also covers the vascular response during acute inflammation, highlighting its importance in the immune response. Understand the differences between acute and chronic inflammation.