Inflammatory Response Overview Quiz

Inflammatory Response Overview

• Inflammatory response is a cascade of events at the site of infection or injury, characterized by redness, swelling, pain, and heat.
• Acute inflammation is a short-term response to infection, while chronic inflammation is a long-term response to cell damage (e.g., IBS, arthritis).
• Immune cells like neutrophils, macrophages, dendritic cells, and mast cells are recruited to the site.

Types of Immune Cells

• Neutrophils: Most abundant, circulating blood cells that die after ~8 hours; phagocytic cells.
• Macrophages: Resident cells that encounter microbes first; phagocytes, located in external barriers (e.g., gastrointestinal tract, skin, alveoli).
• Dendritic Cells: Resident tissue cells that sense danger and release cytokines.
• Mast Cells: Resident in skin and mucosal tissues, activated by PAMPs, cytokines, or antibodies releasing histamine and cytokines to promote vasodilation and inflammation.

Inflammatory Response Steps

• Before injury/infection: Monocytes and neutrophils circulate; resident macrophages, dendritic cells, and mast cells reside in tissues.
• Injury/infection: Local tissue damage triggers pain. Bacterial entry. Activation of immune cells (PRRs/PAMPs, leading to cytokine release).
• Inflammation initiation: Cytokines (e.g., TNF, IL-8, IL-1), chemokines, histamine, and bioactive lipids released by damaged cells and activated immune cells cause vasodilation, increased capillary permeability, and attract immune cells.

Capillary Alterations

• Vasodilation (increased capillary and venule diameter) allows for immune cell circulation.
• Increased capillary permeability (swelling/edema) allows inflammatory mediators to enter tissues.
• Blood volume increases, flow slows down, facilitating immune cell extravasation.

Extravasation (Immune Cell Migration)

• Rolling: Endothelial cells become activated and express adhesion molecules (selectins) on their surface, causing weak leukocyte attachment that rolls along endothelial surface.
• Activation: Cytokines (TNF, IL-1) induce endothelial cells to express ICAMs (intercellular adhesion molecules). Chemokines activate leukocytes to express high-affinity integrins.
• Arrest: Strong leukocyte adhesion due to interactions between leukocyte integrins and ICAMs on the endothelial surfaces that halt leukocytes to spread on surface.
• Diapedesis: Leukocytes cross the endothelial cell junctions and enter the tissues.

Chemotaxis and Phagocytosis

• Chemoattractants (chemokines): Indicate the site of infection and guide immune cell migration.
• Neutrophils: Early responders to infection.
• Monocytes (macrophages): Provide long-term protection.
• Dendritic cells/macrophages: Travel to lymph nodes to present antigens.

Inflammatory Mediators: Cytokines

• Cytokines: Communicate between immune cells.
• Mechanism: Production, secretion, binding to receptors induce cellular response in target cells (e.g., proliferation, differentiation, cell death).
• Types: IL-1 (proinflammatory from macrophages), TNF (proinflammatory from macrophages and neutrophils), IL-8 (recruitment/activation of neutrophils).

Chemokines

• Chemokines: Subgroup of cytokines, small & structurally related; cause leukocyte adhesiveness, cell movement, and chemotaxis.
• Concentration Gradient: Released at infection site by macrophages and damaged cells forming concentration gradient.
• Types: CC and CXC families (classified by conserved cysteine residues in their amino terminal), attracting different immune cells (e.g., monocytes and macrophages, neutrophils).