3 Flashcards
What is inflammation?
Inflammation is a non-specific, dynamic, local physiological tissue response to injury, infection, or cell death. It aims to restrict damage, remove the causative agent, allow immune access, and initiate repair.
What are the two main types of inflammation?
Acute Inflammation – Initial, transient response.
Chronic Inflammation – Prolonged, follows acute inflammation if the cause persists.
What are the key aims of the inflammatory response?
Restrict damage or infection to a localized area.
Remove the causative agent and damaged tissue.
Allow immune cells and molecules to access the site.
Initiate tissue repair.
What are the cardinal signs of acute inflammation?
Redness (rubor)
Heat (calor)
Swelling (tumor)
Pain (dolor)
Loss of function (functio laesa)
What are the major cellular players in inflammation?
Neutrophils (acute inflammation)
Macrophages (chronic inflammation)
Mast cells (release histamine)
Lymphocytes and plasma cells (chronic immune responses)
What are the main causes of acute inflammation?
Infection, physical trauma, toxins, ischemia, and immune reactions.
What is oedema?
An accumulation of fluid in tissues due to increased vascular permeability.
Which cell type dominates in the first 24 hours of acute inflammation?
Neutrophils.
What triggers mast cells to release histamine?
Injury, IgE cross-linking, complement components (C3a, C5a), and physical stimuli.
What are the major mediators of acute inflammation?
Histamine – Vasodilation, increased permeability.
Arachidonic acid derivatives (prostaglandins, leukotrienes) – Inflammation regulation.
Platelet-activating factor (PAF) – Leukocyte activation.
Nitric oxide (NO) – Vasodilation, microbial killing.
Cytokines (IL-1, TNF-α, IL-6, CXCL8, IL-12) – Coordinate immune response.
What is the function of IL-1β?
Local effects: Activates vascular endothelium, lymphocytes, tissue destruction, and increases effector cell access.
Systemic effects: Induces fever and IL-6 production.
What is the function of TNF-α?
Local effects: Increases vascular permeability, allowing IgG and complement entry.
Systemic effects: Fever, metabolite mobilization, and shock.
What is the function of IL-6?
Local effects: Activates lymphocytes and increases antibody production.
Systemic effects: Fever and acute-phase protein production.
What is the function of CXCL8 (IL-8)?
Recruits neutrophils, basophils, and T cells to infection sites.
What is the function of IL-12?
Activates NK cells and induces CD4 T-cell differentiation into TH1 cells.
What are the four plasma enzyme cascade systems in acute inflammation?
Complement system.
Coagulation factors.
Kinin system.
Fibrinolytic system.
What are the three main pathways of complement activation?
Classical pathway.
Alternative pathway.
Lectin pathway.
What are C3a and C5a?
Anaphylatoxins that increase vascular permeability and recruit immune cells.
What does bradykinin do?
Increases vascular permeability and mediates pain.
What is plasmin’s role in inflammation?
Breaks down fibrin, affecting vascular permeability and complement activation.
What are the four steps of neutrophil migration?
Margination – Leukocytes move to vessel edges.
Adherence – Leukocytes stick to endothelium.
Emigration – Leukocytes exit blood vessels.
Chemotaxis – Leukocytes migrate to injury sites.
What are selectins?
Adhesion molecules that mediate rolling of leukocytes on endothelium.
What is ICAM, and what does it do?
Intercellular adhesion molecule; helps leukocytes bind firmly to endothelium.
What is the role of sialyl Lewis-X?
Binds to selectins for leukocyte rolling.
