Exam 1: Inflammation II Flashcards
Major signs of acute inflammation
Pain, heat, swelling, redness, loss of function
Pro-inflammatory cytokines
TNF-a
IL-1
IL-6
TNF-a
Promotes inflammation
Enhances fibroblast growth, collagen synthesis, and bone resorption
Toxic effects: kill tumor cells, septic shock, sickness behavior, altered lipid metabolism
Activates mast cells, vascular endothelium, macrophages, lymphocytes, neutrophils, fibroblasts
IL-1
IL-a - membrane attached
IL-1B - soluble
Promotes inflammation
Kills tumor cells
Affects leukocytes
Affects the brain - fever, drowsiness, loss of appetite
Affects cell growth
Affects blood flow
Affects metabolism
IL-6
Regulates transition from early neutrophil-dominated inflammatory process to later macrophage-inflammatory process
Produced by muscles during exercise
Anti-inflammatory activity inhibits some function of TNF-a and IL-1
T cells: stimulates Th2 responses, activates Th17 cells, suppresses Treg cells, enhances cytotoxicity
Hepatocytes: acute phase response
Brain: fever
B cells: activates, enhances IgA production
Chemokines
Produced by sentinel cells
Classified in 4 families
Coordinate migration of cells and dictate the course of many inflammatory and immune responses
Have receptors on cell membrane
Families of chemokines
a family
B family
y family
delta family
Vasoactive amines
Mast cells –> histamine –> nitric oxide production, vasodilation, edema
Mast cells –> serotonin –> vasoconstriction/vasodilation
Vasoactive peptides
C5a –> chemotactic for neutrophils and monocytes
Vasoactive lipids
Sentinel cells –> leukotrienes, prostaglandins –> inflammation
What do NSAIDs target
Lipoxygenases and cyclooxygenases in production of leukotrienes and prostaglandins
Appearance of leukocytes during inflammation
0-4 days: neutrophils - first line of defense
0 days - 6 weeks: mononuclear phagocytes - macrophages, second line of defense
4 days - 6 weeks: helper T cells - adaptive immune response
1 - 6 weeks: cytotoxic T cells - cellular immune response
3 - 6 weeks: B cells - cytokines
Systemic effects of acute inflammation
Anorexia, altered sleep patterns, lethargy, cachexia, hemodynamic changes (shock), fever, leukocytosis (neutrophilia), metabolic acidosis (lowered blood pH)
Neutrophilia left shift
In order to produce more neutrophils, bone marrow stimulated to release immature neutrophils
Chronic infection and neutrophil left shift
When suffering from chronic infection - bone marrow already stimulated to produce more neutrophils
Does this by release immature ones
