Nonspecific Defense Flashcards
sweat
salt and lysozyme
goblet cells
produce mucus
siderophore
bacteria that secrete iron-binding proteins that steal iron from body
leukocytes- granulocytes
neutrophils
eosinophils
basophils and mast cells
leukocytes- agranulocytes
B lymphocytes
T lymphocytes
NK lymphocytes
monocytes -> macrophages
NK lymphocytes
induce apoptosis in virus
secrete toxins
differentiate body cells and infected cells
monocytes
wandering or fixed
in the reticuloendothelial system
phagocytosis
diapedesis and chemotaxis: from chemicals released by microbes, damaged tissue, and cytokines
adherence and ingestion
digestion and killing
elimination
diapedesis
cell attacks pathogens in tissue by leaving the blood
chemotaxis
movement of a cell toward an infection site
phagocytosis: adherence and ingestion
formation of phagosome
microbes avoid by virulence factors
host fights back by covering with antimicrobial proteins
opsonins: proteins that increase binding sites on microbes surface
phagocytosis: digestion and killing
phagolysosome formation
release of toxic antimicrobial products
microbes avoid by virulence factors
phagocytosis: elimination
exocytosis
complement system, generally
more than 20 proteins in plasma activated sequentially actions: -enhanced phagocytosis (opsonization) -enhanced inflammation, chemotaxis -lysis of microbes
classic pathway
antibodies take a week to be produced
antibodies attach to antigen, complements reestablish homeostasis
start at C1
properdin pathway (alternative)
bipass C1, start at C3
early in infection
lectin pathway
lectins bind to surface receptors on pathogens
bipass C1, start at C2/C4
interferon
binds to receptors on uninfected cells, making antiviral proteins
(protein kinase and synthetase destroy mRNA and inhibit protein synthesis)
type 1: alpha and beta produced by viral-infected cells (viruses cannot replicate inside)
type 2: gamma produced by activated T cells, NK cells (stimulates macrophages and neutrophils)
lactoferrin
iron-binding glycoprotein found in body fluids
retakes iron from bacteria after they take it
causes of inflammation
- damage
- toxins and enzymes and waste
- damage
- loss of homeostasis
- inflammation
signs: redness, heat, swelling, pain
acute inflammatory process
damaged cells release histamine, prostaglandins, leukotrienes
mast cells, basophils, platelets release histamine in response to C3a, C5a
vasodilation
repair
results of vasodilation
increased phagocyte migration: margination and diapedesis
increased delivery of blood borne antimicrobial products, clotting proteins, oxygen
edema
chronic inflammation
increased production of toxic anti-macrophage products
granulomas
may cause loss of function
fever stimulants
pyrogens
leak into blood stream
fever process
pyrogens go to hypothalamus increase core body temperature induces shivering peripheral vasoconstriction stops sweating increase metabolic rate
effects of fever
increase immune response increase interferon production inhibits microbial growth (decreases plasma iron, increases temp) illness can damage neuronal cells over 38.5C
sebum
decreases pH of skin
defensins
dermicidins, inhibit bacterial growth
mucous membrane chemical defense
lysozyme, HCl
neutrophils
kamikaze, kill pathogens and tissue; create abscesses
eosinophils
attack parasitic helminths, toxins; nonphagocytic
basophils
release inflammatory chemicals
C3b, C4b
enhanced phagocytosis (opsonization)
C3a, C4a, C5a
enhanced inflammation, chemotaxis
MACs, C5-C9
lysis of microbes
