chap 16

Question 1

basic run down of innate immunity

Answer 1

• activated by toll-like receptors on host cell that recognize pamps and so it releases cytokines

Question 2

pamps

Answer 2

• pathogen associated molecular pattern
• lps of gram neg, peptidoglycan, flagella, viral rna/dna
• used to identify if something is a foreign substance in
  body
• signals cytokines

Question 3

what do cytokines do

Answer 3

• activate macrophages
• chemotactic effects
• inflammatory response/Fever
• Activate T, B cells

Question 4

first line of defense(phyical factors)

Answer 4

• skin: comprised of epidermis and dermis; has layer of keratin
  - subcutaneous infection: when skin is penetrated
• mucous membranes: line GI, GU, and respiratory tracts; epithelial and connective tissue layer
  - mucus: traps microbes, moistens surfaces
  - tears and saliva: prevent colonization of microbes
  - hairs and cillia: trap microbes
  - epiglottis, earwax, digestion: eliminates microbes

Question 5

first line of defense(chemical factors)

Answer 5

• skin: sebum forms a film on the skin
  - contains fatty acid, low pH means prevent
  colonization of pathogens
• mucous membrane: saliva(lysozyme, urea, uric acid, antibody), gastric juice(pH 1-3 due to HCl), vaginal secretions(acidic pH), urine(lysozyme, pH 6)
• normal microbiota: microbial antagonism, alteration of physical, chemical conditions prevent colonization by pathogens

Question 6

second line of defense

Answer 6

• granulocytic leukocytes
• agranuloctic leukocyes

Question 7

granulocytic leukocytes

Answer 7

• neutrophils(polymorphonuclear leukocytes): phagocytic;
  active in initial stages of infection(exit blood and enter
  infected tissue ~70%)
• basophils: release components promoting inflammatory
  and allergic responses(histamine)(~1%)
• eosinophils: phagocytic and exit blood; release toxins;
  deal w large multicellular pathogens(~3-5%)

Question 8

agranulocytic leukocytes

Answer 8

• monocytes: differentiate into macrophages and dendritic
  cells in lymphatic tissue(~25%)
  - phagocytic cell types
  - antigen presenting cells( work w adaptive sys)
• lymphocytes
  - natural killer cells: kill infected body cells
  - t cells: are programed to have specific immune
  responses (act on intracellular pathogens)
  - b cells: produce antibodies to bind antigens(act on
  extracellular pathogens)

Question 9

natural killer cells

Answer 9

• destroy host cells that are infected an cancerous(ones that lack MHC antigens)
  - bind nk to targets = stimulate membrane to lysis
  - release granzyme; induce apoptosis on target

Question 10

major histocompatibility complex(MHC)

Answer 10

• self antigen; collection of genes code for antigens on
  surface for identification
  MHC class II: macrophages, dendritic, and B cells
  (antigen presenting cells)
  MHC class I: all other ones not class II
  (nucleated mammalian cells)

Question 11

lymphatic system

Answer 11

• lymphoid system/organs present
• protect against ihaled and ingested microbes
• contain T cells, B cells, dendritic cells and macrophages

Question 12

granulocyte and monocyte role in phagocytosis

Answer 12

• granulocytes and monocytes migrate to infection site
  - monocytes diff into macrophages: fixed and free
  macrophages
  - granulocytes = early stages of infection and
  macrophages = later

Question 13

process of phagocytosis

Answer 13

• chemotaxis: chemicals = microbial products, dead
  tissue, and cytokines
• adherence: using PAMPS to toll like; release cytokines,
  opsonization facilitate phagocytosis, tart coat w opsonin
• ingestion: phagosome formation
• digestion: fusion of phagosome w lysosome; enzyme
  digestion and produce O2 radicals and peroxides

Question 14

opsonins

Answer 14

• combination of innate and adaptive(activate w
  complement/antibodies)
• enhance phagocytosis
• engulf capsulated bacteria w anti-capsular antibodies
• phagocytic cells recognize and ingest bacteria
• SIGNAL FOR EAT

Question 15

what triggers inflammation

Answer 15

• damage by microbial infection, chemical or physical

Question 16

signs/symptoms of inflammation

Answer 16

• red/pain/heat/swelling/ maybe loss of function
• acute and chronic inflammation

Question 17

function of inflammation

Answer 17

• destroy/remove agent
• confine agent to local area
• repair/replace damaged tissue

Question 18

early stages of inflammation

Answer 18

• cytokine release
• tnf tumor necrosis factor(cytotoxin stim by endotoxin release)
• formation of acute - phase proteins(bind pathogens)

Question 19

inflammation stages

Answer 19

• vasodilation
  - release kinins, histamines and prostaglandin
• phagocyte migration(chemotaxis)
• phagocytosis(diapedesis and margination)
• repair(pus form and blood clot)

Question 20

vasodilation(inflammatory response)

Answer 20

• increase blood flow(cause red and heat)
• triggered by chem(histamine, kinins)
• increase permeability = blood cell go area(edema,
  swelling) (due to kinin, leukotrienes(mast cells))
• prostaglandin intensifies effect chemicals; highen pain response
• clotting elements arrive

Question 21

phagocyte migration(inflammatory response)

Answer 21

• respond to cytokines = phagocyte stick to blood vessel
  walls(margination)
• diapedesis(phagocyte squeeze btwn cells, exit blood
  vessels)
• monocytes enter and become free macrophages

Question 22

phagocytosis(inflammatory response)

Answer 22

• removes microbes, damage tissues and pus formation

Question 23

tissue repair(inflammatory response)

Answer 23

• replacement of dead, damaged tissue
• pus formation and clotting occur

Question 24

role of they hypothalamus

Answer 24

• body’s thermostat(regulate body temp)

Question 25

pyrogens(and types)

Answer 25

• substance cause fever, natural, induce rise in body temp

exogenous pyrogens - outside body(bacteria, viruses,
others)
endogenous pyrogens(interleukin-1) - act on
hypothalamus, raise temp set point

Question 26

effect of elevated temperature

Answer 26

• slows pathogen growth
• increase T cell activity
• lowers concentration of available iron

Question 27

complement cascade

Answer 27

• enhances antibodies and phagocytic cells using soluble
  protein factors(20 proteins activate each other CIA proteolytic cleavage)

classical pathway- C3 activated by contact btwn
complement and pathogen via antibodies

alternate pathway - C3 act by contact btwn complement
and pathogen via surface glycolipids complex

lectin pathway - C3 act by contact btwn lectin and
pathogen via surface specific carbohydrates(mannose)

Question 28

effects of complement

Answer 28

• opsonization: activated C3b proteins bind microbe;
  phagocyte bind to C3b(enhances phagocytosis)
• cytolysis: C3b proteins split C5 to C5a + C5b; C5b
  promotes formation of complement protein that inserts in
  the plasma membrane of microbe(forms membrane
  attack complex(MAC), then channel forms causing lysis)
• inflammation: C3a and C5a bind mast cells -> release
  histamine, kinins. C5a also chemoattractant for
  phagocytes

Question 29

interferons

Answer 29

• cytokines that interfere w viral production; in response to
  infection(host-specific)
• not long acting; not stable; toxic in high doses
• effective in acute viral infect; can’t help virus infected cells

type 1 - high antiviral; bind receptor on uninfected to make
resistant to viral infection

type 2 - activate neutrophil and macrophage; increase
MHC antigen on surface

Question 30

antimicrobial substances

Answer 30

• iron binding proteins
• transferrins, lactoferrins, ferritin, hemoglobin(bind free iron in human body)
• compete w pathogen for iron(bc iron need as cofactor of lot enzymes)
• pathogens use siderophores to bind iron

Question 31

antimicrobial peptides(AMPS)

Answer 31

• 12-50 amino acid long, broad spectrum of activity
  - synthesis trig by protein, carbohydrate molecules
  on microbial surfaces
• act against bacteria, virus, fungi, eukaryotic parasites
• kill by lysing, inhibit cell wall syn; hydrolyze DNA and rna
• attract dendritic and mast cells