-
susceptibility
lack of resistance
-
immunity
ability to ward of disease
-
innate immunity
defenses against any pathogen
-
adaptive immunity
defenses against specific pathogens
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Toll-Like Receptors (TLRs)
plasma membrane receptors (flagella, LPS, techoic acids)
-
Function of TLRs
stimulates cytokines which stimulate innate/adaptive immunity
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Physical Factors: Epidermis
tightly packed cells with keratin and protective proteins
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Physical Factors: ciliary escalator
microbes trapped in mucus transport away from lungs
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Physical Factors: lacrimal apparatus
washes eyes
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Chemical Factors: pH of skin
pH 3-5
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Chemical Factors: lysozyme
in perspiration, tears, saliva, and tissue fluids
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Chemical Factors: pH of gastric juice
pH 1.2-3
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Chemical Factors: transferrins
in blood, bind iron
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Chemical Factors: NO (nitric oxide)
ATP production
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3 forms of microbial antagonism
- 1. competitive exclusion
- 2. bacteriocins
- 3. alter conditions (ex. lactic acid production)
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leukocytosis
increased WBC count
-
leukopenia
decrease WBC count
-
neutrophils
- -PMNs/polymorphonuclear leukocytes/polymorphs
- -phagocytic
-
3 lymphocytes
- 1. T cells
- 2. B cells
- 3. Natural Killer Cells
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Natural Killer Cells
- -blood, spleen, lymph nodes
- -kill infected cells
- -release toxic granules perferin/granzymes that make holes in target cell membrane
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3 WBCs
- neutrophils
- basophils
- eosinophils
-
basophils
produce histamine
-
eosinophils
toxic to parasites and some phagocytosis
-
dendritic cells
initiate adaptive immune response
-
monocytes
- -phagocytic as mature macrophages
- -fixed macrophages in lung, liver, and bronchii
- -wandering macrophages roam tissues
-
lymphocytes
involved in specific immunity
-
Inflammation
- -edema (symptoms)
- -acute phase protiens activated
- -vasodilation
- -margination/emigration of WBCs
- -tissue repair
-
histamine/kinins
vasodilation; increased permeability of blood vessels
-
prostoglandins
intensifies histamine and kinin effects
-
leukotrienes
increased permeability of blood vessels; phagocytic attachment
-
chemicals released by damaged cells
- -histamine
- -kinins
- -prostoglandins
- -leukotrienes
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fever
abnormally high body temp
-
What temp is the hypothalamus usually set at?
37 degrees C
-
Endogenous pyrogen
gram-neg. endotoxin cause phagocytes to release interleukin-1
-
______ releases ______ that reset the hypothalamus to a higher body temp
hypothalamus, prostoglandins
-
shivering
body increase rate of metabolism which increases body temp
-
how to lower body temp:
eliminate IL-1
-
advantages of fever
- 1. increase transferrins (binding iron)
- 2. increase IL-1 activity
- 3. interferon more effective
-
disadvantages of fever
- 1. tachycardia (rapid heart rate)
- 2. acidosis (acid in blood; pH imbalance)
- 3. dehydration/electrolyte imbalance
- 4. seizures
- 5. delirium
- 6. coma
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Complement System
- -opsonization
- -inflammation
- -cytolysis
-
opsonization
enhancement of phagocytosis by coating with C3b
-
cytolysis
MAC (membrane attack complex)
-
How many proteins produced by liver in CS
30 proteins
-
T/F: there are clotting factors in CS
false
-
T/F: amount of reactive product amplified with each reaction
true
-
T/F: inactive until split into fragments
true
-
T/F: one reaction triggers another
true
-
3 pathways of CS
- -classical
- -alternative
- -lectin
-
Classical Pathway
antibodies involved
-
Alternative Pathway
- no antibodies involved
- factors B, P, D
-
Lectin Pathway
- lectin: carbs
- -starts process
-
Ways Bacteria Evade CS
- capsules
- surface lipid-carbs
- enzymatic digestion of C5a
-
How do bacteria use capsules to evade CS
prevent C activation
-
How do bacteria use surface lipid-carbs to evade CS?
prevent MAC formation
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