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Immunology > Lecture 3&4 early recognition and inflammation > Flashcards

Lecture 3&4 early recognition and inflammation Flashcards

1
Q

___________ cells recognize invading microbes

A

sentinel cells (guard cells)

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2
Q

T/F pathogens grow fast, must be detected and destroyed quickly

A

TRUE

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3
Q

What are the 3 types of sentinel (guard) cells that recognize pathogens

A

mast cells
macrophages
dendritic cell

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4
Q

how do sentinel cells recognize pathogens

A

they notice alarm signals by using their PRRs

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5
Q

what is a PRR

A

pattern recognition receptors

these identify PAMPs and DAMPs

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6
Q

what is a PAMP

A

Pathogen Associated Molecular Patterns

alarms signals are generated by: invading microorganisms (exogenous signals)

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7
Q

what is a DAMP

A

Damage Associated Molecular Pattern
(sometimes called Alarmins)

alarms signals are generated by: dead or dying host cells

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8
Q

DAMPs and PAMPs are identified by _________ present on ___________ cells located throughout the body so that leads to cytokines

A

PRRs (pattern recognition receptors)
sentinel

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9
Q

examples of PAMPs

A

bacterial lipopolysaccharides
bacterial peptidoglycan
bacterial DNA
Viral nucleic acids

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10
Q

Lipopolysaccharides are gram _______

A

negative

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11
Q

peptidoglycan are gram _______

A

positive

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12
Q

some DAMPs are released when cells _____ (intracellular) or generated when _______________ is damaged (extracellular)

A

die
connective tissue

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13
Q

when host cells die what happens to the mitochondria

A

may be recognized as the bacteria they once were

mitochondria were originally sing celled and its DNA is un-methylated so it presents as bacterial DNA

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14
Q

list some intracellular DAMPs

A

HMGB1 (most important)
uric acid
adenosine

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15
Q

list some extracellular DAMPs

A

hyaluronic acid
elastin
collagen derived peptides

**form connective tissue

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16
Q

why is HMGB-1 an important DAMP

A

it affects the epithelium, endothelium, dendritic cells, neutrophils, and macrophages

leads to severe inflammation

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17
Q

what are the categories of PRRs

A

soluble
within vesicles
cytoplasmic
membrane-bound

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18
Q

what kind of PRR are TLRs

A

membrane-bound

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19
Q

what are TLRs

A

Toll-like receptors; transmembrane glycoprotein receptors present on many different cell types including sentinel cells

most important PRRs

play a critical role in microbial sensing by recognizing viruses, fungi, and bacteria

located on cell surface to recognize extracellular invaders OR located in cell to recognize intracellular invaders

20
Q

mammals posses _____to____ different functional TLRs. Humans and cattle have TLR__ to TLR___

A

10 to 12
1 to 10

21
Q

what are the cell surface TLRs and what do they recognize

A

1,2,4,5,6,11

mainly recognize bacterial/fungal proteins, lipoproteins and LPA

22
Q

what are the intracellular TLRs and what do they recognize

A

3,7,8,9,10

recognize viral and bacterial nucleic acids

23
Q

why is inflammatory bowl disease so common in German Shepards

A

they have several single-nucleotide polymorphisms (SNPs) in the TLR4 and TLR5 genes

this suggest that their TLR4 and 5 have reduced the ability to defend against bacterial invasion resulting in predisposition to intestinal infections

24
Q

RIG-like receptors are another family of PRRs expressed within the ___________. They recognize __________

A

cytosol
viral dsRNA

25
Q

NLRs stand for

A

NOD-like receptors

NOD= nucleotide-binding oligomerization domain

26
Q

what happens when a PAMP binds to TLR

A

TLR4 recognizes LPS (lipopolysaccharide= type of PAMP)

signal that PAMP and TLR have binded travels through sentinel cell

transcriptional factors get turned on

caspase-1 is then activated which turns cytokines on, leading to cytokines being released resulting in inflammation

27
Q

when exposed to infectious agents or their PAMPs, sentinel cells synthesize and secrete 3 major cytokines

what are the 3 pro-inflammatory cytokines

A

TNF-alpha
IL-1
IL-6

28
Q

sentinel cells trigger the release of cytokines (TNF-alpha, IL-1, and IL-6) leading to inflammation

How do these cytokines effect the hypothalamus, liver and bone marrow?

A

hypothalamus: fever, anorexia, sleepiness, depression

liver: iron sequestration (bacteria require iron to survive)

bone marrow: increased white cell production

smooth muscle: break down amino acid chains to get energy

natures way to make you stay home while you’re sick

29
Q

tissue reaction that rapidly delivers mediators of host defense to the sites of infection and tissue damage

A

inflammation

30
Q

what are the 3 essential roles inflammation plays in combating infection

A
  1. deliver additional effector molecules and cells to sites of infection to increase the killing of invading microbes by the front-line macrophages
  2. provide a physical barrier presenting the spread of infection
  3. promote the repair of injured tissue
31
Q

MAIN PURPOSE of inflammation

A

focus the immune response to the site of the injury or infection

32
Q

3 steps to the acute inflammatory response

A

surface wound introduces bacteria which activate resident effector cells to secrete cytokines

vasodilation and increased vascular permeability allow fluid, protein and inflammatory cells to leave blood and enter tissue

the infected tissue becomes inflamed, causing redness, heat, swelling and pain as leukocytes destroy microbes clear damaged cells and promote more inflammation/repair

33
Q

cardinal signs of inflammation and why these occur

A

redness: increased blood flow to area of injury

heat: increased blood flow and action of pyrogens (fever-inducing agents)

swelling: due to increased extravascular fluid and phagocyte infiltration to damaged area

pain: local tissue destruction and irritation of sensory nerve receptors

if whole organ/tissue is involved– loss of function may occur

34
Q

autosomal recessive immunodeficiency in holstein

A

BLAD (bovine leukocyte adhesion deficiency)

neutrophil cant get out of vessel to kill of infection

35
Q

what initiates inflammation at the site of infection

A

response of macrophages to pathogens

36
Q

list of pro-inflammatory mediators

A

cytokines
chemokines
vasoactive peptides
vasoactive lipids
vasoactive amines
coagulation system

37
Q

effects of IL-1 on the cells of the body

A

macrophages see pathogen and produce IL-1

effects metabolism, blood flow, cell growth, leukocytes, kills cells, promotes inflammation

most important: affects the brain causing drowsiness, loss of appetite, and fever

38
Q

effects of TNF-alpha on the cells of the body

A

macrophage/monocyte/T cells/ mast cells notice pathogen and produce TNF-alpha

TNF-alpha activates cells. promotes inflammation, enhances collagen synthesis, bone reabsorption but kills tumor cells

39
Q

in low quantities of pro-inflammatory cytokines what are the clinical signs

A

local inflammation
macrophage and complement activation

40
Q

in moderate quantities of pro-inflammatory cytokines what are the clinical signs

A

fever
lethargy
loss of appetite
neutrophilia

41
Q

in high quantities of pro-inflammatory cytokines what are the clinical signs

A

vasodilation
increased vascular permeability
acute respiratory distress syndrome

42
Q

septic shock can occur in cows with _____________. Endotoxin from the bacteria induces high quantities of pro-inflammatory _________

A

gram negative bacterial mastitis
cytokines

43
Q

what are the two vasoactive amines

A

histamine (most important) and serotonin

44
Q

vasoactive peptides C5a and C__ are called ______________, promote histamine release from mast cells. C__ is also a potent attractant for _________________

A

3a
anaphylotoxins
5a
neutrophils and monocytes

45
Q

what activates the coagulation system

A

fluid from the blood vessels leak

large quantities of thrombin (clotting enzyme) is generated and fibrin is deposited forming a barrier

46
Q
A

Immunology (12 decks)

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