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Microbiology and Immunology > lecture 3 > Flashcards

lecture 3 Flashcards

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1
Q

first line of defense

A
  • innate immune system
  • barriers within it
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2
Q

barriers

A
  • are able to. keep most of the pathogens away
  • we might not even realize we were exposed to them
  • can keep them away from our tissues and body
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3
Q

what happens if pathogens breach the barriers

A
  • innate immune cells
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4
Q

myeloid origin

A

gives rise to phagocytes:

  • dendritic cells
  • neutrophils
  • macrophages/monocytes
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5
Q

lymphoid origin
(these are not all the things it can give rise to, just the ones involved in innate immunity)

A

gives rise to lymphocytes
natural killer cells

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6
Q

macrophages

A
  • are a differentiatied type of monocyte
    (monocytes that have been circulating in the blood that come out of blood become macrophages)
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7
Q

phagocytes

A
  • kill extracellular pthogens via phagocytois
  • first responders to infection
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8
Q

lymphocytes

A
  • kill intracellular viruses via apoptosis
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9
Q

phagocytosis

A
  • stretches out membrane,
  • “cell eating”
  • this forms phagosome (around the extracellular pathogen)
  • the phagosome fuses with lysosome that contains the toxic, killing agents that will kill the pathogen
  • creates a phagolysosome
  • debris from there is expeld from cell
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10
Q

phagolysosome

A
  • toxins in it are toxic to the cell also, so must be contained
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11
Q

phagocytosis steps

A
  • fuses with lysosome
  • pH drops
  • enzymes that were in lysosome get activated
  • killing of pathogen in phagolysosome
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12
Q

phagosome

A
  • ## not toxic at first, bacteria allow the pathogen to live here by blocking following steps
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13
Q

macrophages

A
  • can “eat up” a huge amount of cells at a time
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14
Q

lyssoome

A
  • contains acid
  • enzymes
  • antimicrobials
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15
Q

low pH

A
  • this can be detrimental to the cells that want to survive in there
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16
Q

NADPH oxidase

A
  • makes reactive oxygen species that are toxic to the cell
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17
Q

myelopersoxidase

A
  • makes bleach that is toxic to the pathogen
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18
Q

lactoferrin

A
  • enzyme that captures iron (Fe2+) that is essential for bacterial growth,
  • process called nutritional immunity, way that cells try to sequester essential nutrients from the pathogens
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19
Q

defensins

A
  • also found in lysosomes
  • create pores on pathogen membrane, then lyse cell
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20
Q

lysosome

A
  • degrades peptidoglycan to kill bacteria, mainly gram positive
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21
Q

nutritional immunity

A
  • host cell and pathogen are fighting for nutrients
  • keeping nutrients from pathgogen prevents them from gorwing
  • e.g. taking way co factor iron prevents it from growing
  • lactoferrin binds iron to keep it unavailable from pathogen
  • transferrin also sequesters iron
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22
Q

trace metals that are typically sequestered from pathogens in nutritional immmunitu?

A
  • co factors in metabolic enzymes
  • e.g. iron, zinc, managenese
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23
Q

consequence of infection

A
  • low iron in blod
  • making so much of the components that sequester iron, makes it unavailable to ur own bell
  • leads to hypoferremia of infection
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24
Q

neutrophils

A
  • eat the pathogens once they catch up with them
    0 very abundant
  • replicate quickly
  • about 50-70 percent of blood circulating leukocytes
  • swarm in large numbers to site of infection
  • main component of pus
  • can be used as a measure of infection
  • have a life span of only a few days
  • will replicate as long as the infection signals are there
  • exit blood and rapidly enter infected tissues
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25
Q

Multi-lobed nucleus

A

have packaged their genetic material (DNA) in multiple spheres instead of one big sphere like in most other cell types. These types of nuclei are called lobular nuclei

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26
Q

components of neutrophils

A
  • multi lobed nucleus
  • granules
  • phagosome
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27
Q

NETosis

Neutrophil Extracellular Traps

A
  • release chromatin from chromosomes associated with the enzymes and antimicrobial proteins
  • produces nets that capture the pathogens
  • the nets are decorated with antimicrobial proteins
  • ensnares extracellular pathogens
  • the associated antimicrobial proteins intoxicate microbes
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28
Q

what antimciorbial proteins are used by NETs to intoxicate microbes

A
  • antimicrobial peptides, MPO, elastase
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29
Q

sign of infection

A
  • neutrophils are used in clinical settings to measure for infection
  • in blood results, if the majority of WBC are neutrophils, signals that person has an infection
30
Q

neutropenia

A
  • people that are unable to produce high numbers of neutrophils ( or none at all)
  • patients are highly susceptible to a wide range of pathogens
  • innate immune system is highly comprosied
31
Q

how to combat neutropenia

A
  • restore neutrophil levels through blood transufsion
  • transfusion of Buffy coat
  • must be done quite frequently especially during infection, because neutrophils die quite quickly.
32
Q

neutropenic sespsi

A
  • septic shock
  • life threatening needs immediate attention
  • infections in neutropenic patients
  • if the infection is not controlled
33
Q

macrophages

A
  • professional phagocytes
  • good at ingesting pathogens and killing them
  • have pseudopods.
  • also have a role in adaptive immunity
  • last for a long time (months to years)
  • differentiate from monocytes that circulate in the blood and enter tissues
34
Q

resident macrophages

A
  • there ar e professional macrophages that are tissue specific, that survey the area for the pathogens
    (resident macrophages)
  • have specialized functions depending on location
35
Q

tissue-specific macrophaes

A
  • eyes
  • digestive and resp tract
  • brain
36
Q

dendritic cells

A
  • immature dendritic cells circulate in blood and reside in lymphoid organs and peripheral tissue
  • have phagososomes, processes, lysosomes
  • important role in adaptive immunity
  • bridge between the two
37
Q

immature dendritic cells

A
  • good phagoycytes
38
Q

mature dendritic cells

A
  • role in adaptive immunity
  • antigen presenting cells
39
Q

Natural killer cells

A
  • lymphocytes
  • not phagocytose
  • kill intracellular viruses
  • by targetting the virus infected cells via apoptosis
  • cytotoxic granules
  • circulate the blood
  • important role in virus infected cells, and in killing cancer cellsc
40
Q

cytoplasmic granules

A
  • contain perforin and granzyme that trigger apoptosis
  • recognize that the cell is infected, release the two enxymes
41
Q

how do NK cells work

A
  • recognize that the cell Is infected
  • reaches target cell that has infection signals on sruface
  • granules converge and reroute themselves to an areas of contact between the two cells
  • contents of the granules are expelled
  • cell death
  • happens quickly
42
Q

perforin

A
  • released from granule
  • forms a pore in the cell membrane which helps deliver granzyme to the inside of cell
43
Q

granzyme

A
  • turns on apoptosis in cell
44
Q

apoptosis

A
  • general process by which a cell dies
  • usually done at the end of cell’s lifetime
  • Genzyme speeds up this process
  • pro caspase: turns on the caspaces which turns on the apoptosis process, leads to degradation of the genetic material of the cell
  • degrades also the viral nucleic acidswh
45
Q

why does granzyme also kill viral nucleic acids?

A
  • to ensure that the virus does not escape and infect other cells
  • prevents viral replication
46
Q

When are NK cells released

A
  • NK cell mediated killing is the second wave of cells
  • comes after signalling molecules called inteferons
  • can control viral infection usually
  • if innate cannot control, activation of t cells
47
Q

how are pathogens detected

A
  • need signals to get there but also need something to allow them to recognize the ahogen
  • done through a sort of signal transduction pathway
  • with PRRs
48
Q

Pathogen recognition and detection

A
  • PRR recognizes characteristics of the outside of that extracellular pathogen
  • those PRR receptors can also be internal (intracellular pathogen that is inside of the cytosol , there are also receptors inside the cell to catch it)
  • triggers phagocytosis
  • also triggers the production of cytokines and chemokines to call more cells to battle
49
Q

pattern recognition receptors

A
  • essential receptors of innate immunity
  • expressed at surface and within many cell types (WBC, some lymphocytes, and epithelial cells)
  • low specificity, can recognize broad characteristics of pathogens
  • germ-line encoded
  • can also recognize damage signals
50
Q

germ-line encoded

A
  • ## encoded in genome, passed through progeny, cannot change
51
Q

innate immunity (with PRRs)

A
  • specificity inherited in genome
  • triggers immediate response (when receptors recognize pathogen, triggers immediate phagocytosis immediately and release of cytokines and chemo)
  • recognize broad classes of pathogens.
52
Q

What do PRRs recongize

A

PAMPS
- pathogen associated molecular patterns

53
Q

PAMPS

A
  • common in many pathogens
  • can be on cell wall (on outside of pathogen) e.g. cell wall structure
  • oligosaccharides
    -pettidoglycans
  • lipopolysccahrides
  • unmethylated CpG DNA in DNA
54
Q

PAMPS for vacteria

A
  • lipopolysaccharides
  • peptidoglycans
  • lipoproteins
  • flagellin
  • lipoteichoic acid (LTA)
  • DNA
55
Q

PAMPS for virus

A
  • protein capsid
56
Q

PAMPS for parasite

A
  • GPI anchor
57
Q

PAMPS for yeast

A
  • zymosan
58
Q

key properties of MPAMPS

A
  • must be only found in pathogens and not in bodies
  • very conserved for pathogens (low mutation rate, stays the same)
  • usually critical for survival or pathogenesis of pathogen
  • makes this an excellen target for reoconition
  • used in clinical settings to distunigh between types of pathogens
  • detections of PAMPS is critical to the initiation of immune responses
59
Q

examples of PAMPS

A
  • Exposed glycolipids on gram positive bacteria
    or peptidoglycan(conserved and exposed)
  • LPS on gram negative bacteria
60
Q

look for other examples of PAMPS in lecture notes

A
61
Q

requirements to be a PAMP

A
  • must be conserved
  • must be broadly found in groups of pathogens
62
Q

PRRS in humans

A
  • we have few receptors but they recognize a broad range of characteoriesitcs
63
Q

surface prrS

A
  • recognizee components on the outside of pathogens
  • recognize exposed structures on extracellular pathogens
  • e.g. LPS, peptidoglycan, flagellin
64
Q

Endosomal PRRs

A
  • recognize components released during degradatoion
  • regonzie intracellular pathogenic PAMPS in endosomes and vacuoles
65
Q

Candida albicans PAMPS

A

-

66
Q

first step of phagocytosis process

A
  • binding of PRRs to PAMPS
  • Pseudopods engulf pathogen
  • phagosome formation
  • fusing with lyosome
67
Q

strategies for bacteria in immane evasion

A
  • producing capsular polysaccharides that cover their PAMPS to become unrecognizable, e.f. K. pneuomniae
  • or PAMP variation e.g. N. gonnorahe changes its flagellin structure to prevent immune cell recognition, some bacteria remove their flagella to accomplish this
68
Q

innate cells summary

A
  • phagocytes in tissues are waiting for a breach of barriers
  • breach
  • bacteria and viruses with extraceullar PAMPS are “eaten” by phagocytes
  • signal molecules are produced to call more cells
  • ## if the cells get infected by virus, make signals that the infection is happening, the virus-infected cells will be killed via apoptosis.
69
Q

how can intracellular bacteria survive phagocytosis?

A
  • inhibit fusion of phagosome wit lysosome, and survive there (e.g. tuberculosis)
  • may have enzymes that prevent the killing by the toxic lysosome enzymes, so they can survive in that enviornment
  • the bacteria can also escape the phagolysosome
    (e.g. listeria)
70
Q
A

Microbiology and Immunology (4 decks)

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