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Microbiology > Innate Immune System > Flashcards

Innate Immune System Flashcards

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1
Q

What are the different components of Innate Immunity

A

Phagocytosis
Complement System
Interferons
Natural Killer Cells

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2
Q

What is another term for innate immunity? Adaptive Immunity?

A

Innate: natural
Adaptive: acquired

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3
Q

Does infection have to result in disease?

A

No - it does not have to result in disease. Infection and disease are very different. Overtime we brush our teeth for example we get an infection, but we do not acquire a disease from this

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4
Q

What are the different soluble factors involved in innate immunity? Adaptive Immunity?

A

Innate: lysozyme, complement system, acute phase proteins (C-reactive proteins)
Adaptive: antibodies

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5
Q

What cells are involved in innate immunity? Adaptive immunity?

A

Innate: natural killer cells and phagocytes

Adaptive immunity: T lymphocytes

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6
Q

Difference between innate immunity and adaptive immunity

A

Innate: non specific, no memory, resistance not improved by repeated contact
Adaptive: specific, memory, resistance improved by repeated contact

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7
Q

Defences against entry into the body

A
  • lysozyme in most tears, nasal secretions and saliva
  • sebaceous gland secretions( fatty acids in the skin tend to have more antimicrobial properties active against gram positive)
  • commensal organisms in gut and vagina
  • spermine in the semen
  • mucuous
  • cilia lining in the trachea
  • acid in the stomach
  • skin
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8
Q

What kind of bacteria can typically survive the acid of the stomach

A

spore forming bacteria (can survive pH of typically 2)

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9
Q

Does the innate immune system change over time?

A

Yes, but it can only weaken (as we age) - it cannot improve and get stronger

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10
Q

What are the main mechanisms to limit entry in the innate immune system?

A

Skin, membranes and normal flora

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11
Q

How does skin limit entry into body?

A
  • normally impermeable to a number of infectious agents
  • hostile environment for many bacteria
  • lactic acid and fatty acids in sweat and sebaceous secretions lower the pH
  • loss of skin – burns can cause serious infections
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12
Q

What do burn units do to protect their patients?

A

are all positively pressured - air cannot get into rooms carrying microorganisms this way

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13
Q

How do membranes limit entry inside the body?

A
  • line the inner surfaces of the body and secrete mucous
  • inhibit bacterial adherence, inhibit entry
  • ciliary action– remove microbes and other foreign particles
  • flushing action - tears, saliva, urine, all protect epithelial surfaces
  • presence of antimicrobial compounds (acid in gastric juice, spermine and zinc in semen, lactoperoxidase, and lysozyme in nasal secretions, tears and saliva)
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14
Q

How does normal flora limit entry into the body

A

bacteria and fungi are permanent residents on the body surfaces (skin and mucosal membranes), they also suppress the growth of pathogenic microbes (have a protective layer, compete for nutrients and produce inhibitory compounds such as acids and colicins)

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15
Q

More about normal microflora….

A
  • prevents the attachment of pathogens because of a lack of space on the tissue and lack of food for the pathogens to feed on
  • normal microflora can also produce antibacterial properties that kill off pathogens (lowering pH, for example as happens in the vagina)
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16
Q

When does c. difficile usually colonize the gut

A

usually colonizes the gut when the gut microflora is depleted after being on antibiotics (clostridium is a spore former and can survive in the gut at very low pH’s)

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17
Q

How does the innate immunity limit growth of pathogens?

A
  • phagocytosis ( macrophages, polymorphonuclear granulocytes)
  • soluble chemical factors( bactericidal enzymes)
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18
Q

What are macrophages?

A
  • promonocytes (in bone marrow) -> circulating blood monocytes -> mature macrophages in tissues
  • concentrated in lung, liver, lining of lymph nodes , well placed to filter off foreign material
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19
Q

Polymorphs

A
  • dominant white cell in the bloodstream
  • share common haemopoietic precursor
  • no mitochondria (capable of carrying out very fast glycolysis reactions)
  • non-dividing, short lived, segmented nucleus
  • granular cytoplasm
20
Q

Explain phagocytosis

A
  • There are specific molecules on the pathogen, and specific molecules on the phagocytes that mediate this interaction between the pathogen and the phagocyte
  • The phagocyte does not recognize the bacterial cell - it only recognizes the irregular patterns on the pathogen
  • there is only an interaction between PAMPS and PRRs
21
Q

PAMPS

A

pathogen associated molecular pattern

-on the microbe (LPS, protein)

22
Q

PRRs

A

pathogen recognition receptors - on the phagocyte

23
Q

What is a way that the pathogen can hide from the bacterial cell

A

It can hide inside the bacterial cell

  • micobacterium tuberculosis does this and hides inside the phagocyte
  • mutations on the PAMP can also cause misidentification of the pathogen- mutation changes the marker on the pathogen that the phagocyte is looking for, so the phagocyte is not recognizing the pathogen anymore
24
Q

What is the most common PRR

A

light toll receptors (LTRs)

- PAMPS can be any protein that is present on the bacterial cell

25
Q

What is the significance of granules in phagocytosis?

A
  • inside the granules that are inside of the phagocyte, the phagocyte can release a large amount of antimicrobial properties (if the pathogen is not contained within the vacuole of the phagocyte though, the antimicrobial properties released can cause death of the phagocyte itself)
  • inside the vacuole, the phagocyte can pump in reactive O2 of N species via the granules and can cause complete degradation of the pathogen
  • in O2 dependant killing, the degraded microbe is released to the outside
26
Q

What are the 4 steps of phagocytosis

A
  1. attachment by pattern recognition receptors
  2. pseudopodia forming a phagosome
  3. granule fusion and killing (complete formation of the phagolysosome)
  4. release of microbial products
27
Q

Phagocytosis and the complement system

A
  • contact dependant
  • formyl methionyl peptides attract leukocytes - move by chemotaxis until the pathogen is engulfed
    (weak signal however)
  • complement proteins work by the cascade reaction - product of one reaction serves as the initiator of the next reaction
  • blood clotting, for example (highly controlled)
28
Q

Which components of the alternative complement pathway cause mast cell degranulation

A

C5a and C3a

29
Q

C5a and C3a release chemicals that mediate what?

A
  1. Increased vascular/ capillary permeability that allows flow of fluid and plasma components to site of infection (acute inflammatory response)
  2. chemotactic attraction of polymorphs through blood vessel walls to C3b-coated bacteria
30
Q

Polymorphs have what on their surface to allow them to bind tightly to bacteria, allowing phagocytosis to occur?

A

C3b

31
Q

When do acute phase proteins come into play?

A

They increase in concentration in plasma in response to injury and inflammation
- C-reactive protein, mannose binding protein, bind to PAMPS, can fix complement ans opsonize bacteria

  • acute phase proteins let us know how long ago an infection has occurred
32
Q

What do antimicrobial factors do

A

They act within phagocytic cells but also within body fluids

  • tears and saliva contain lysozyme
  • blood contains lactoferrin , which binds iron and makes it unavailable for bacteria to use
33
Q

What are interferons

A

They are soluble factors that are released in response to a viral infection

  • interferons prevent the viral replication in neighbouring cells
  • the infected cells are the ones that secrete the interferons, causing other cells around them to be resistant to the viral replication
  • interferons protect against al related viruses that share the same receptor
34
Q

When are interferons used treatment

A

For LAST resort in treatment in hepatitis and some cancers

  • tends to be a lot of side effects
  • these act as the hormones of the immune system- sensing of higher than normal levels of interferons, the immune system kicks in and causes a large number of side effects
35
Q

Natural Killer Cells

A
  • bind to receptors on virus-infected cells, causing activation of the natural killer cell and release of granules
    (perforin that inserts into the host membrane forming a MAC)
  • allows the entry of a second molecule, granzyme B that leads to apoptosis
    (this is used when our body gets infected by a virus - our body can kill the cell that is infected to prevent the spread and replication of the virus)
36
Q

Can viruses replicate on their own?

A

No- they’re obligate intracellular parasites and do not have the machinery to carry out replication on their own - they use host cell tissue for this

37
Q

Eosinophils

A
  • these combat large parasites (like helminths)
    • these are two large to be engulfed by phagocytes
  • these bind to C3b which cause activation
  • several toxic compounds released that damage the membrane via hole formation
38
Q

What are the 4 steps of phagocytosis?

A
  1. attachment by pattern recognition receptors (PAMP and the receptor)
  2. pseudopodia forming a phagosome
  3. complete formation of the phagolysosome (fusion of the granule with the vacuole)
  4. release of the microbial products
39
Q

Why do we need the complement system? Why can’t we just rely on phagocytosis?

A

Phagocytosis is contact dependent

  • clearly this cannot happen unless both become physically close to each other - there is a need for a mechanism that mobilized the phagocytes from a far - bacteria do produce formyl methanol peptides that attract leukocytes from far away (known as chemotaxis)
  • this is a weak signal however! This is why the body relies on the complement system
40
Q

What protein does the complement system start off with?

A

C3

41
Q

When C3 becomes activated at the start of the complement system, what are its two breakdown products?

A

C3b and C3a

42
Q

What is the difference between the C3a and C3b proteins?

A

C3a is a mediator of inflammation, while C3b goes on to activate the MAC, or can start opsonization

43
Q

What does C3b go on to produce in the complement pathway?

A

C3b complexes with Factor B

-> C3bB is acted upon by enzyme factor D to produce C3bBb (aka C3 convertase)

44
Q

What does C3 convertase do initially in the complement system?

A

Split C3 into more C3b and C3a

45
Q

Under what situations does C3bBb require to have action inside the cell

A

C3bBb is a very unstable enzyme and degrades easily, but in the presence of carbs or other bacterial surface molecules, C3 converts is no longer susceptible to breakdown
- ONLY works when its needed!

46
Q

What are the different roles of C3b in the body?

A
  • C3b binds to microbial surface on the cell and acts as opsonin - opsonin is the molecule that coats the bacterial surface and allows for phagocytic recognition
  • C3b and C3 converts can also act on the next component, C5
  • C5 is split into C5a and C5b
  • C5b is joined by C6, C7, C8, and C9
  • these together get inserted into the lipid layer and form the membrane attack complex- this leads to cell lysis
47
Q

What are the 2 different things that C3a and C5a can do in the cell?

A
  • they cause mast cell degranulation and release chemical mediators that:
    1. increase vascular/ capillary permeability - allows flow of fluid and plasma components to the site of infection - part of the acute inflammatory response
    2. chemotactic attraction of polymorphs through blood vessel walls to C3b coated bacteria
    • polymorphs have a receptor for C3b on surface so they bind tightly to the bacteria and phagocytosis occurs

Microbiology (16 decks)

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