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B4W1 > INNATE IMMUNITY AND THE INFLAMMATORY PROCESS > Flashcards

INNATE IMMUNITY AND THE INFLAMMATORY PROCESS Flashcards

1
Q

how is skin a physical barrier to pathogens?

A

it has many layers of keratinised cells and the periodic shedding helps to remove pathogens from the surface. the skin also has glands which secrete sebaceous oil which inhibits the growth of certain pathogens.

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2
Q

how are mucous membranes a first line of defence? give examples

A

the mucous is slightly viscous so traps many microbes. e.g. in the nose there is also hairs, in the upper respiratory tract there is also cilia and swallowing mucous can take pathogens to the stomach where the gastric juice destroys them

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3
Q

how do eyes defend against pathogens?

A

the lacrimal apparatus manufactures and drains away tears in response to irritants. lining spread tears over the surface of the eye, diluting pathogens and keeping them from settling on the surface. tears contain lysozymes

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4
Q

what are some first line defences against pathogens?

A

skin, mucous membranes, tears, saliva, urine, vaginal secretions, sneezing, coughing, defecation, vomiting, perspiration, gastric juice

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5
Q

what are interferons?

A

proteins that diffuse to uninfected cells and induce synthesis of antiviral proteins to interfere with viral replication.

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6
Q

what releases interferons?

A

lymphocytes macrophages and fibroblasts infected with viruses can release them.

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7
Q

what can iron-building proteins do to defend against pathogens? give some examples

A

inhibit the growth of certain bacteria by reducing the amount of iron available. e.g. transferrin, lactoferrin, ferritin and haemoglobin

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8
Q

what do antimicrobial proteins do?

A

they kill microbes, attract dendritic cells and mast cells to participate in an immune response.

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9
Q

where can we find natural killer cells?

A

blood, spleen, lymph nodes and red bone marrow

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10
Q

describe the steps of a natural killer cell?

A

NK cells bind to target cells and this causes the release of cytotoxic granules from NK cells. some granules contain perforin which inserts into the plasma membrane of the target cell and created perforations. as a result, extracellular fluid flows into the target cell and the cell bursts. other granules may release granzymes which induce the cell to undergo apoptosis.

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11
Q

what can natural killer cells release?

A

granzymes or perforin

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12
Q

what is an issue with natural killer cells?

A

they kill the infected cell but do not destroy the microbes inside so when the cell bursts/dies these microbes are released and must be destroyed by phagocytes

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13
Q

describe the 2 different types of macrophages?

A

when an infection occurs, monocytes migrate to this area and enlarge and develop into actively phagocytic macrophages whereas other macrophages can be fixed and stand guard in specific tissues.

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14
Q

describe the steps taken in phagocytosis?

A
  1. chemotaxis= phagocytes are attracted to the site of damage by chemicals.
  2. adherence= the phagocyte attaches to the microbe via PAMP
  3. ingestion= the plasma membrane of the phagocyte extends projections called pseudopods that engulf the pathogen by surrounding it and fusing
  4. digestion = phagosome merges with lysosome to form phagolysosomes. the lysosomes break down microbial cell walls and degrade the insides. respiratory burst can also happen here
  5. killing= any material not degraded further by the above is called residual bodies
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15
Q

describe the respiratory burst?

A

its a rapid increase in the production of reactive oxygen species during phagocytosis. the immune cells use NADPH oxidase to reduce O2- to an oxygen free radical and then to H2O2. these damage microbial membrane and can activate microbicidal enzymes.

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16
Q

describe the 3 stages of the inflammatory response?

A

vasodilation and increased permeability of blood vessels
emigration of phagocytes from the blood into the interstitial fluid
tissue repair

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17
Q

after tissue injury, what immediate changes do we get in the blood vessels?

A

vasodilation of arterioles to allow more blood to damaged area
increased permeability of capillaries so defensive proteins can enter the injured area from the blood

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18
Q

what cells release histamine? what is the effect?

A

mast cells, basophils, platelets, neutrophils and macrophages. it causes vasodilation and increased permeability of blood vessels.

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19
Q

What effect do kinins have? give an example of one

A

they induce vasodilation and increase permeability and serve as chemotactic agents for phagocytes. e.g. bradykinin

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20
Q

where are prostaglandins secreted from? what effect do they have?

A

from damaged cells.
they intensify the effects of histamine and kinins and can stimulate the emigration of phagocytes through capillary walls

21
Q

where are leukotrienes secreted from? what’s their effect?

A

basophils and mast cells.

they increase permeability, act as chemotactic agents that attract phagocytes

22
Q

what are some of the effects of activating the complement system?

A

stimulates histamine release
attracts neutrophils by chemotaxis
promotes phagocytosis
destroys bacteria

23
Q

why do we get pain in inflammation?

A

it results from injury to neurone and from toxic chemicals released by microbes. kinins can affect some nerve endings. prostaglandins prolong and intensify the pain and pain could be due to increased pressure caused by oedema.

24
Q

how can blood clotting factors assist with the immune response?

A

fibrinogen is converted to an insoluble, thick mesh of fibrin threads that localise and trap invading microbes, blocking their spread.

25
Q

what is leukocytosis?

A

a large increase in white blood cells

26
Q

describe extravasation?

A

As large amounts of blood accumulate, neutrophils begin to stick to the inner surface of the endothelium of blood vessels. Then the neutrophils begin to squeeze through the walls of the blood vessels to reach the damaged area

27
Q

what is pus?

A

a collection of dead cells and fluid

28
Q

how do we remove pus from our bodies?

A

it can reach the surface or can drain into an internal cavity and be dispersed or it can be gradually destroyed and absorbed.

29
Q

why do we occasionally get a fever with inflammation?

A

bacterial toxins can elevate the body temperature e.g. interleukin-1.

30
Q

what is the effect of a fever during inflammation?

A

it intensifies the effect of interferons, inhibits the growth of some microbes and speeds up the body’s reactions that aid repair.

31
Q

what are the main components of the innate immune response?

A

physical barriers, phagocytic leukocytes, dendritic cells, natural killer cells, circulating plasma proteins

32
Q

what are the 2 types of adaptive immune responses?

A 
humeral immunity (controlled by B cells and antibodies)
cell-mediated immunity (controlled by T cells)
33
Q

what are cytokines?

A

small protein hormones that stimulate or inhibit many normal cell functions.

34
Q

which cells secrete cytokines?

A

lymphocytes, antigen-presenting cells, fibroblasts, endothelial cells, monocytes, hepatocytes and kidney cells

35
Q

what is the function of Tumour Necrosis Factor?

A

produced by macrophages, stimulate accumulation of neutrophils and macrophages at sites of inflammation and stimulates the killing of microbes

36
Q

what is the function of macrophage migration inhibiting factor?

A

produced by cytotoxic T cells to prevent macrophages from leaving the site of infection

37
Q

what is the complement system?

A

a multi-catalytic system of multiple proteins with enzymatic activity. it is stimulated by some pathogens and regulates acute inflammation. early components carry out opsonisation whilst terminal components may kill pathogens directly by lysis.

38
Q

describe the steps of opsonisation in the complement system?

A

inactive C3 splits into active C3a and C3b. C3b binds to the surface of microbes. when C5a binds to the macrophages surface then it will engulf the pathogen.

39
Q

describe how the complement system forms a membrane attack complex?

A

C5 converts converts C5 into C5a and C5b. C5 sits on the surface of the pathogen so when cleaved C5a leaves but C5b stays attached to the pathogen. C6 C7 and C8 come and join and form C5b678 complex. next a lot of C9 molecules join, polymerase into a ring shape and form the membrane attack complex-a pore.

40
Q

how does the membrane attack complex kill a pathogen?

A

if enough pores/membrane attack complexes form then there will be an inflow of extracellular fluid and this will result in cytolysis.

41
Q

what are the 3 pathways of the complement system?

A

classical, alternative and lectin

42
Q

what is the classical pathway of the complement system?

A

it is initiated by antibodies binding to antigens and this activate C3.

43
Q

what is the alternative pathway of the complement system?

A

this is initiated when C3 converts forms C3b which binds to the surface of pathogens

44
Q

what is the lectin pathway of the complement system?

A

it is initiated when proteins bind to a pathogen

45
Q

what are the 3 functions of the complement system?

A

opsonisation, membrane attack complexes, enhances inflammation

46
Q

how does the complement system enhance inflammation?

A

C3a and C5a stimulate mast cells to release histamine which causes vasodilation and increased permeability.

47
Q

if neutrophils can’t catch a pathogen, how do they neutralise them?

A

they extrude their DNA to form neutrophil extracellular traps so the pathogen becomes immobile and then other phagocytic cells are able to catch up with the pathogen and ingest it.

48
Q

what’s the role of dendritic cells?

A

The main function of these innate cells is to capture, process, and present antigens to adaptive immune cells- links innate and adaptive immunity.

49
Q

what are chemokines?

A

chemotactic cytokines

B4W1 (10 decks)

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