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Basic Immunology- Module 1 > Evolution of Inflammatory Diseases > Flashcards

Evolution of Inflammatory Diseases Flashcards

1
Q

Give 2 examples of potentially lethal inflammatory responses?

A

anaphylaxis and septic shock

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2
Q

What is the advantage and disadvantge of increased mucus production by goblet cells?

A

enhances epithelial barrier defenses but leads to mucus plug formation and reduced gas exchange at respiratory epithelia

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3
Q

Why might you expect taht the cost-benefit trade-off of the inflammatory response in modern populations is not optimised to the current environmnet?

A

there have been massive changes in environmental factors in the past century- poplation density; diet; hygiene; antibiotics; vaccines

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4
Q

What are the 2 main plasma antioxidants?

A

urate and bilirubin

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5
Q

What is the function of lipoxins?

A

inhibit the recruitment of neutrophils and promote the recruitment of monocytes

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6
Q

what is hte function of monocytes in the resolution and repair phase of inflammation?

A

remove dead cells and initiate tissue remodelling

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7
Q

What is the function of resolvins and protectins?

A

transform growth factor b and growth factors produced by macrophages; intiation of tissue repair

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8
Q

What happens if macroaphges and T cells cannot resolve an an infection?

A

chronic inflammatory state ensues with granuloma formation and teritiary lymphoid tissue formation

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9
Q

What is the function of granulomas?

A

an attempt to wall off intruders by layers of macropahges

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10
Q

What cell senses the proteolytic activity of proteases produced by helminths?

A

basophils

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11
Q

Why might allergens induce inflammation?

A

mimic the virulence of parasites (e.g act as a protease) or irritate the mucosal epithelia

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12
Q

What are foreign bodies?

A

indigestible particles that are either too largeto be phagocytosed or cause phagosomal memrbane daamge in macropahges

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13
Q

What is frustrated phagocytosis?

A

phagocytic cup is formed but cannot close to form a phagosome (e.g large size of shapre)

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14
Q

What happens if a foreign body is too large for a phagocytic cup to be ofrmed?

A

macropahge forms a granuloma around the body

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15
Q

What are the actions of ATP released by necrotic cells?

A

binds to purinoceptors at the maceroaphge surface resulting in K efflux which activates the NLPR3 inflammasome; activates nociceptors- reports tissue injury to the nervous system

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16
Q

What is the action of HMGB1 released by necrotic cells?

A

binds to RAGE and TLRs to induce an inflammatory response

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17
Q

What is the non-canonical patwhay of release of intracellular proteins

A

not via the ER and golgi; mediated by activated caspase 1 i.e the inflammasomes (requires ATP)

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18
Q

When might the non-canonical secretory pathway be invovled?

A

HMGB1 is released from macropahges when TLR4 is stimulated with LPS in the absence of necrotic death

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19
Q

What hapens when there is disurption of the basement membrane?

A

unschedulaed epithelail-mesenchymal interactions which indicate the presence of tissue damage

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20
Q

What are the 2 class of microbial induce?

A

PAMPs and virulence factors

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21
Q

Give examples of non-microbial inducers?

A

allergens; irritants; foreign bodies; toxic compounds

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22
Q

How does the growth factor heregulin act as an endogenous inducer in the airway epithelium?

A

hergulin is apically expressed whereas its receptors are basolaterally expressed, when there is epithelial injury, hergulin can bind to its receptors and initiate a tissue-repair response

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23
Q

What happens when urate crytals reach a certain size?

A

detected by macroaphges and treated as foreign bodies, phagocytosis triggers activation of NLRP3 and IL production

24
Q

What are AGEs?

A

products of non-enzymatic glycation of long-lived proteins eg collagen

25
Q

When do AGEs accumulate?

A

hyperglycaemic or pro-oxidative conditions- diabetes, ageing

26
Q

What receptor recognises AGE?

A

RAGE

27
Q

What are the 7 groups of inflammatory mediator?

A

vasoactive amines; vasoactive peptides; fragments of copmlement components ; lipid mediators; cytokines; chemokines and proteolytic enymes

28
Q

give examples of vasoactive amines?

A

histamine and serotonin

29
Q

Give an example of a vasoactive peptide that is stored in its active form in secretory vesicles?

A

substance p

30
Q

Give an example of a vasoactive peptide that is generated by proteolytic processing extracellularly?

A

kinins; FDPs

31
Q

What cells release substance p?

A

sensory neurons

32
Q

What activates cytosolic phospholipase A2?

A

intracellular Ca ions

33
Q

What does phosphlipase A2 break phosphatidylcholine into?

A

arachidonic acid and lysophosphatidic acid

34
Q

What do COX enzymes break arachidonic acid into

A

prostaglandins and thromboxanes

35
Q

what do lipoxygenases break up arachiodonic acid into?

A

leukotrienes and lipoxins

36
Q

Which transcription factors mediate the generic stress resposne?

A

FOXO

37
Q

Are cell states discrete or graded?

A

discrete- transitions happen in an all-or non manner

38
Q

What induces para-inflammatory response?

A

tissue malfunction- not overt tissues injury or infection

39
Q

What is the function?

A

cell is expressing signals saying it needs help to restore tissue functionality and homeostasis

40
Q

What is disease tolerance?

A

the immune system protecting itself from infectious diseases by reducing the negative impact on infections on host fitness

41
Q

What are the 3 strategies of host defence against infection?

A

avoidance; resistance and tolerance

42
Q

What is immunopathology?

A

the negative impact of immune defenses on host fitness

43
Q

What determines the optimal immune response?

A

balance between efficient pathogen clearance and an acceptable level of immunopathology

44
Q

What are teh 2 types of fitness costs associated with infections?

A

pathogens can direcrtly damage the host tissues or the immune repsonse

45
Q

What determines the balance of tolerance and resistance against a pathogen?

A

pathogen specific and conditions could promote tolerance for one whilst resistance against another eg tolerance to plasmodium was found to compromise the resistance against salmonella in mice

46
Q

How can increased tolerance to tissue damage be achieved generally?

A

tissue protection and repair

47
Q

When do the pathological outcomes of infections arise?

A

when the degree of tissue damage or alteration of host physiology exceeds the capacity of tolerance mechanisms- to restore homeostasis

48
Q

What are the 4 factors that determine tolerance capacity?

A

intrinsic damage susceptibility; renewal and repair capacity; functional autonomy; damage sequela

49
Q

What type of immune defenses do immune privileged sites employ?

A

low immunopathological potential- secretory IGA and anti-microbial peptides

50
Q

What are cellular stress responses?

A

inducible adaptations to adverse conditions- adverse condition is sensed by dediated stress response pathway–transcirptional master regulator–induction of stress response genes

51
Q

What is the cellular response pathway in heat schock?

A

activates transcrption factor HSF-1 leading to induction of genes that control refolding or degradation of misfolded proteins- preventing proteotoxicity

52
Q

What is the cellular response to oxidative stress?

A

activation of Nrf2 which induces proteins that scavenge free radicals, eliminate damaged proteins, metabolize oxidized membrnae lipis and repair damaged DNA

53
Q

What happens in ER stress?

A

ATF6; PERK and IRE1 are activated which reduce new protein synthesis; eliminate misfolded proteins from the ER and restore calcium and ROS homeostasis

54
Q

What is pre-conditioning or hormesis?

A

when cellular stress reponse pathways are activated by a mild stressor they become more tolerant to a more severe insult

55
Q

How is protection from malaria in sickle haemoglobin mutations explained by hormesis?

A

mutation results in accumulation of free heme in plasma, a mild stressor that induces tolerance mechanisms and provides host protection against malria induced tissue damage (mediated by free haem)

56
Q

Why would reducing toxic levels of ROS have cytoprotective functiosn for most types of stress?

A

ROS is elevated under most stress conditions adn high levels of ROS make ells more sensitive to the damaging effects of most types of stress

57
Q

What are the 2 aspects of pathogen virulence?

A

pathogen intrinsic and host-intrinsic- susceptbility to a pathogens damage or immune repsonse it illicits

Basic Immunology- Module 1 (31 decks)

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