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immunology Flashcards

1
Q

what is inflammation?

A
  • Swelling, redness, heat and pain.

Cells signalled to move to an area that has been damaged. The more things that move there increases the swelling. Redness and heat is from blood.

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2
Q

types of inflammation?

A

ACUTE
- Fast
- Injury
- Resolves fast.

CHRONIC
- Long term
- Disease process / injury
- Unresolved inflammation

SYSTEMIC
- Long term
- Low level
- Unresolved inflammation.

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3
Q

what do cytokines do?

A

activate other immune cells.

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4
Q

what do chemokines do?

A

drive motion or movement of other cell so they come into that area.

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5
Q

acute inflammation steps.

A

DANGER SIGNAL - Injury – fungi, bacteria coming into body.
Cells that are in that area receive signals. This produces chemical signals.

CYTOKINE AND CHEMOKINE - Including cytokines and chemokine. Cytokine – activate other immune cells. Chemokines – drive motion or movement of other cell so they come into that area.

RECRUITMENT OF CELLS AND PHAGOCYTOSIS – what we can see is the capillaries become leakier. Junctions become leakier from the chemical signals. Cells pootling and squeeze through to go to the tissue following the signals. Cells are highly phagocytic – engulf invading micro to dissolve them.

RESOLUTION OF INFLAMMATION – so that this does not keep happening.

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6
Q

three immune cells.

A

Macrophages – “big eater” eat and kill.
Neutrophils – Fast come into that area eat things. Puss = neutrophils are dead.
Lymphocytes – t and b cells. Come into sight of inflammation.

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7
Q

immune molecules

A
  • Cytokines – activating.
  • Chemokine s- mobilising other immune cells
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8
Q

what does bone marrow do?

A

nesury school for our immune cells. Stem cells found in bone marrow. Can turn into myeloid to turn into macrophages or neutrophils. Or lymphocytes.

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9
Q

non-immune molecules.

A

Hormone – produced in brain.
Angiogenic molecules – drive new blood vessel formation.
Acute phase proteins – in liver to help fight acute infection

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10
Q

macrophages function.

A

Grow up in the bone marrow (with the other immune cells).
Some we know will stay in the tissue.
Live in blood circulation as monocytes. Immature macrocytes.
Mature into macrophages as they move into tissue
Phagocytose pathogens and destroy them.
Produce molecules Activate and recruit other immune cells. (cytokines and chemokines)

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11
Q

how we detect pathogens?

A

Macrophages have receptors to detect: self vs non-self.
Pattern recognition receptors on macrophage. Able to recognise. PAMPs found on pathogens that are not usually found in our own cells.

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12
Q

neutrophil function.

A

Grow up in the bone marrow.
Circulate in the blood. Rapidly produced in bone marrow after infection or injury.

Leave the blood and enter the tissue. Recruited out of the blood when needed. Chemokines that are produced by macrophages attract passing neutrophils. Chemokines drive this whole process.

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13
Q

How does a neutrophil fight a pathogen?

A
  • Phagocytosis (eating them)
  • Degranulation (release toxic chemicals)
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14
Q

resolving an immune response.

A

Macrophages also have wound healing abilities.

When talking about resolution of inflammation. Has to do with organs and non-immune responses.

Inflammatory response are not just local.
Cells activated during an immune response travel through the blood making cytokines and chemokines. Activates cells in other organs to help fight the infection

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15
Q

Describe the possible consequences of unresolved inflammation.

A

Damage to the underlying tissue.

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16
Q

how does exercise change the frequency of circulating immune cells.

A

Neutrophils, increase the number of cells. peak increase at 2-3 hr post ex. start to go down after 6-9hr.

17
Q

mechanisms of neutrophils

A

more blood - increased blood flow in exercise = more cells.
more cells made - increased plasma cortisol during E. these influence how the bone marrow make cells. therefore need more neutrophils.
more cells released - Demarginating from blood vessels in spleen, liver, lung blood vessels during exercise.

18
Q

what hormones are released during exercise?

A

Release of catecholamines (adrenaline) and glaucochroites (cortisol) during exercise.
- Cortisol increases neutrophil production in bone marrow = early phase, neutrophilia.
- Gets them up really quickly post exercise.

19
Q

how does exercise change the function of circulating neutrophils?

A
  • Increased killing ability (degranulation = release of toxins)
  • Increased tissue migration potential. They can get out of blood vessels and into tissue quicker.
  • Increased ability to respond to catecholamines and glucocorticoids. Respond better.
20
Q

how exercise affects neutrophils ability of phagocytosis?

A

After acute exercise, more neutrophils are able to phagocytose. BUT per cell, they are less good at it than in an infection.
After chronic exercise – phagocytosis activity decreases.

21
Q

why do endurance athletes differ with immunity.

A

Endurance athletes have lower frequency of circulating immune cells
- immune depression (lower numbers, decreased function). Consequence of training. Higher risk of infection.
Immune depression means increased infection risk
- Athletes need to take extra care to avoid infection

22
Q

how does the temperature effect the immune system in exercise?

A

HEAT
- If athletes core temperature is over 39 degrees:
- Increased circulating cell frequency.
- Increased cell function.
COLD
- Suppressed immune function

23
Q

how does the altitude effect the immune system in exercise?

A

Limited effect. No much at all. Effects red blood cells but not white – immune.

24
Q

how does pollution effect the immune system in exercise?

A

Nobody really knows.
2008 Olympic – athletes had stuff in lungs.

25
Q

how does gravity effect the immune system in exercise?

A

Re-entry to normal gravity is associated with leukocytosis. More Immune cells.
Prolonged space flight – link to reduced immune function.

26
Q

what is demargination?

A

the mobilisation of “parked” neutrophils from blood vessel walls.

27
Q

obesity as an inflammatory disease.

A

Cells - Macrophages * Neutrophils * Other immune cells. Increased in obese people.
Molecules - Cytokines. Measure the cytokines in obese.
Organs - Liver * Brain * Muscles * Heart * Kidneys. Inflammatory things.

28
Q

systemic inflammation.

A

(whole body) al; through your body not localised.
- Inflammatory cells (neutrophils, macrophages) infiltrate into fat.
- Accumulate in obesity. Come in and stay in fat.
- Inflammatory cytokines secreted in high amounts.
- Inflammation leads to tissue degeneration and organ dysfunction.

29
Q

Inflammation and obesity - evidence

A

Inflammatory cytokines in adipose tissue of obese but not lean mice
Inflammatory mediators in metabolic organs of people
- adipose tissue * liver * pancreas * brain * muscle

30
Q

difference between acute and systemic inflammation process.

A

same cells, same processes. Acute through an infection or injury. Systemic trigger is metabolic. Starts off the inflammation.
caused by excess nutrition. mediated by adipocytes, create their own cells to create inflammation. it is self sustaining, and carries on as it does not get signals to stop.

31
Q

Detecting DAMAGE in obesity

A

Cells recognise damage from obesity effects and induce inflammation.

Cells recognise excess nutrition as a pathogen and induce inflammation.

PAMP may be an error. Which would create an unresolved of inflammatory response. Higher risk of metabolic diseases.

32
Q

three possible theories of the systemic inflammation.

A

Stressed or dying cells immune cells recruited to fix damage. More cells keep getting brought in that damage more things.

  1. nutrient composition alters gut microbiota start to make more fatty. acids fatty acids activate PRRs. Can make more fatty acids. Nature of the food coming in.
  2. bigger adipocytes make more inflammatory cytokines. As you get after your fat cells get bigger. That means they can make more stuff.

Making damage that cannot be resolved. That the food itself can effect the bacteria and can keep the inflammation going and bigger cells.

33
Q

type 2 diabetes.

A
  • Insulin resistance.
  • Crossover between inflammatory cell signalling and insulin signalling. So some of inflammatory cytokines signal the same one as insulin.
  • Exercise alone improves insulin sensitivity in obese people.
  • Anti-inflammatory drugs to treat.
34
Q

microbiome in an obese person. (dybosis)

A

Influenced by diet.
Less diversity in the obese person.
Intestinal junctions broken down, get bacteria and going into places they shouldn’t be.

35
Q

how does exercise influence microbial diversity?

A

Exercise increases microbial diversity in obese people. Makes it more like a healthy person.

36
Q

what is bariatric surgery?

A
  • best long-term weight loss (>15 yr)
  • attenuation of the metabolic syndrome:
  • decreased oxidative stress and inflammation
  • modulation of sex steroids
  • modulation of gut hormones
  • modulation of cellular energetics
  • modulation of immune system better.
  • modulation of adipokines.
  • changes in gut microflora

physiology (11 decks)

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