immune system Flashcards
where did intial links with sport and the immune system come from?
athletes complaining of illness following intensitive competition higher than the rate of the population or at any other time in their season
what is the difference in % in URTI symptoms in marathon runners compared to control group of runners who didn’t run it?
and what factor increases the %?
urti - upper respiratory tract infections (minor illnesses)
13% of marathon runners
2% of controls
more likely the more km run in the weeks leading up to marathon
what is the difference in % of urti incidence of older women doing moderate, low and sedentary activity?
50% of sedentary
% much lower in low and even lower in moderate
(contradicts marathon runners results)
what does the J shaped curve explain?
risk of urti dependent on exercise and intensity
end of J at low intensity at average/low risk
middle of J at moderate insensity at low risk
high intensity at end of J and much higher risk
how do we defend against pathogens innately/’frist line of defence’?
- anatomical barriers - mucus, skin and low pH in stomach
- chemical barriers
- immune cells - granulocytes, monocytes and natural killer (destroy infection by killing host cells but non-specific killing anything foreign)
how do we defend against pathogens acquired?
specific and previous exposure required
cells - develop immune cells to destroy illness e.g cytotoxic t cells
humoral - atnibodies
which WBCs engage in which functions?
phagocytosis (engulf and destory) - neutrophil & monocyte
destory parasites - eosinophil
inflammation - basophil
immune response - lymphocyte
effect of exercise on circulating white blood cells/leukocytes?
and specifically neutrophils and lymphocytes
exercise produces increase in leukocytes (leukocytosis)
after exercise falls to resting levels
lymphocytes - go below baseline level after exercise so open to infection
2 hours later rise in neutrophil
difference in response (straight after vs dalyed) = biphasic response
what is meant by ‘demargination’?
and what does it explain?
during exercise, increase in shear stress and catecholamines meanes adherence of WBCs to walls of vessels decreases
therefore more immune cells in blood as come away from walls
what are the 2 response after exercise by WBCs?
immediate & delayed
what is involved in the immediate response of WBCs after exercise?
increased catecholamines and shear stress
decreased endothelial adherence (demargination)
so increased circulating lymphocytes and neutrophils
what is involved in the delayed response of WBCs after exercise?
cortisol levels might not reach peak until following exercise
cortisol increases release of neutrophils from bone marrows but lag when doing this as transport etc.
what is lymphocytopemia and what is the result of it?
fall in levels of lymphocytes following exercise which can lead to ‘open window hypothesis’ meaning vulnerability to infection
what is the function of neutrophil?
how to check if working properly?
part of innate immune system
open up, absorb antigen, digest and get rid of - phagocytosis
degranulation and respriatory burst gives idea of whether doing correct function
what is the response of neutrophil to acute exercise?
increase immediate and after 2 hours
fall in function after exercise and 2 hours after so more but not as good at their job - function inhibited
what is the response of neutrophil to different types of training?
explanations for this?
intensified training - decrease in neutrophil function as more release of neutrophils from bone marrow due to higher cortisol levels and mature ones run out (depleted stores after chronic training) and new naive cells aren’t as good
what is selective proliferation?
when well have immune cells with specific surface antigen receptor
foreign agents when ill and need specific surface antigen receptor to fit it
make lots more of certain immune cell which has that antigen to get rid of all forgein agents - selective proliferation
describe lymphocyte proliferaton during exercise?
way at looking at lymphocyte function
proliferation doesn’t change in controls
marathon runners - for 3 hours after decline in ability to selectively proliferate lymphocytes
due to increased cortisol levels inhibiting
how do lymphocytes start out and what will be formed in the case of viral or bacterial infections?
t or b cell always start as naive t helper cells
either go to t helper 1 to t (viral) or 2 to b (bacterial) lymphocytes
response of lymphocytes to viral infection?
increase in t helper 1 cells and increased t lympocytes
produce ifn, il2 and tnf beta
known as cell-mediated immunity - intracellular pathogens - receptors to detect antigens
response of lymphocytes to bacterial infection?
t helper 2 cells increasing b lymphcytes
creating antibodies of il4, il10 and il13 increasing
known as humoral immunity - extracellular pathogens - antibodies
what is the cell mediated response to severe exercise?
how is cell mediated repsonse measured?
decline in cell mediated immune response after exercise
measure by seeing how many pricks which have gone in skin inflame - larger inflammation if good immune response as ‘fighting infection’
effect of cycling to fatigue and cytokine production?
ifn increased after exercise (t)
no change in il4 (b)
what is the il6 response to exercise?
marker of inflammation
increase following exercise
are you more likely to produce t or b lymphocytes during exercise?
b lymphocytes from t helper 2 sites due to catecholamines increasing levels of e.g il10
which counter regulates t helper 2 sites which produce t lymphocytes
why getting stressed may decrease immunity due to increase level of adrenaline which is a catecholamine which limits t lymphocytes
what is the difference between humoral and cell-mediated immunity?
humoral - produces antibodies to destroy extra-cellular antigens/pathogens and involves B cells for bacterial infections
cell mediated - produces immune cells e.g phagocytes to destory intra-cellular antigens/pathogens and involves T cells for viral infections
