L6 Helminth immunology Flashcards
What do chronic infections prove?
People can have parasites for a long time, shows they can survive the immune system
Describe an experiment to show
Schistosoma worms put from monkey and from mouse into a new host.
Monkey - non immunised Monkey,
Monkey - Mouse immunised monkey, Worms survived and established
Mouse - non infected monkey, Partial success, worms survived but egg laying interrupted.
Mouse - mouse-immunised monkey, Failure, all worms killed in 44 hours.
What did the monkey/mouse schistosoma experiment show?
Worms acquire molecules from host to put on skin, so host can’t immunologically recognise worm.
Effect is antibody dependent. Mouse-immunised monkey has antigens against mouse molecules, which worms have acquired.
Worms are constantly removing and replacing tegument.
Describe the tegument
Multilayered mambrane, constantly renewed so can repair any immunological damage.
Schistosomes have glutathione peroxidase on surface to protect from free radical damage.
What is concomitant immunity?
No immune response against adults once they have established, but will prevent more infection.
What does the immune response against schsistosomes?
Adults - use a molecular disguise, tegual renewal.
Schistosomulae - Attacked by IgE and IgG. Stimulates complement cascade and can puncture tegument. Antibody dependent cell mediated cytotoxicity.
Antibodies also attract esosinophils.
Describe the vertebrate gut as a habitat
‘external’ to body - maybe separated from host immune system
Mucous membrane - secretes IgA
Enterocytes take up antigen and act as APCs
describe an experiment showing spontaneous cure and why isn’t this usually the case.
Rats infected with N. brasiliensis. 9 days after infection, immune response acts to remove worms.
12 days later, all gone.Spontaneous cure.
However, not really relevant to environment, as wouldn’t get massive infection at start - Trickle infections are more accurate. (no. worms increases gradually) but host can’t spontaneously cure themself.
What is the immune response to N. brasiliensis?
T cell mediated, using IgE and mast cells.
Histamine release from mast cells caused by IgE, influx to intestine. Maybe directly damaging to worms, or indirect - gut physiology is unsuitable for worms, or more permeable to other effector molecules.
Type 1 Hypersensitivity response.
Why may worms survive?
Low rate of worm delivery, giving worms time to adapt to the immmune response.
Maybe, parasites modulate host immune response, prolonging survival.
Describe an experiment to show immunomodulation of helminthes.
4 groups of mice:
1) infected with adult worms
2) Infected w adult worms then immunised
3) Sham infection then immunised
4) No initial infection then immunised
Infected with irradiated Heligmosomoides polygyrus larvae.
Repeat infection on day 49.
Results: 4) Vaccination causes immunity on repeat infection on day 49.
2) Immunisation fails if worms already present in gut.
3)Sham infection shows manipulation of host to give worms isn’t source of infection in 2.
Sometimes what can high T cell activity in an immune response cause?
High pathology, especially in filarial worm infections.
However, low activity of T cells causes little control of infection, but low pathology.
