Page 941 - Veterinary Immunology, 10th Edition

smooth muscle contraction and increase vascular permeability. The
VetBooks.ir IL-13 promotes parasite expulsion by stimulating epithelial cell

proliferation. Presumably the rapid epithelial cell turnover acts as
an “epithelial elevator” to assist in expelling worms. IL-33 also

induces the expulsion of adult worms. Tissue edema can inhibit
helminth invasion. Increased permeability, epithelial cell
proliferation, smooth muscle contraction, and mucus production all
contribute to worm expulsion. This expulsion is accompanied by

mucosal mast cell infiltration, intestinal eosinophilia, elevated
serum IgE, and elevated parasite-specific IgG1 levels.
The violent contractions of the intestinal muscles caused by
histamine and the increase in the permeability of intestinal

capillaries cause an efflux of fluid into the intestinal lumen,
resulting in dislodgment and expulsion of many worms. (This has
been characterized as “weep and sweep.”) In sheep that have just
undergone “self-cure,” IgE antibody levels are high, and

experimental administration of helminth antigens will cause acute
anaphylaxis (Chapter 30). A similar reaction is seen in fascioliasis in
calves, where peak PCA antibody titers coincide with expulsion of
the parasite.

Variations among worms.

Tissue helminths may be thought of as xenografts. That is, grafts
between individuals of two different species. The intensity of the
graft rejection process can vary between different hosts and
between different worms. Inbred mouse strains differ in their

ability to expel intestinal nematodes such as T. muris. Since inbred
mice are genetically homogeneous, these variations in resistance to
T. muris must be due to differences among the worms. We know

that strains of worms differ in their ability to trigger Th1 and Th2
responses. This may be due to manipulation of the immune
response by each worm. For example, T. muris can produce a
protein related to IFN-γ that suppresses Th2 responses and so
enhances worm survival. Alternatively, these differences may be

due to parasite numbers. Thus low-level trickle infestations of T.
muris provoke a Th1 response, and the parasites persist. If higher
doses of parasites are administered, mice mount Th2 responses and

expel the parasites. A threshold of infection is likely critical for the

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