Sequential Mesenteric Lymph Node Histological Response following <i>Trichinella spiralis</i> Infection

Abstract

The histology of mouse secondary lymphoid tissue was examined following infection of Trichinella spiralis. ICR/CD-1 mice were orally infected with 200 T. spiralis and sacrificed at either 0, 3, 7, 14, 28 or 56 days after nematode administration. The animals were bled and sacrificed, and mesenteric lymph nodes were removed from each animal. They were fixed in 10% neutral buffered formalin, embedded in paraffin, and cut in 4-µm sections. Examination of serial sections demonstrated the sequential development of histological alteration in these regional lymph nodes. Hyperplasia was detected as early as 3 days after infection. Progressive changes occurring between 7 and 28 days after larval inoculation included hyperplasia with concurrent congestion of medullary sinuses, with increased numbers of neutrophils, histiocytes, lymphocytes, and eosinophils. Microscopic appearance of nodes removed from 56-day infected mice was similar to that noted for control tissues.

Dominance of Immunoglobulin G2c in the Antiphosphorylcholine Response of Rats Infected withTrichinella spiralis

“…MLNs are sites of intense B-and T-lymphocyte activity between 8 and 16 days after infection with T. spiralis in rats and mice (13,22). The increased cellular activity in the MLN is correlated with the expulsion of the adult worms.…”

Echinococcus granulosus infection in mice: host responses during primary and secondary infection

“…The fall in serum IgE during the first 5 days after antigen challenge coincides with migration of eosinophils and macrophages into t h e tissues and with the peak period of PSC destruction and may represent sequestration of serum IgE by tissue mast cells, eosinophils and phagocytes. There is evidence that parasite mitogens directly induce proliferation and maturation of pre-plasma cells in advance of macrophage-and T-cell-dependent germinal centre development (Cook, Trapp & Williams, 1981;Morrison, Murray & Hinson, 1982;Molinari, Hess & Wesley, 1982) which may represent one mechanism by which specific antibody synthesis evades T-cell-mediated regulation and successfully participates in protoscolecidaJ. mechanisms.…”