The mucosal and systemic response to phosphorylcholine in mice infected with Trichinella spiralis.

The presence of phosphorylcholine (PC) in Trichinella was confirmed by ELISA and Western blot experiments with the PC-specific myeloma TEPC-15. Anti-PC antibody production was detected in ELISA by cross-reaction with the PC-positive somatic polysaccharide of Aspergillus and the synthetic conjugate phosphorylcholine-bovine serum albumin conjugate and by inhibition with phosphorylcholine chloride (PCCl). The kinetics of the serum and mucosal anti-PC immunoglobulin response were determined following infection of CFW mice. Anti-PC IgA was a minor fraction of the serum response. In primary infections IgG binding to Trichinella antigen was partially inhibited by PCCl incubation, but by Day 6 following challenge infections, incubation with PCCl did not reduce IgG binding. PCCl incubation also reduced serum IgM binding to Trichinella antigen following primary infections, and in contrast to IgG, a reduction occurred following challenge infection as well. Following primary and challenge infections PCCl incubations also reduced bile IgA binding to Trichinella antigen. The kinetics and subclass distribution of the anti-Trichinella PC response were equivalent to the group I response reported for synthetic PC-protein conjugates. Anti-PC IgA production indicates that class switching occurred without maturation of the response. Immunization by feeding Trichinella antigen plus cholera toxin, in contrast to infection with larvae, did not affect anti-PC antibody production following infection. Since the response was not anamnestic and the serum IgG response was not downregulated, larval infection and antigen feeding differ in the anti-PC responses they induce. The anti-PC response does not appear to be protective in Trichinella infections in mice.