A study of chemical and cellular changes induced by Trichinella infections

The progressive host responses to the invading larvae of Trichinella spiralis and Trichinella pseudospiralis were monitored in the peritoneal cavity and skeletal muscles of mice;Activated peritoneal macrophages, obtained 15 days after oral infection of mice with T. spiralis, were found to secrete a transiently appearing protein (TAP). This protein has been purified by the use of polyacrylamide gel electrophoresis and isoelectrofocusing techniques. Chemical analysis revealed that TAP is acidic due to the high content of glutamic and aspartic acids. With 50% of its total amino acids being non-polar, this 50,000 dalton molecule tends to crystallize at its isoelectric point (5.7) and in deionized water. High-titer (1.5 x 10(\u27-5)) specific antibodies (IgG) to TAP were used to demonstrate that peritoneal macrophages are solely responsible for TAP production;The biological function of TAP is not known. It is not a plasma protein, a constituent substance in the cytoplasm of resident white blood cells, a membrane-bound molecule, an elastase or a plasminogen activator. However, TAP may have an immuno-regulatory function;T. spiralis and T. pseudospiralis infections of murine skeletal muscles were investigated using synchronous infections for histological studies and asynchronous infections for ultrastructural studies. The penetration of muscle cells by either species induces marked morphological changes in the host cells including: (1) an increase in the amount of endoplasmic reticulum, ribosomes, mitochondria and Golgi apparatus; (2) an increase in the size of muscle cell nuclei with enlarged nucleoli; and (3) degeneration and loss of myofilaments;In comparision with T. spiralis infected muscle cells, cells infected with T. pseudospiralis show a slower rate of myofilament degeneration and lighter basophilic staining and remain elongated and non-encapsulated;Tissue autoradiography plus various superimposed and concomitant infections with both species indicate that T. spiralis-infected muscle cells are intrinsically responsible for capsule formation. Encapsulation is independent of host fibroblasts and the presence of T. pseudospiralis. The lower content of guanosine and cytidine-rich RNA in the cytoplasm of T. pseudospiralis infected muscle cells suggests that collagen mRNA may not be present for the encapsulation processes