Takashi Miyazato

Reactive oxygen intermediates from eosinophils in mice infected with Hymenolepis nana

A large number of eosinophils were recruited to the intestinal villi after infection with Hymenolepis nana. Eosinophil numbers were increased more rapidly in challenged mice than in primary infected mice. Local intestinal eosinophils from challenged mice showed more extracellular oxygen radical release, as assessed by histochemical mothods using nitro blue tetrazolium, accompanied with tissue injury and larval degradation. Intestinal eosinophils isolated from the lamina propria induced specific oxygen radical generation in response to H. nana oncosphere extract as measured by luminol‐dependent chemiluminescence. This response was stronger in challenged mice than in primary infected mice. Radical generation from uninfected mice was negligible. Lipid peroxidation in the small intestine, as measured by formation of malondialdehyde, was increased during H. nana challenge infection, the peak activity coinciding with the elimination of challenge larvae. Continuous administration of a NADPH oxidase inhibitor to sensitized mice interfered with the degeneration of challenge larvae. These results suggest that intestinal eosinophils may be the major contributor to oxygen radical production in response to H. nana and that reactive oxygen species may play a part of effector molecule in the resistance to reinfection with H. nana

Ultrastructural aspects of immune damage to Hymenolepis nana oncospheres in mice

Abstract When Hymenoiepis nana eggs were inoculated orally into unimmunized mice, the oncosphere larvae penetrated the intestinal villi and underwent postembryonic development. The ultra-structural changes during the 48 h after infection were characterized by the development of microvillar protrusions on the surface of the epithelium, development of many membranous vesicles in the epithelium, and proliferation of undifferentiated cells in the parenchyma with a rapid disappearance of penetration gland cells and muscle cells. The epithelium of larvae from a challenge infection of mice that had been immunized by oral infection with eggs was severely damaged as shown by the increased electron density, shrinking of the cytoplasm and formation of large empty vacuoles. Development of microvillar protrusions and intraepithelial vesicles were not seen. Changes of internal structure were similar to those changes seen in the larvae of unimmunized mice. It was evident that host immunity, resulting in the ultimate death of challenge larvae during 24 h after challenge, was primarily directed against the epithelium of the larva. Host cells which firmly adhered to the larva in unimmunized mice were monocytes and macrophages with occasional infiltration of eosinophils and plasma cells, whereas the host cells in immunized mice were almost exclusively eosinophils and macrophages. It was suggested that the degeneration of larvae in immunized mice was caused by the action of specific antibody directed against larval epithelium. The cooperative action of antibody and eosinophils or macrophages in killing challenge larvae was also suggested.

Circulating immunoglobulins and complement in mice with Hymenolepis nana infection

Abstract Changes in the circulating immunoglobulins and complement in ddY mice were assayed at various times after immunizing and challenge infections with Hymenolepis nana eggs. The levels of IgG1 and IgG2a consistently increased during 3–4 weeks after immunizing infection. The increase of these immunoglobulins after challenge infection was quicker and more intense than that following immunization. It was not possible to correlate increased levels of IgG1 and IgG2a with the onset of destruction of challenge larvae in immunized mice. IgM concentrations increased slightly during 4 days after immunization but challenge infection did not further increase IgM levels. IgA and IgG2b levels showed no significant change during the course of the infection. Serum C3 levels showed no discernible change after either immunizing or challenge infections. An attempt to specifically suppress the acquisition of resistance by administration of the complement-depleting agent, cobra venom factor (CoF), before immunization failed and depletion of complement activity with CoF that was administered just before challenge infection also failed to affect resistance. These results suggest that complement has no critical role in either induction of the response nor in the anamnestic response to H. nana infection in mice.