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猫条虫Taenia taeniaeformis感染成立における宿主-寄生虫相互作用の解析
| Title: | 猫条虫Taenia taeniaeformis感染成立における宿主-寄生虫相互作用の解析 |
| Other Titles: | Studies on the host-parasite relationship in Taenia taeniaeformis infection in the intermediate host（mouse and rat）． |
| Authors: | 石渡, 賢治1 Browse this author |
| Authors(alt): | Ishiwata, Kenji1 |
| Issue Date: | 25-Mar-1992 |
| Publisher: | Hokkaido University |
| Abstract: | Mechanisms of protection， and the host－parasite relationships in hydatidosis/cysticercosis were investigated using the laboratory model of Taenia taeniaefomis in mice and rats． Responses to Taenia taeniaeformis infection were studied in mice with severe combined immunodeficiency （scid）， which lack functional T and B lymphocytes． These responses were compared with those in their immunologically normal counterparts C． B－17 mice （a BALB/c strain），which are genetically resistant to the parasite． The results suggested that in host responses to larval T． taeniaeformis， polymorphonuclear leucocyte accumulation and encapsulation by fibrosis are T and B cell independent， while eosinophi1 and macrophage infiltration， as well as resistance to infection are T and/or B cell dependent． Additionally，there may be an association between host cell necrosis around larvae and T and/or B cell responses． Challenge infection in scid mice supplemented with thymocytes or splenocytes from C． B－17 confirmed the importance of T cells in protection against T． taeniaeformis infection． Staining properties， kinetics and degranulation of mast cells accumulating around the metacestodes of T． taeniaeformis in the liver of rats were studied． These hepatic mast cells are observed in very small numbers in the liver of infected mice， prompting a study to discern the stimulus for mast cell proliferation in the rat． Mast cells in the liver of infected rats began to proliferate from 2 wks postinfection （p. i.）， reaching a peak at 4 wks p. i. Numbers then decreased gradually． Mast cell accumulation was unremarkable in the congenitally athymic nude rat， indicating that mast cell proliferation is thymus dependent． Histochemical analysis of the host capsule of infected rats revealed that most cells appearing in the early stage of infection were of the mucosal mast cell type． As infection progressed however， their character changed to one midway between mucosal mast cells and connective tissue mast cells． This type of cell first appeared at 28 days p. i. By 70 days p. i. cells that appeared to be normal connective tissue mast cells were also observed． These observations suggest that mast cell differentiation／maturation occur within the host capsule． In vitro studies were then initiated to more critically assess the phenomena observed in T． taeniaeformis infection of the rat． Firstly， a method for artificial activation of T． taeniaeformis oncospheres needed to be developed． Co－culturing activated oncospheres with normal or infected rat serum caused their lysis within 30 minutes． Heat inactivation of serum at 56℃ for 30 min． removed this effect， showing that a non-specific heat labile factor was responsible for the lysis．Activated oncospheres were then added to normal rat peritoneal cells after being precultured with immune or normal rat serum for estimating the passive immunization in vivo． Peritoneal cells mainly granulocytes adhered to oncospheres from both pretreatment groups in large numbers，but oncosphere destruction was not observed up to 150 min later． Mice pre-treated with carrageenan （CAR） or diethylstilbestrol （DES） were assessed for macrophage function． CAR depressed phagocyte function，while DES stimulated it， as assessed by carbon clearance test． Pre-treated mice were then challenged with T． taeniaeformis eggs per os. Paradoxically， cyst formation was lower in CAR－treated mice， while that in DES－treated mice was the same as in controls． Finally， the contribution of the parasite to modulation of the host’s immune system was investigated． Strains of T． taeniaeformis adapted to rats had lower survival than mouse strains when inoculated into mice， but caused a higher degree of immune－suppression． This immune－suppression manifested as a lower responsiveness of splenocytes to Con A （mitogen） stimulation at 12 days p. i. Supernatant removed from in vitro larval culture also caused suppression of mitogen－induced proliferation when added to normal mouse splenocyte culture. The greatest suppression was caused by supernatant from rat－adapted larvae． Above experiments showed that survival larvae induce immune－suppression，although the relation， which stronger suppression caused by larvae leads higher susceptibility of host， could not be suggested． Remarkable factor of protection against larval T. taeniaeformis infection could not be cleared， however， these results may support that resistance consists of several mechanisms． |
| Conffering University: | 北海道大学 |
| Degree Report Number: | 甲第3086号 |
| Degree Level: | 博士 |
| Degree Discipline: | 獣医学 |
| Type: | theses (doctoral) |
| URI: | http://hdl.handle.net/2115/49798 |
| Appears in Collections: | 学位論文 (Theses) > 博士 （獣医学）
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Submitter: 石渡 賢治
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