Atsushi YAMATODANI
Department of Medical Physics, School of Allied Health Sciences, Faculty of Medicine, Osaka University, Yamadaoka 2-2, Suita, Osaka, 565 Japan.

Kumiko NAGATA
Haruki OKAMURA
Toshihide TAMURA
Department of Bacteriology, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo, 663 Japan.

Kazuo NAGAI
Department of Pharmacology, Hyogo College of Medicine, 1-1, Mukogawa-cho, Nishinomiya, Hyogo, 663 Japan.

Abstract
Effects of the infection with larval Ascaris suum on the immune system seem to be primarily induced by the tissue injury of target organs. In this study, the tissue damage caused by the larval migration was substantiated by measuring enzymatic activities. The activities of both transaminases, GOT and GPT in sera of infected mice peaked on the 5th day of infection when the number of larvae in the liver was maximal. The total activities of histidine decarboxylase (L-histidine carboxylase, EC 4.1.1.22) (HDC) in the liver or in the lung increased when the larvae migrated to respective organs. The infected mice normally recovered from the debility after the remove of larvae from the lung. However, the administration of a histamine H2-receptor antagonist, famotidine, interfered with the recovery. In the circulation, the corticosterone level significantly increased from the 3rd day and peaked on the 7th day of infection (p<0.01). On the other hand, catecholamines (adrenalin, nor adrenalin and dopamine) significantly decreased to below normal levels on the 8th day (p<0.02, 0.05 and 0.01, respectively) These data suggest that the systemic feedback regulation with corticosterone that is induced by local tissue damages may affect the immune system.