The Serial Changes of Antibody Production, Macrophage Migration Inhibition Test (MIT) and Histopathologic Examination in an Experimental Hypersensitivity Pneumonitis in Rabbits

We developed a hypersensitivity pneumonitis model by sensitizing rabbits intratracheally (IT) twice after two subcutaneous sensitizations (SS), and investigated the serial changes in the production of antibody against micropolyspora faeni (Mf), macrophage migration inhibition test (MIT), and histopa...

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Published inNihon Kyōbu Shikkan Gakkai zasshi Vol. 28; no. 1; pp. 113 - 120
Main Authors Okazaki, Nozomu, Yamaguchi, Etsuro, Itoh, Akihide, Abe, Shosaku, Terai, Tsugio, Kawakami, Yoshikazu
Format Journal Article
LanguageEnglish
Japanese
Published Japan The Japanese Respiratory Society 1990
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Summary:We developed a hypersensitivity pneumonitis model by sensitizing rabbits intratracheally (IT) twice after two subcutaneous sensitizations (SS), and investigated the serial changes in the production of antibody against micropolyspora faeni (Mf), macrophage migration inhibition test (MIT), and histopathologic features. On the third day after the last IT, the proportions of neutrophils in bronchoalveolar lavage fluid (BALF) increased. The antibody levels of Mf specific-antigen in BALF decreased transiently, but those in serum began to increase. The number of AFC in spleen increased rapidly. Histopathologic examination revealed alveolitis and prominent acute pneumonia. On the seventh day after the last IT, the proportion of lymphocytes in BALF, the antibody levels of Mf specific-antigen in BALF, the number of AFC in BALF, and the percent inhibition of MIT were highest. Histopathologic features were characterized by the formation of prominent epithelioid granulomas. On the fourteenth day after the last IT, these features retured to the state of untreated group. These results indicate that the lesions in this HP model are formed by both type III and type IV immune reactions (Coombs-Gall). It was concluded that the seventh day after the last IT was most appropriate for the study of pathophysiology of human HP.
Bibliography:ObjectType-Article-2
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ISSN:0301-1542
1883-471X
DOI:10.11389/jjrs1963.28.113