Hisato Yamasaki

Hypersensitivity pneumonitis induced by a smut fungus Ustilago esculenta.

A case of hypersensitivity pneumonitis caused by a smut fungus Ustilago esculenta is presented.

Purification and characterization of the serotype-specific polysaccharide antigen of Trichosporon cutaneum serotype. II: A disease-related antigen of Japanese summer-type hypersensitivity pneumonitis

Summer‐type hypersensitivity pneumonitis (SHP) is a unique type of hypersensitivity pneumonitis and the most prevalent in Japan. Our previous study clarified that the causative agent of the disease is Trichosporon cutaneum, and that the patients with SHP have high litres of antibodies against the serotype‐specific antigen of polysaccharide nature which exist in the high molecular weight fraction of the culture supernatant of the yeast. In this study, we purified the serotype‐specific antigen of serotype II T. cutaneum by gel filtration and affinity chromatography using a monoclonal antibody, D‐8, specific for a high molecular weight antigen of serotype II T. cutaneum, and elucidated the structure of the antigen. This affinity‐purified antigen was shown to be an essentially acidic polysaccharide comprising mannose, xylose, and glucuronic acid (6:44:4.7). Chemical analysis showed that this polysaccharide antigen contains a (1–3)‐linked mannan backbone attached with short side chains of (1–4)‐linked mannose and a small proportion of (1–2)‐linked xylose residues by substituting the 2‐ or 4‐positions of the (1–3)‐linked mannose residues of the main chain. Approximately one‐fifth of the side chains were terminated with glucuronic acid residues. The antigenic epitope of the serotype‐specific antigen was shown to involve the terminal glucoronic acid residues as revealed by immunodiffusion test and sandwich enzyme‐linked immunosorbent assay using monoclonal antibody D‐8.

Hypersensitivity pneumonitis resulting from Aspergillus fumigatus in a greenhouse.

A 57-y-old female who had cultivated vegetables in a plastic greenhouse developed a case of hypersensitivity pneumonitis from Aspergillus fumigatus. This report exemplifies a potential hazard caused by a thermotolerant fungus, A. fumigatus, in a poorly constructed greenhouse.

Experimental Hypersensitivity Pneumonitis in Mice Induced by Trichosporon cutaneum: Histologic and Immunologic Features and Effect of in Vivo Depletion of T Cell Subsets

An animal model of hypersensitivity pneumonitis (HP) was developed in C57Black/6J mice by repeated intratracheal inoculations with particulate Trichosporon cutaneum, a causative agent of Japanese summer-type HP. We observed severe alveolitis and bronchiolitis with infiltration of lymphocytes, macrophages, and neutrophils in the lung lesions. Granuloma formation was occasionally seen. Bronchoalveolar lavage (BAL) of the experimental animals showed an increase in the number of lymphocytes, macrophages, neutrophils, and in the total cell yield. Phenotypic analysis of the BAL lymphocytes by flow cytometry revealed that 43.1 +/- 3.1% of lymphocytes were Thy1.2+ (CD3+) cells and that the L3T4+ (CD4+) cells (36.3 +/- 3.5%) predominated over the Lyt2+ (CD8+) cells (18.5 +/- 1.2%). As for the humoral immune response, the specific IgA antibody activities in the BAL fluids well reflected the specific pulmonary inflammatory responses. Studies of lymphocyte depletion were performed by in vivo administration of anti-CD4 and anti-CD8 monoclonal antibodies. Depletions of CD4+ cells and of both CD4+ and CD8+ cells diminished the pulmonary lesions and specific IgA antibody activities in the BAL fluids. These results indicate that CD4+ cells may play a major role in the inflammatory process of this animal model.

Arachidonic Acid Release Is Closely Related to the Fcγ Receptor-Mediated Superoxide Generation in Macrophages

Stimulation of macrophages with IgG2 immune complexes induced dose‐dependently the O2− generation and the release of arachidonic acid and its metabolites. This FcγR‐mediated O2− generation was inhibited by a phospholipase A2 inhibitor, 4‐p‐bromophenacyl bromide (4‐pBPB), in parallel to the dose‐dependent inhibition of arachidonic acid release. The main arachidonic acid metabolites released were shown to be prostaglandin E2 and thromboxane B2 and blocking of the production of these metabolites by indomethacin did not inhibit the O2− generation. Inhibition of the FcγR‐mediated O2− generation and the arachidonic acid release by the C‐kinase inhibitor, 1‐(5‐isoquinolinesulfonyl)‐2‐methylpiperazine (H‐7), was less intense than by 4‐pBPB. These results support the previously proposed hypothesis that arachidonic acid acts as an intracellular activator of the FcγR‐mediated O2− generation in macrophages. Although the C‐kinase activation may also contribute to the activation of the O2−‐generating system, arachidonic acid release appears to play a major role in FcγR‐mediated O2− generation. In contrast, activation of C‐kinase seems to be contributing mainly in the induction of both the arachidonic acid release and O2− generation by 12‐o‐tetradecanoylphorbol 13‐acetate (TPA). Furthermore, suboptimal concentrations of TPA and arachidonate were found to act synergistically to stimulate O2− generation and the inhibition study suggested a positive synergism between C‐kinase and arachidonic acid release to induce O2− generation. This synergistic action may have general importance in receptor‐mediated O2− generation.

A case of alpha-fetoprotein-producing large cell carcinoma of the lung.

α-fetoprotein (AFP) 産生原発性肺大細胞癌の1症例を経験したので報告する. 症例は72才男性, 右中肺野の腫瘤状陰影を指摘され入院となった. 肺の組織学的検査では大細胞癌の診断を得たが, 血清AFPが37,400ng/mlと異常高値を呈していた. 酵素抗体法により, 腫瘍組織からのAFP産生を証明した. 剖検所見では原発性肝癌, 精巣癌, 縦隔腫瘍などは認めなかった.