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Biomedical subjects

C Asagami

Publications and source records attributed to C Asagami.

At least 19 recordsLinked to original sources
PubMed1997

Establishment and characterization of a novel human cell line exhibiting both immunophenotypic markers of monocyte/macrophage and natural killer cell lineages from peripheral blood of a patient with atopic dermatitis.

Large amounts of homogeneous cells are not always available for in vitro studies of inflammatory skin disorders. Here we demonstrate that a novel cell line, termed YAA, has been established from peripheral blood mononuclear cells, which were separated by the Ficoll method, of a patient with atopic dermatitis. YAA cells were grown in suspension culture. The cytochemical staining showed a positive reaction for alpha-naphthyl butyrate esterase, which was completely inhibited by sodium fluoride, but a negative result for periodic acid-Schiff, peroxidase and alkaline phosphatase. A large population of YAA cells exhibited phenotype of CD33 and CD56 but neither of CD2 nor CD3. The phorbol ester-stimulated YAA cells produced a considerable amount of tumor necrosis factor-alpha. These findings suggest that YAA might be a monocytoid line with an additional phenotype specific for natural killer cells.

Adult↗
PubMed1996

Establishment and characterization of a novel human promonocytic cell line from peripheral blood of a patient with psoriasis.

Human monocyte/macrophage lineages have unique phagocytic and immune-regulatory functions. We established a promonocytic cell line from the peripheral blood of a patient with psoriasis vulgaris. The newly established cells, termed YAP cells, grew in a suspension culture. In Wright-Giemsa-stained preparations, YAP cells were round or polygonal in shape. Transmission electron microscopy showed that the cells had clear nuclei with well-defined nucleoli. There were frequent mitochondria, a relatively abundant endoplasmic reticulum profile, free ribosomes and an occasional Golgi apparatus. Cytochemical studies showed a positive reaction for alpha-naphthyl butyrate esterase, which was completely inhibited by sodium fluoride, a diffuse positive reaction for periodic acid-Schiff, and a negative result for alkaline phosphatase and peroxidase. A large population of YAP cells reacted with the CD4, CD11b, CD25 and CD33 surface markers, but not with CD2, CD3, CD8 or CD19. We also found that YAP cells produced considerable amounts of TNF alpha, which was detected in the culture supernatant when the cells were treated with 1 ng/ml 12-O-tetradecanoylphorbol-13-acetate (TPA). Chromosome analyses showed that YAP cells contained a variety of marker chromosomes. It should be stressed that YAP cells were derived from a patient with a non-neoplastic disorder, whereas most monocytic cell lines previously reported are of malignant origin. This newly established cell line might be valuable for studying the pathogenesis of psoriasis, especially the role of monocytes/macrophages in the aetiology of the disease.

Adult↗
PubMed1996

Human melanoma cell lines deficient in GD3 ganglioside expression exhibit altered growth and tumorigenic characteristics.

We have selected GD3-deficient human melanoma cell lines, in order to investigate the function of GD3 ganglioside. This was done by treating SK-MEL-28 cells with anti-GD3 antibody (R24) and rabbit complement and subsequent subcloning of the surviving cells, resulting in the derivation of two cell lines deficient in the cell surface expression of GD3. Neither cell line (designated SK-MEL-28-N1 and SK-MEL-28-N2) had detectable cell surface expression of GD3 as analyzed with monoclonal antibody R24, and no GD3 was detectable in either cell line by glycolipid isolation, thin-layer chromatography, or resorcinol-HC1 spray, but thin-layer chromatography immunostaining with monoclonal antibody R24 showed the presence of low amounts of GD3 in both N1 and N2 (1/40 of the amount in the parent cell line in N1 and 1/500 in N2). In SK-MEL-28-N1, the residual GD3 was shown by immunofluorescence assays on permeabilized cells to be present in discrete intracellular organelles, suggesting that these cells have a defect in the transport of GD3 as well as in its synthesis. Both SK-MEL-28-N1 and -N2 had an increase in detectable GM3 expression. The mutant cell lines had altered cell morphology in comparison to the parent cell line and both had slower growth rates in vitro and lower tumorgenicity in nu/nu mice. These results indicate that GD3 ganglioside plays an important role in proliferation and growth of melanoma cells.

Animals↗
PubMed1996

A case of herpes zoster associated with colitis.

A 58-year-old Japanese woman who had herpes zoster in association with colitis was successfully treated with intravenously administrated acyclovir. Vesicular lesions with red haloes ranged from the left side of her buttock to the left extremity, corresponding to the L4 to S2 dermatomes. Her colitis was considered to have been induced by varicella-zoster virus, based on the facts that the clinical courses were correlated and that the innervation of the affected site of the colon corresponded to an infected dermatome (S2).

Acyclovir↗
PubMed1996

Significance of antibodies to streptococcal M protein in psoriatic arthritis and their association with HLA-A*0207.

Psoriatic arthritis (PA) is an immune disease associated with HLA-A2 in the Japanese population. To investigate mechanisms the association between HLA-A2 and PA, we examined in vivo immune responsiveness to Streptococcus pyogenes. Recombinant M proteins for the subtype specific N-terminal half (AB region) and conserved C-terminal half (C region) were produced separately. IgG antibody level against each region was measured by ELISA in 31 PA patients, 88 patients with psoriasis vulgaris, 6 patients with rheumatoid arthritis and 77 healthy controls. We found that IgG antibody levels against the C region were markedly higher in the PA patient group than in the other disease groups or controls. Further, IgG antibody levels were higher in PA patients with spondylitis and polyarticular arthritis than in PA patients with rheumatoid-like arthritis and arthritis mutilans. In contrast, no significant difference in the IgG antibody levels against the AB region was observed among the tested groups. HLA-A2 DNA typing showed that HLA-A*0207 was associated with PA (RR = 17.6; pcorr < 0.01) and the IgG antibody responses to the C region correlated well with the presence of HLA-A*0207. These results suggest that streptococcal infection may be involved in the pathogenesis of PA by participating in the HLA-linked immune responsiveness.

Antibodies, Bacterial↗
PubMed1996

Putative linkage between HLA class I polymorphism and the susceptibility to malignant melanoma.

Human leukocyte antigen (HLA) frequencies in 67 melanoma patients were compared to 120 controls in Japan. The frequency of HLA-B13 was increased in melanoma patients compared to controls and was particularly common in nodular melanoma HLA-B61 was decreased in melanoma patients. Almost 50% of acral lentiginous melanoma patients expressed HLA-B51 compared to 0% of nodular melanomas.

Asian People↗
PubMed1996

Immune response to Streptococcus pyogenes and the susceptibility to psoriasis.

Monoclonal antibodies directed against type 12 Group A streptococcal cell wall antigens cross-react with nuclei and cytoplasm of cells from skin and synovium from controls, uninvolved skin of psoriatics and psoriatic plaques. Patients with psoriasis had high serum titres of antibody against the M12 (C-region) streptococcal antigen compared to controls. An abnormal immune response directed against a "self' antigen after initiation by Group A streptococcal infection may play an important role in the exacerbation or development of psoriasis.

Antibodies, Monoclonal↗
PubMed1995

Polysialogangliosides expressed by amelanotic melanoma: a possible explanation for the poor response to anti-monosialoganglioside antibody 202 in a patient with melanoma.

A 52-year-old Japanese woman developed numerous amelanotic metastatic melanomas on the skin and in various organs three years after a surgical operation for primary melanoma on the right axilla. The patient was treated with monosialoganglioside specific monoclonal antibody 202; however, no apparent clinical effects were observed. Ganglioside analysis of a metastatic tumor demonstrated that it expressed GM3, GM2, GD3, GD2, and polysialogangliosides. Since polysialogangliosides rarely appear in melanomas, their expression may explain the patient's poor response to MAb 202. The relationship between ganglioside composition and the effect of anti-ganglioside monoclonal antibody is discussed.

Antibodies, Monoclonal↗
PubMed1995

Necrotizing fasciitis due to Pasteurella multocida infection.

Necrotizing fasciitis is a potentially fatal clinical disease caused by infection with various bacteria in addition to streptococci, which are common causative agents. We report on a rare case of this disease in association with Pasteurella multocida infection. A 58-year-old man had systemic features of shock after a 15-hour history of a painful swelling on the right lower leg. The swelling led to skin blistering and necrosis from which P. multocida was isolated. Those lesions progressed rapidly. The patient also had a history of chronic liver injury as described in previous reports.

Blister↗
PubMed1995

Immunohistological reaction mechanism of anti-monosialoganglioside monoclonal antibody, MAb 202, showing predominant cytotoxicity for malignant melanoma.

Mouse monoclonal IgM antibody (MAb 202) can cause melanoma cell necrosis in vivo. We analysed its immune mechanism in three melanoma patients to whom MAb 202 was administered. After the MAb 202 administration, histopathological analysis showed necrosis of melanoma cells expressing only GM3 in two patients. Another patient carrying both GM3 and GD3 showed infiltration of lymphocytes within the tumor nest but no tumor cells or nest necrosis. Immunohistological examination using anti-mouse IgM antibody revealed MAb 202 bound on the surface of melanoma cells in two patients but not in the third (positive for both GM3 and GD3). In vitro, MAb 202 reacted with the melanoma cells of the same two patients, but not with any other tissues of these individuals. We found no reaction of MAb 202 to non-melanoma cells including normal melanocytes and glia cells. Our trials suggest, 1) MAb 202 reacts directly to monosialogangliosides on the melanoma cell surface and then leads to the cytotoxicity reaction, or 2) MAb 202 induces lymphocyte infiltration and possibly then promotes the secretion of some cytokines.

Adult↗
PubMed1993

Structure determination of glycosphingolipids of cultured human keratinocytes.

From cultured human keratinocytes, seven glycolipid fractions were isolated by DEAE and silica-gel column chromatographies, and further by HPLC on a silica-gel column. By means of 1H-NMR spectroscopy, fast atom bombardment mass spectrometry and GLC-mass spectrometry, one fraction was determined to contain acylglucosylceramides, which consist of amide linked omega-hydroxy fatty acids (C30:0, C30:1, C32:1 and C34:1), fatty acids linked to the omega-hydroxy fatty acids through ester linkages (C14:1, C16:1, C18:1 and C18:2), a long-chain base (d18-sphingenine), and beta-glucose. Five of the other fractions contained glucosylceramides, and the seventh fraction contained a mixture of glucosylceramides and galactosylceramides. Glucosylceramides containing long-chain omega-hydroxy fatty acids, which are assumed to be immediate precursors of the acylglucosylceramides, were hardly detected in these glycolipid fractions. Six glucosylceramide fractions were separated due to differences in their fatty acids and sphingosines. On comparison with the results reported in our previous paper, the acylglucosylceramide content of the cultured human keratinocytes was about half that of human epidermis. Under the culture conditions used, the human keratinocytes did not differentiate into granular or horny cells. Taken together, the results suggest that the synthesis of acylglucosylceramides is not activated much in the cultured keratinocytes, but would be more activated in differentiated cells.

Adult↗
PubMed1993

Iatrogenic benign lymphoplasia induced by allergic contact dermatitis from squaric acid dibutylester: immunohistologic study of cellular infiltrates.

We report of a 62-year-old male patient with a dull red itchy nodule on the induction area of allergic contact dermatitis to squaric acid dibutylester, which had been used for the therapy of alopecia universalis. The excised biopsy specimen showed dense infiltration of lymphoid cells in the dermis and subcutaneous tissue, associated with the formation of lymphoid follicles. Immunohistologic analysis of the infiltrates indicated mixed proliferation of T- and B-cells. A biopsy specimen from the challenge area showed spongiosis in the epidermis and lymphoid cell infiltration in the upper dermis, while the infiltrates consisted mainly of T-cells. The following points are discussed: (i) the lesion had an iatrogenic origin and the causative agent was quite evident; (ii) the route of allergen application was only through the epidermis and not directly in the dermis; (iii) lymphoid cell infiltrates of the induction and challenge areas were different.

Allergens↗
PubMed1993

Inhibitory effect of azelastine, a potent antiallergic agent, on release of tumor necrosis factor-alpha from activated human peripheral blood mononuclear cells and U937 cells.

It is generally accepted that tumor necrosis factor-alpha (TNF-alpha) is a multifunctional cytokine which is involved in the regulation of inflammation as well as immunity. In the present study, we investigated whether azelastine, a potent antiallergic agent, affects release of TNF-alpha from peripheral blood mononuclear cells (PBMC) and U937 cell line in vitro. When human PBMC and U937 cells were stimulated by phytohemagglutinin (PHA) and 12-0-tetradecanoyl-phorbol-13-acetate (TPA), respectively, the cells released significant amounts of TNF-alpha as determined by TNF-alpha-specific enzyme immunoassay. TNF-alpha levels in the culture supernatant of PHA-stimulated human PBMC and TPA-activated U937 cells decreased in a dose-dependent manner when these cells were cultured in the presence of azelastine. This inhibitory effect of azelastine was obtained at concentrations where the drug produced no toxicity. Moreover, azelastine also inhibited release of TNF-alpha from U937 cells which were already activated by TPA. These results suggest that the inhibitory effect of azelastine on TNF-alpha release plays an important role in its antiallergic action in addition to inhibition and/or antagonism of histamine and leukotrienes, which has been previously reported.

Depression, Chemical↗