Biomedical subjects

Hidero Kitasato

Publications and source records attributed to Hidero Kitasato.

22 records · Page 2Linked to original sources

PubMed2002

Antiinflammatory effect of retrovirally transfected interleukin-10 on monosodium urate monohydrate crystal-induced acute inflammation in murine air pouches.

OBJECTIVE: To investigate the role of interleukin-10 (IL-10) in the inflammatory response, the antiinflammatory effect of retrovirally transfected IL-10 was evaluated both in vitro and in vivo. METHODS: A recombinant retrovirus containing the murine IL-10 gene was constructed using the pLXSN vector and was designated as LXSN-IL-10. Murine IL-10 was introduced into embryonic C57BL/6J fibroblast cells using LXSN-IL-10 to create C57-IL-10 cells. The effect of IL-10 in the culture supernatant of these cells was then evaluated by determining changes in the production of tumor necrosis factor alpha (TNFalpha), macrophage inflammatory protein 1alpha (MIP-1alpha), and MIP-1beta by macrophages. The antiinflammatory effect of C57-IL-10 cells was also investigated using an in vivo model of monosodium urate monohydrate (MSU) crystal-induced acute inflammation. RESULTS: The IL-10 gene transcript and its product were detected by reverse transcriptase-polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The level of IL-10 in the culture supernatant of C57-IL-10 cells was estimated to be 50 ng/ml. The culture supernatant of these cells exerted the biologic activity of IL-10, showing inhibition of TNFalpha, MIP-1alpha, and MIP-1beta production by macrophages. Injection of C57-IL-10 cells into murine air pouches significantly inhibited MSU crystal-induced cellular infiltration (P < 0.01) and production of the mouse CXC chemokine KC (P < 0.05). These findings were consistent with the results obtained by the injection of recombinant human IL-10 into air pouches. CONCLUSION: In this murine air pouch model of MSU crystal-induced inflammation, IL-10 seemed to inhibit the recruitment of neutrophils at least partly by suppressing KC production. These findings seem to suggest that IL-10 gene therapy may be useful for inflammatory diseases.

Air↗

PubMed2002

Multiple palmar epidermoid cysts.

Implantation of epidermal fragments into the dermis has been pointed out as the cause of common epidermal cysts. However, some palmoplantar epidermoid cysts have been reported to be caused by human papillomavirus (HPV) infection or to be derived from eccrine ducts. A 65-year-old left-handed woman presented with extraordinary multiple epidermoid cysts on the palm and volar aspect of the fingers of her left hand. HPV infection was not detected by immunohistochemistry, in situ hybridization and polymerase chain reaction. Histological investigation revealed syringeal structures within the cyst wall and in the cyst cavity. Carcinoembryonic antigen was observed in these syringeal structures but was not specifically stained in the cyst wall cells by immunohistochemistry. The cytokeratin composition of the cyst wall cells was similar to that of the nonadnexal epidermis.

Aged↗

PubMed2002

[Identification and classification of beta-lactamases in clinical isolates of bacteria].

Emergence of bacterial resistance has rendered ineffective a number of previously valuable antibiotic treatments and now threatens the effectiveness of others. beta-Lactam resistance is no longer predominantly a hospital-treated problem; it has now become an important issue in community medicine. More than 100-beta-lactamases have been identified and classified according to their structure, substrate specificity, and whether they are chromosomal or plasmid-mediated. beta-Lactamase production is rare among Gram-positive pathogens, important exceptions being Staphylococcus aureus and Enterococcus faecalis. By contrast, many Gram-negative pathogens are beta-lactamase-positive; inducible and/or hyper-productive strains are particularly challenging in the clinical setting. Surveillance programs have shown that, in general, beta-lactam resistance is on the increase, and that the plasmid-mediated beta-lactamase have developed rapidly over past decade such as ESBLs and carbapenemases.

Gram-Negative Bacteria↗

PubMedDate not supplied

Down-regulation of lipoxin A4 receptor by thromboxane A2 signaling in RAW246.7 cells in vitro and bleomycin-induced lung fibrosis in vivo.

Lipoxins (LXs) are members of eicosanoid family that can be endogenously produced during cell-to-cell interactions such as platelet-leukocyte interactions. Anti-inflammatory function of lipoxin A4 (LXA4) as "braking signals" is mediated by the receptor. On the other hand, thromboxane A2 (TXA2) produced by catalysis of cyclooxygenase and thromboxane synthetase is released during platelet aggregation as a vasoconstrictor and a pro-inflammatory factor. To investigate interaction of TXA2 receptor (TP) and LXA4 receptor, effects of a TP agonist and a thromboxane synthetase inhibitor on expression of LXA4 receptor were examined in vitro and in vivo. A TP agonist, U46619 showed a down-regulation of LXA4 receptor induced by interleukin-1beta (IL-1beta) in RAW246.7 cells. In bleomycin-induced lung fibrosis in mice, administration of a thromboxane synthetase inhibitor DP-1904 increased LXA4 receptor mRNA and decreased type I collagen mRNA. In vitro experiments indicate that LXA4 significantly prevented enhanced proliferation of NIH3T3 fibroblasts and the collagen expression by transforming growth factor-beta (TGF-beta). These results suggest that TXA2-TP signaling could cause negative regulation of lipoxin A4 receptor under the transcriptional level during inflammatory process mediated by IL-1beta and TGF-beta induce the expression of LXA4 receptor. Furthermore, the down-regulation of LXA4 receptor by TXA2 implies a possibility that a cellular signaling by TXA2 may have a novel and potential function as a pro-inflammatory factor to inhibit anti-inflammatory effect of LXA4. Concomitantly, selective blockade of TXA2-TP signaling could be suggested to lead to anti-inflammation through active role of LXA4.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗