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101.
102.
Infection mechanism of biofilm‐forming Staphylococcus aureus on indwelling foreign materials in mice
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Taro Makino Shiro Jimi Takuto Oyama Yuki Nakano Kouichi Hamamoto Kanako Mamishin Tomoko Yahiro Shuuji Hara Tohru Takata Hiroyuki Ohjimi 《International wound journal》2015,12(2):122-131
Indwelling foreign‐body infections are a critical medical problem, especially in immunocompromised patients. To examine the pathogenicity of biofilm‐forming bacteria settling on foreign materials, mice implanted with plastic discs were infected with Staphylococcus aureus. After opening a wide subcutaneous pocket on the dorsal side of mice with or without temporal leukocytopenia, a plastic sheet was placed in the left subcutaneous space; subsequently, bacteria in a planktonic state were dispersed over the subcutaneous space. Bacterial numbers were examined 7 days after inoculation. In subcutaneous tissue on the right, S. aureus was found only in leukocytopenic mice. Meanwhile, bacteria were detected on the plastic and neighbouring tissue in both leukocytopenic and normal mice; however, colony‐forming analysis indicated that leukocytopenic mice possessed significantly more bacteria. Tissue reaction against bacteria was pathologically examined. Invading S. aureus induced severe inflammation. In transient leukocytopenic mice, bacterial microcolonies formed on the plastic as well as in the developed necrotic tissue – both of which were shielded from inflammatory cell infiltration – result in bacteraemia. These results indicate that biofilm‐forming S. aureus settling on indwelling foreign material are tolerant against host immunity and assault neighbouring tissue, which may lead to chronic wound infection. 相似文献
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Ryo Fukuda M.D. Naruaki Kohge Shuji Akagi Nguten Thanh Xuan Alejandro Tokuda Shiro Fukumoto 《Journal of gastroenterology》1993,28(2):254-258
To investigate whether hepatitis causes mutation in the viral genome, DNA sequences in the pre-core region of duck hepatitis
B virus (DHBV) DNA were analyzed in both ducks with hepatitis and without hepatitis. Five DHBV carrier ducks were injected
with DHBV particle proteins purified from duck serum with Freund’s complete adjuvant (FCA) intrahepatically from 14 day posthatch
for 9 weeks (immunized group). Serum was drawn at the end of the 1st and 4th week after the 1st injection of DHBV particle
protein and ducks were killed at the end of the 9th week to obtain the liver. Another five ducks without treatment were used
as controls. All ducks of the immunized group showed moderate to severe hepatitis at the 9th week. All ducks in the immunized
group showed one mutation except one duck that showed two mutations only at the 9th week. Mutations were observed in the 5th,
13th, 21st, 22nd, and 28th codon of the precore region. All of them were point mutation at the 3rd base in the triplets. The
frequency of mutation was different in each duck from 20% to 60% but not 100%. There was no mutations in ducks in control
group. These results suggest that hepatitis causes mutation in the pre-core lesion genome of duck hepatitis B virus. 相似文献
105.
106.
Value of thyroid specific peroxidase and Ki‐67 stains in preoperative cytology for thyroid follicular tumors
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107.
108.
Influence of PD‐L1 cross‐linking on cell death in PD‐L1‐expressing cell lines and bovine lymphocytes
Ryoyo Ikebuchi Satoru Konnai Tomohiro Okagawa Kazumasa Yokoyama Chie Nakajima Yasuhiko Suzuki Shiro Murata Kazuhiko Ohashi 《Immunology》2014,142(4):551-561
Programmed death‐ligand 1 (PD‐L1) blockade is accepted as a novel strategy for the reactivation of exhausted T cells that express programmed death‐1 (PD‐1). However, the mechanism of PD‐L1‐mediated inhibitory signalling after PD‐L1 cross‐linking by anti‐PD‐L1 monoclonal antibody (mAb) or PD‐1–immunogloblin fusion protein (PD‐1‐Ig) is still unknown, although it may induce cell death of PD‐L1+ cells required for regular immune reactions. In this study, PD‐1‐Ig or anti‐PD‐L1 mAb treatment was tested in cell lines that expressed PD‐L1 and bovine lymphocytes to investigate whether the treatment induces immune reactivation or PD‐L1‐mediated cell death. PD‐L1 cross‐linking by PD‐1‐Ig or anti‐PD‐L1 mAb primarily increased the number of dead cells in PD‐L1high cells, but not in PD‐L1low cells; these cells were prepared from Cos‐7 cells in which bovine PD‐L1 expression was induced by transfection. The PD‐L1‐mediated cell death also occurred in Cos‐7 and HeLa cells transfected with vectors only encoding the extracellular region of PD‐L1. In bovine lymphocytes, the anti‐PD‐L1 mAb treatment up‐regulated interferon‐γ (IFN‐γ) production, whereas PD‐1‐Ig treatment decreased this cytokine production and cell proliferation. The IFN‐γ production in B‐cell‐depleted peripheral blood mononuclear cells was not reduced by PD‐1‐Ig treatment and the percentages of dead cells in PD‐L1+ B cells were increased by PD‐1‐Ig treatment, indicating that PD‐1‐Ig‐induced immunosuppression in bovine lymphocytes could be caused by PD‐L1‐mediated B‐cell death. This study provides novel information for the understanding of signalling through PD‐L1. 相似文献
109.
110.