Search

Your search keyword '"Arakaki, Rieko"' showing total 8 results
Start Over Author "Arakaki, Rieko" Journal plos one
8 results on '"Arakaki, Rieko"'

2. Effect of CNT exposure on alveolar macrophages

Author

Otsuka, Kunihiro, Yamada, Koichi, Taquahashi, Yuhji, Arakaki, Rieko, Ushio, Aya, Saito, Masako, Yamada, Akiko, Tsunematsu, Takaaki, Kudo, Yasusei, Kanno, Jun, and Ishimaru, Naozumi

Subjects
fibrosis, respiratory system, alveolar macrophage, Carbon nanotube, Taquann methods, lung
Abstract

Background Nanomaterials are widely used in various fields. Although the toxicity of carbon nanotubes (CNTs) in pulmonary tissues has been demonstrated, the toxicological effect of CNTs on the immune system in the lung remains unclear. Methods and finding In this study, exposure to Taquann-treated multi-walled CNTs (T-CNTs) was performed using aerosols generated in an inhalation chamber. At 12 months after T-CNT exposure, alveolar inflammation with macrophage accumulation and hypertrophy of the alveolar walls were observed. In addition, fibrotic lesions were enhanced by T-CNT exposure. The macrophages in the bronchoalveolar lavage fluid of T-CNT-exposed mice were not largely shifted to any particular population, and were a mixed phenotype with M1 and M2 polarization. Moreover, the alveolar macrophages of T-CNT-exposed mice produced matrix metalloprotinase-12. Conclusions These results suggest that T-CNT exposure promoted chronic inflammation and fibrotic lesion formation in profibrotic macrophages for prolonged periods.

Published
2018

3. Anti-Inflammatory Effects of Rebamipide Eyedrop Administration on Ocular Lesions in a Murine Model of Primary Sjögren's Syndrome

Author

Arakaki, Rieko, primary, Eguchi, Hiroshi, additional, Yamada, Akiko, additional, Kudo, Yasusei, additional, Iwasa, Akihiko, additional, Enkhmaa, Tserennadmid, additional, Hotta, Fumika, additional, Mitamura-Aizawa, Sayaka, additional, Mitamura, Yoshinori, additional, Hayashi, Yoshio, additional, and Ishimaru, Naozumi, additional

Published
2014
Full Text
View/download PDF

8. Cathepsin L Inhibition Prevents Murine Autoimmune Diabetes via Suppression of CD8+ T Cell Activity.

Author

Yamada, Akiko, Ishimaru, Naozumi, Arakaki, Rieko, Katunuma, Nobuhiko, and Hayashi, Yoshio

Subjects
DIABETES, AUTOIMMUNE diseases, T cells, CYCLOPHOSPHAMIDE, ANTIRHEUMATIC agents, ANTINEOPLASTIC agents, GENES, RNA, NUCLEIC acids
Abstract

Background: Type 1 diabetes (T1D) is an autoimmune disease resulting from defects in central and peripheral tolerance and characterized by T cell-mediated destruction of islet β cells. To determine whether specific lysosomal proteases might influence the outcome of a T cell-mediated autoimmune response, we examined the functional significance of cathepsin inhibition on autoimmune T1D-prone non-obese diabetic (NOD) mice. Methods and Findings: Here it was found that specific inhibition of cathepsin L affords strong protection from cyclophosphamide (CY)-induced insulitis and diabetes of NOD mice at the advanced stage of CD8+ T cell infiltration via inhibiting granzyme activity. It was discovered that cathepsin L inhibition prevents cytotoxic activity of CD8+ T cells in the pancreatic islets through controlling dipeptidyl peptidase I activity. Moreover, the gene targeting for cathepsin L with application of in vivo siRNA administration successfully prevented CY-induced diabetes of NOD mice. Finally, cathepsin L mRNA expression of peripheral CD8+ T cells from NOD mice developing spontaneous T1D was significantly increased compared with that from control mice. Conclusions: Our results identified a novel function of cathepsin L as an enzyme whose activity is essential for the progression of CD8+ T cell-mediated autoimmune diabetes, and inhibition of cathepsin L as a powerful therapeutic strategy for autoimmune diabetes. [ABSTRACT FROM AUTHOR]

Published
2010
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results