Mayumi Ota
Dokkyo University
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Publication
Featured researches published by Mayumi Ota.
Molecular Medicine Reports | 2011
Kenya Kohyama; Masayuki Hashimoto; Shyuzo Abe; Kazumi Kodaira; Tatsuo Yukawa; Soichiro Hozawa; Junichiro Morioka; Hiroaki Inamura; Megumi Yano; Mayumi Ota; Hironori Sagara; Motohiro Kurosawa
It is well known that aspirin-exacerbated respiratory disease (AERD) is more common in women than in men, however, whether gene polymorphisms of the thromboxane A2 receptor (TBXA2R) and chemoattractant receptor-homologous molecules expressed on Th2 cells (CRTH2) are associated with the susceptibility of AERD remains unknown. In this study, we examined the gene polymorphisms in a Japanese population. DNA specimens were obtained from the following three groups: 96 patients with AERD, 500 patients with aspirin-tolerant asthma (ATA) and 100 normal controls. The target DNA sequence of each gene was amplified, and an allelic discrimination assay for single nucleotide polymorphisms relating to expression of each gene was carried out. The frequencies of the CC/CT genotype of TBXA2R +795T>C were higher than those of the TT genotype in AERD patients compared to ATA patients (P=0.015). In female AERD patients, but not in males, frequencies of the CC/CT genotype were higher than those of the TT genotype of TBXA2R +795T>C compared to female ATA patients (P=0.013). Also, frequencies of the TT genotype of CRTH2 -466T>C were higher than those of the CC/CT genotype in AERD patients compared to ATA patients (P=0.034). In female AERD patients, but not in male, frequencies of the TT genotype were higher than those of the CC/CT genotype of CRTH2 -466T>C in AERD patients compared to female ATA patients (P=0.046). Based on our investigations, no significant relationship was found between the genotype and the clinical characteristics according to these gene polymorphisms in AERD patients. Our results suggest that an association between the TBXA2R and CRTH2 gene polymorphisms with AERD may exist in the Japanese population.
International Archives of Allergy and Immunology | 2011
Kenya Kohyama; Shyuzo Abe; Kazumi Kodaira; Tatsuo Yukawa; Soichiro Hozawa; Junichiro Morioka; Hiroaki Inamura; Mayumi Ota; Hironori Sagara; Lawrence B. Schwartz; Motohiro Kurosawa
Background: There has been no report that investigated β2-adrenergic receptor (ADRB2) gene polymorphism in patients with aspirin-exacerbated respiratory disease (AERD). Methods: DNA in the specimens in three groups of study subjects classified patients with AERD, patients with aspirin-tolerant asthma (ATA) and normal controls was extracted, and the target DNA sequence of the ADRB2 was amplified using a set of primers to generate an amplicon of 219 bp in length. Allelic discrimination assay for single nucleotide polymorphisms relating to the ADRB2 gene expression was carried out by using a previously described single nucleotide polymorphism detective system, sequence-specific thermal-elution chromatography. Results: The frequency of the Gly variant allele in patients with AERD was significantly lower than that in patients with ATA (p = 0.007), and the odds ratio (OR) of AERD to ATA associated with wild-type ArgArg homozygote was 3.300. Frequencies of wild-type ArgArg homozygote are significantly higher than those of variant-type ArgGly/GlyGly genotype in patients with AERD compared with those with ATA (p < 0.001, OR = 3.153). In patients with AERD, frequencies of wild-type ArgArg homozygote in both female and male patients are significantly higher than those of variant-type ArgGly/GlyGly genotype in male patients compared with those with ATA (p < 0.001, OR = 5.128 and p = 0.007, OR = 4.367, respectively). Also, in patients with AERD, frequencies of wild-type ArgArg homozygote in female patients are significantly higher than those of variant-type ArgGly/GlyGly genotype in female patients compared with those with ATA (p = 0.002, OR = 2.825). Conclusions: We were the first to analyze Arg16Gly ADRB2 gene polymorphism in Japanese patients with AERD, and showed that Arg16Gly ADRB2 gene polymorphism in Japanese patients with AERD is different from that in the patients with ATA.
American Journal of Physiology-lung Cellular and Molecular Physiology | 2009
Masakata Yoshioka; Hironori Sagara; Fumiyuki Takahashi; Norihiro Harada; Kazuto Nishio; Akio Mori; Hiroko Ushio; Kazue Shimizu; Takenori Okada; Mayumi Ota; Yoichi M. Ito; Osamu Nagashima; Ryo Atsuta; Toshihiro Suzuki; Takeshi Fukuda; Yoshinosuke Fukuchi; Kazuhisa Takahashi
Multidrug resistance-associated protein 1 (MRP1) is a cysteinyl leukotriene (CysLT) export pump expressed on mast cells. CysLTs are crucial mediators in allergic airway disease. However, biological significance of MRP1 in allergic airway inflammation has not yet been elucidated. In this study, we sensitized wild-type control mice (mrp1(+/+)) and MRP1-deficient mice (mrp1(-/-)) to ovalbumin (OVA) and challenged them with OVA by aerosol. Airway inflammation and goblet cell hyperplasia after OVA exposure were reduced in mrp1(-/-) mice compared with mrp1(+/+) mice. Furthermore, CysLT levels in bronchoalveolar lavage fluid (BALF) from OVA-exposed mrp1(-/-) mice were significantly lower than those from OVA-exposed mrp1(+/+) mice. Levels of OVA-specific IgE, IL-4, and IL-13 in BALF were also decreased in OVA-exposed mrp1(-/-) mice. IgE-mediated release of CysLTs from murine bone marrow-derived mast cells was markedly impaired by MRP1 deficiency. Our results indicate that MRP1 plays an important role in the development of allergic airway inflammation through regulation of IgE-mediated CysLT export from mast cells.
International Archives of Allergy and Immunology | 2001
Hironori Sagara; Sohei Makino; Naomi Chibana; Mayumi Ota; Stephen T. Holgate; Martin K. Church; Takeshi Fukuda
Inflammation of the airways is a cardinal feature of asthma. It has recently been recognized that mast cells may contribute to this process by cytokine secretion. Activation of a number of transcription factors, such as NF-ĸB, results in the de novo synthesis of a wide spectrum of cytokines including TNFα, IL-8 and GM-CSF. We have assessed the activation of NF-ĸB by exposure of purified lung mast cells to TNFα (5 ng/ml), SCF (10 ng/ml) and anti-IgE (1 µg/ml). Mast cells were identified by cytospin immunocytochemistry using the antitryptase antibody AA-1 and activated NF-ĸB visualized by the antibody 2c7 (Upjohn) which recognizes a site revealed only on its dissociation from I-ĸB. In addition, the effects of theophylline and other modulatory drugs have been examined on NF-ĸB activation and consequential cytokine secretion. Results show that TNFα increased the percentage of cells staining positive for activated NF-ĸB from 8.4 ± 4.8 to 63 ± 4.5 within 15 min. Anti-IgE caused a slow increase from 4.3 ± 0.4 to 45.4 ± 13.3% at 4 h. Theophylline at 20 µg/ml decreased TNFα and anti-IgE induced NF-ĸB activation by 37.3 ± 2.1 and 25.3 ± 1.3%, respectively. Secretion of TNFα, IL-8 and GM-CSF was also inhibited by 20 µg/ml theophylline. The suppression of NF-ĸB activation indicates that theophylline, in addition to its bronchodilator actions, has anti-inflammatory activity which is likely to be pertinent to the treatment of bronchial asthma.
american thoracic society international conference | 2010
Hironori Sagara; Hiroyuki Masuda; Mayumi Ota; Takenori Okada; Kazumi Akimoto; Takeshi Fukuda; Makoto Fueki; Naoto Fueki
american thoracic society international conference | 2010
Takeshi Fukuda; Tatsuo Yukawa; Hironori Sagara; Akihiro Takemasa; Mayumi Ota; Kumiya Sugiyama; Hirokuni Hirata; Yoshiki Ishii; Yasutsugu Fukushima
american thoracic society international conference | 2009
Naoto Fueki; Hironori Sagara; Makoto Fueki; A Hashii; Mayumi Ota; Takenori Okada; Kumiya Sugiyama; Kazumi Akimoto; Sohei Makino; Takeshi Fukuda
The Journal of Allergy and Clinical Immunology | 2006
Hironori Sagara; Kumiya Sugiyama; Takenori Okada; Mayumi Ota; Takeshi Fukuda
The Journal of Allergy and Clinical Immunology | 2006
N. Fueki; Hironori Sagara; Mayumi Ota; Kazumi Akimoto; Takenori Okada; Kumiya Sugiyama; M. Fueki
Japanese Journal of Allergology | 2005
Hironori Sagara; Mayumi Ota; Takenori Okada; Kazumi Akimoto; Takeshi Fukuda