Hiroyuki Kayaba
Akita University
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Publication
Featured researches published by Hiroyuki Kayaba.
Allergy | 2007
Wataru Ito; Takahito Chiba; Arihiko Kanehiro; Hikari Kato; Kazutoshi Yamaguchi; Shigeharu Ueki; Hiroyuki Kayaba; Junichi Chihara
Background:u2002 Hepatocyte growth factor (HGF) is known to influence a number of cell types, and regulate various biologic activities including cell migration, proliferation, and survival. In a recent study, we found that, in vivo, HGF suppresses allergic airway inflammation, i.e. the infiltration of inflammatory cells including eosinophils into the airway, and further, that HGF reduces Th2 cytokine levels; however, the directly physiologic role of HGF with eosinophils remains unclear. In this study, we investigate the potential of recombinant HGF to regulate the factor‐induced chemotaxis of human eosinophils.
International Archives of Allergy and Immunology | 2008
Wataru Ito; Masahide Takeda; Masako Tanabe; Junko Kihara; Hikari Kato; Takahito Chiba; Kazutoshi Yamaguchi; Shigeharu Ueki; Arihiko Kanehiro; Hiroyuki Kayaba; Junichi Chihara
Hepatocyte growth factor (HGF) is known to influence a number of cell types and regulate various biological activities including cytokine production, cell migration, proliferation and survival. Thus, HGF is now recognized to be a key factor in the prevention and attenuation of disease progression. We have reported that HGF reduces allergic airway inflammation, airway hyperresponsiveness, remodeling and development of Th2 cytokines as well as growth factors such as transforming growth factor-β in vivo. In vitro, HGF directly attenuates chemotaxis of eosinophils in the absence of Th2 cytokines and modulates mitogen-activated protein kinases, which play an important role in eosinophil migration. In this review, we discuss the physiological role of HGF in allergic inflammation and its mechanism of anti-inflammatory effects, including the regulation of eosinophil functions.
Allergy | 2009
Noriko Kobayashi; Yoshiyuki Yamada; Wataru Ito; Shigeharu Ueki; Hiroyuki Kayaba; Hajime Nakamura; Junji Yodoi; Junichi Chihara
Background:u2002 Human thioredoxin (TRX) is one of redox‐active proteins that regulate reactive oxidative metabolisms. In recent study, we found that serum levels of TRX were elevated in asthmatic patients with exacerbation; however, few details are known about the physiological role of TRX in allergic inflammation, involving eosinophil infiltration.
International Archives of Allergy and Immunology | 2007
Takahito Chiba; Akira Kanda; Shigeharu Ueki; Wataru Ito; Kazutoshi Yamaguchi; Yumiko Kamada; Masahide Takeda; Tomomi Tanigai; Hajime Oyamada; Hiroyuki Kayaba; Junichi Chihara
Prostaglandin D2 (PGD2), a major prostanoid produced by activated mast cells, has long been implicated in allergic diseases. Recent studies have shown that PGD2 exerts its effects through two different G-protein-coupled receptors (GPCRs), the D-prostanoid receptor (DP) and the chemoattractant receptor-homologous molecule expressed on T helper type-2 cells (CRTH2), expressed in various human tissues. The PGD2/CRTH2 system mediates the chemotaxis of eosinophils, basophils, and Th2 cells, which are involved in the induction of allergic inflammation. We have reported that normal human bronchial epithelial cells (NHBE) and epithelial cell lines (NCI-H292) expressed CRTH2, and PGD2 induces production of IL-8 and GM-CSF. This review discusses the role of CRTH2/DP on epithelial cells and mentions a possible novel receptor for PGD2.
International Archives of Allergy and Immunology | 2008
Wataru Ito; Masahide Takeda; Miyoshi Fujita; Yumiko Kamada; Hikari Kato; Takahito Chiba; Kazutoshi Yamaguchi; Shigeharu Ueki; Hiroyuki Kayaba; Junichi Chihara
Background:Reactive oxygen species (ROS) and eosinophilic granule proteins such as eosinophil-derived neurotoxin (EDN) are known to damage bronchial tissue and cause airway hyperresponsiveness (AHR) in asthma. Hepatocyte growth factor (HGF) regulates various biological activities and is known to be a multifunctional factor. In our previous study, we found that HGF suppressed allergic airway inflammation and AHR in a murine model of asthma. However, there have been few reports regarding the detailed mechanism of the anti-allergic effect of HGF in asthma. In this study, we investigated the potential of recombinant HGF to regulate the production of ROS and the release of EDN from human eosinophils. Methods:Eosinophils were isolated from subjects with mild eosinophilia by modified CD16-negative selection. We investigated the expression of CD69, an activation marker of eosinophils, on eosinophils, using flow cytometry. Further, ROS production from eosinophils was analyzed using luminol-dependent chemiluminescence, and EDN release was measured by ELISA. Results:Treatment with HGF suppressed interleukin-5-induced upregulation of CD69 expression, ROS production and EDN release from human eosinophils. Conclusion:Taken together, these data suggest that in asthma, HGF attenuates allergic airway inflammation and AHR through at least the suppression of ROS production and EDN release from eosinophils.
Allergy and Asthma Proceedings | 2008
Yumiko Kamada; Hiroyuki Kayaba; Wataru Ito; Sigeharu Ueki; Yoshimi Kobayashi; Yoshiyuki Yamada; Norihiro Saito; Tomoe Takahashi; Hajime Oyamada; Junichi Chihara
The monitoring of airway inflammation is mandatory for the improved control of bronchial asthma. We previously reported that intracellular EG2 levels of eosinophils, a marker of bronchial asthma increased in asthma patients. In this study, we hypothesized that eosinophil EG2(+) expression increases during airway inflammation in asthmatic individuals. Eosinophil EG2(+) and percentage eosinophil EG2(+) with whole blood flow cytometry, eosinophil counts, serum total IgE, serum eosinophil cationic protein, eosinophil-derived neurotoxin, and percent of forced expiratory volume in 1 second/force vital capacity (FEV(1)/FVC) were measured in 33 asthmatic patients and 22 healthy volunteers. The relationships between these markers were evaluated. Comparisons were made on EG2(+) expression between attack and asymptomatic periods in six asthmatic patients. EG2(+) expression was significantly greater in the asthmatic patients than in healthy subjects. Furthermore, the EG2(+) expression showed a significant increase during attacks. EG2(+) expression inversely correlated with the FEV(1)/FVC. These results suggest that EG2(+) expression may be a useful clinical marker of airway inflammation in asthma.
Tohoku Journal of Experimental Medicine | 2007
Hiroaki Yoshino; Hiroyuki Kayaba; Tatsuzo Hebiguchi; Mayako Morii; Taku Hebiguchi; Wataru Ito; Junichi Chihara; Tetsuo Kato
Journal of Pediatric Surgery | 2007
Hiroaki Yoshino; Hiroyuki Kayaba; Tatsuzo Hebiguchi; Mayako Morii; Taku Hebiguchi; Wataru Itoh; Junichi Chihara; Tetsuo Kato
american thoracic society international conference | 2009
Shigeharu Ueki; G Mahemuti; H Kato; Masahide Takeda; J Kihara; M Tanabe; Wataru Ito; Hiroyuki Kayaba; Junichi Chihara
american thoracic society international conference | 2009
Wataru Ito; Noriko Kobayashi; Masahide Takeda; Tomomi Tanigai; Yoshiyuki Yamada; Shigeharu Ueki; Hajime Nakamura; Hiroyuki Kayaba; Junji Yodoi; Junichi Chihara