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Dive into the research topics where Osamu Narumoto is active.

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Featured researches published by Osamu Narumoto.


Lung | 2007

Efficacy of Corticosteroids in the Treatment of Community-Acquired Pneumonia Requiring Hospitalization

Katsunaka Mikami; Masaru Suzuki; Hiroshi Kitagawa; Masaki Kawakami; Nobuaki Hirota; Hiromichi Yamaguchi; Osamu Narumoto; Yoshiko Kichikawa; Makoto Kawai; Hiroyuki Tashimo; Hidenori Arai; Tadashi Horiuchi; Yoshio Sakamoto

BackgroundRecent studies suggested that administration of corticosteroids may improve clinical outcomes in patients with severe pneumonia.ObjectivesThe aim of this study was to assess the effectiveness of corticosteroids as an adjunctive therapy in community-acquired pneumonia (CAP) requiring hospitalization.Design and SettingAn open label, prospective, randomized control study was conducted from September 2003 to February 2004 in a community general hospital in Japan.PatientsThirty-one adult CAP patients who required hospitalization were enrolled.Measurements and ResultsFifteen patients received 40 mg of prednisolone intravenously for 3 days (steroid group). Sixteen patients did not receive prednisolone (control group). Both groups were also evaluated for their adrenal function. The primary endpoint was length of hospital stay. Secondary endpoints were duration of intravenous (IV) antibiotics and time required to stabilize vital signs. Both groups demonstrated similar baseline characteristics and length of hospital stay, and yet a shorter duration of IV antibiotics was observed in the steroid group (p < 0.05). In addition, vital signs were stabilized earlier in the steroid group (p < 0.05). These differences were more prominent in the moderate–severe subgroup but not as significant in the mild–moderate subgroup. The prevalence of relative adrenal insufficiency (RAI) in both groups was high (43%), yet there was no difference in baseline characteristics between patients, with or without RAI. In multiple regression models, RAI seemed to have no influence on clinical courses.ConclusionsIn moderate–severe CAP, administration of corticosteroids promotes resolution of clinical symptoms and reduces the duration of intravenous antibiotic therapy.


Cellular Immunology | 2012

The role of CCR7 in allergic airway inflammation induced by house dust mite exposure

Masaki Kawakami; Osamu Narumoto; Yukiko Matsuo; Kazuhide Horiguchi; Satomi Horiguchi; Naohide Yamashita; Masahiro Sakaguchi; Martin Lipp; Takahide Nagase; Naomi Yamashita

House dust mite (HDM), the most common allergen, activate both the IgE-associated and innate immune responses. To clarify the process of sensitization, we investigated the role of the CCL21, CCL19, and CCR7 axis in a mouse model of HDM-induced allergic asthma. HDM inhalation without systemic immunization resulted in a HDM-specific IgE response. CCR7-knockout (CCR7KO) mice exhibited greater airway inflammation and IgE responses compared to wild-type mice. We examined FoxP3 expression in these mice to clarify the contribution of regulatory cells to the responses. FoxP3 expression was higher in the lungs but not in the lymph nodes of CCR7KO mice compared to wild-type mice. In CCR7KO mice, FoxP3-positive cells were found in lung, but we observed higher release of IL-13, IL-5, TGF-β, IL-17, and HMGB1 in bronchoalveolar lavage fluid. We demonstrate here that immuno-regulation through CCR7 expression in T cells plays a role in HDM-specific sensitization in the airway.


Experimental and Molecular Pathology | 2012

Suppressive effects of a pyrazole derivative of curcumin on airway inflammation and remodeling.

Osamu Narumoto; Yukiko Matsuo; Masahiro Sakaguchi; Shunsuke Shoji; Naohide Yamashita; David Schubert; Kazuho Abe; Kazuhide Horiguchi; Takahide Nagase; Naomi Yamashita

To advance the control of airway epithelial cell function and asthma, we investigated the effects of a new curcumin derivative, CNB001, which possesses improved pharmacological properties. Normal human bronchial epithelial (NHBE) cells were stimulated with synthetic double-stranded RNA, Poly(I:C). CNB001 significantly suppressed IL-6, TNF-α, and GM-CSF production by NHBE cells, and did so more effectively than did curcumin or dexamethasone (DEX). CNB001 significantly inhibited the decrease of E-cadherin mRNA expression and increase of vimentin mRNA expression observed in NHBE cells induced by a combination of TGF-β1 and TNF-α, which are markers of airway remodeling. In NHBE cells stimulated by TGF-β1, CNB001 significantly downregulated the level of active serine peptidase inhibitor clade E member (SERPINE) 1, which is also reported to be related to airway remodeling. Whereas DEX alone significantly increased the active SERPINE1 level, the combination of DEX and CNB001 significantly suppressed active SERPINE1. In addition, CNB001 significantly suppressed neutrophil infiltration, IL-6, TNF-α, IL-13 and active SERPINE1 production in bronchoalveolar lavage fluid of the murine asthma model, which was not observed in the case of DEX. In conclusion, the curcumin derivative, CNB001, is a promising candidate to treat asthma associated with neutrophilic airway inflammation and remodeling.


Biochemical and Biophysical Research Communications | 2010

Down-regulation of secreted lymphocyte antigen-6/urokinase-type plasminogen activator receptor-related peptide-1 (SLURP-1), an endogenous allosteric α7 nicotinic acetylcholine receptor modulator, in murine and human asthmatic conditions

Osamu Narumoto; Kazuhide Horiguchi; Satomi Horiguchi; Yasuhiro Moriwaki; Hiromi Takano-Ohmuro; Shunsuke Shoji; Hidemi Misawa; Naohide Yamashita; Takahide Nagase; Koichiro Kawashima; Naomi Yamashita

Whereas acetylcholine (ACh) acts as a bronchoconstrictor and stimulator of mucus secretion from bronchial epithelium, it acts via alpha7 nicotinic Ach receptors (nAChRs) on macrophages in the airways to exert anti-inflammatory effects by reducing synthesis of pro-inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-alpha). Moreover, the effects of ACh are modified by secreted ly-6/urokinase-type plasminogen activator receptor-related peptide-1 (SLURP-1), a positive allosteric modulator of alpha7 nAChR signaling. Our aim was to explore the roles played by SLURP-1 in the pathophysiology of asthma by assessing SLURP-1 expression in the OVA-sensitized murine asthma model and in cultured human bronchial epithelial cells. Using real-time PCR we found that expression of SLURP-1 mRNA is down-regulated in the lungs of asthmatic model mice, as compared to healthy mice. In addition, immunohistochemical studies confirmed the diminished expression of SLURP-1 in the bronchioles of asthmatic mice, and showed it was due to extensive metaplasia of mucus-secreting cells and the concomitant loss of ciliated epithelial cells. Expression of SLURP-1 mRNA and protein was also significantly down-regulated in human epithelial cells stimulated with the pro-inflammatory cytokine interleukin-13 (IL-13), which is related to asthmatic condition. Thus SLURP-1 appears to be down-regulated in both an animal model of asthma and human epithelial cells treated with an inflammatory cytokine related to asthma. Those findings suggest that diminished expression of SLURP-1 in asthma attenuates its negative regulation of airway inflammation, and that perhaps changes in SLURP-1 expression could serve as a marker of airway damage in asthma.


PLOS ONE | 2014

Lymphotoxin β receptor signaling induces IL-8 production in human bronchial epithelial cells.

Yu Mikami; Hirotaka Matsuzaki; Masafumi Horie; Satoshi Noguchi; Taisuke Jo; Osamu Narumoto; Tadashi Kohyama; Hajime Takizawa; Takahide Nagase; Yasuhiro Yamauchi

Asthma-related mortality has been decreasing due to inhaled corticosteroid use, but severe asthma remains a major clinical problem. One characteristic of severe asthma is resistance to steroid therapy, which is related to neutrophilic inflammation. Recently, the tumor necrosis factor superfamily member (TNFSF) 14/LIGHT has been recognized as a key mediator in severe asthmatic airway inflammation. However, the profiles and intracellular mechanisms of cytokine/chemokine production induced in cells by LIGHT are poorly understood. We aimed to elucidate the molecular mechanism of LIGHT-induced cytokine/chemokine production by bronchial epithelial cells. Human bronchial epithelial cells express lymphotoxin β receptor (LTβR), but not herpesvirus entry mediator, which are receptors for LIGHT. LIGHT induced various cytokines/chemokines, such as interleukin (IL)-6, oncostatin M, monocyte chemotactic protein-1, growth-regulated protein α and IL-8. Specific siRNA for LTβR attenuated IL-6 and IL-8 production by BEAS-2B and normal human bronchial epithelial cells. LIGHT activated intracellular signaling, such as mitogen-activated protein kinase and nuclear factor-κB (NF-κB) signaling. LIGHT also induced luciferase activity of NF-κB response element, but not of activator protein-1 or serum response element. Specific inhibitors of phosphorylation of extracellular signal-regulated kinase (Erk) and that of inhibitor κB attenuated IL-8 production, suggesting that LIGHT-LTβR signaling induces IL-8 production via the Erk and NF-κB pathways. LIGHT, via LTβR signaling, may contribute to exacerbation of airway neutrophilic inflammation through cytokine and chemokine production by bronchial epithelial cells.


Biochemical and Biophysical Research Communications | 2013

Effect of secreted lymphocyte antigen-6/urokinase-type plasminogen activator receptor-related peptide-1 (SLURP-1) on airway epithelial cells

Osamu Narumoto; Yuichi Niikura; Satoshi Ishii; Hirofumi Morihara; Saki Okashiro; Takashi Nakahari; Takashi Nakano; Hitoshi Matsumura; Chikao Shimamoto; Yasuhiro Moriwaki; Hidemi Misawa; Naohide Yamashita; Takahide Nagase; Koichiro Kawashima; Naomi Yamashita

Acetylcholine (ACh) exerts various anti-inflammatory effects through α7 nicotinic ACh receptors (nAChRs). We have previously shown that secreted lymphocyte antigen-6/urokinase-type plasminogen activator receptor-related peptide-1 (SLURP-1), a positive allosteric modulator of α7 nAChR signaling, is down-regulated both in an animal model of asthma and in human epithelial cells treated with an inflammatory cytokine related to asthma. Our aim of this study was to explore the effect of SLURP-1, signal through α7 nAChR, in the pathophysiology of airway inflammation. Cytokine production was examined using human epithelial cells. Ciliary beat frequency of murine trachea was measured using a high speed camera. The IL-6 and TNF-α production by human epithelial cells was augmented by siRNA of SLURP-1 and α7 nicotinic ACh receptor. The cytokine production was also dose-dependently suppressed by human recombinant SLURP-1 (rSLURP-1). The ciliary beat frequency and amplitude of murine epithelial cells were augmented by PNU282987, a selective α7 nAChR agonist. Those findings suggested that SLURP-1 and stimulus through α7 nicotinic ACh receptors actively controlled asthmatic condition by stimulating ciliary beating and also by suppressing airway inflammation.


PLOS ONE | 2015

Interleukin-17A and Toll-Like Receptor 3 Ligand Poly(I:C) Synergistically Induced Neutrophil Chemoattractant Production by Bronchial Epithelial Cells

Hirotaka Matsuzaki; Yu Mikami; Kousuke Makita; Hideyuki Takeshima; Masafumi Horie; Satoshi Noguchi; Taisuke Jo; Osamu Narumoto; Tadashi Kohyama; Hajime Takizawa; Takahide Nagase; Yasuhiro Yamauchi

Chronic inflammatory airway diseases, such as bronchial asthma and chronic obstructive pulmonary disease, are common respiratory disorders worldwide. Exacerbations of these diseases are frequent and worsen patients’ respiratory condition and overall health. However, the mechanisms of exacerbation have not been fully elucidated. Recently, it was reported that interleukin (IL)-17A might play an important role in neutrophilic inflammation, which is characteristic of such exacerbations, through increased production of neutrophil chemoattractants. Therefore, we hypothesized that IL-17A was involved in the pathogenesis of acute exacerbation, due to viral infection in chronic inflammatory airway diseases. In this study, we assessed chemokine production by bronchial epithelial cells and investigated the underlying mechanisms. Comprehensive chemokine analysis showed that, compared with poly(I:C) alone, co-stimulation of BEAS-2B cells with IL-17A and poly(I:C) strongly induced production of such neutrophil chemoattractants as CXC chemokine ligand (CXCL)8, growth-related oncogene (GRO), and CXCL1. Co-stimulation synergistically induced CXCL8 and CXCL1 mRNA and protein production by BEAS-2B cells and normal human bronchial epithelial cells. Poly(I:C) induced chemokine expression by BEAS-2B cells mainly via Toll-like receptor 3/TIR-domain-containing adapter-inducing interferon-β–mediated signals. The co-stimulation with IL-17A and poly(I:C) markedly activated the p38 and extracellular-signal-regulated kinase 1/2 pathway, compared with poly(I:C), although there was little change in nuclear factor-κB translocation into the nucleus or the transcriptional activities of nuclear factor-κB and activator protein 1. IL-17A promoted stabilization of CXCL8 mRNA in BEAS-2B cells treated with poly(I:C). In conclusion, IL-17A appears to be involved in the pathogenesis of chronic inflammatory airway disease exacerbation, due to viral infection by promoting release of neutrophil chemoattractants from bronchial epithelial cells.


Internal Medicine | 2018

Acute Arterial Thrombosis during Postoperative Adjuvant Cisplatin-based Chemotherapy for Completely Resected Lung Adenocarcinoma

Chihiro Sato; Kenichi Okuda; Hiroyuki Tamiya; Kota Yamamoto; Katsuyuki Hoshina; Osamu Narumoto; Hirokazu Urushiyama; Satoshi Noguchi; Yosuke Amano; Kosuke Watanabe; Akihisa Mitani; Hidenori Kage; Goh Tanaka; Yasuhiro Yamauchi; Daiya Takai; Takahide Nagase

A malignant tumor can cause hypercoagulation and it also often coexists with thrombosis. Cisplatin-based chemotherapy can also induce adverse vascular effects, including arterial thrombosis. We herein report a case of acute arterial thrombosis in a patient undergoing postoperative adjuvant cisplatin-based chemotherapy for completely resected lung cancer. The patient complained of acute leg pain after chemotherapy, and computed tomography revealed multiple thrombi from the thoracic to popliteal arteries. Arterial thrombosis during adjuvant chemotherapy is extremely rare; however, careful clinical observation of patients receiving cisplatin-based chemotherapy is important, because arterial thrombosis, even in the absence of the primary malignant tumor, is possible.


Clinical Respiratory Journal | 2018

Utility of bronchoscopy in the definitive diagnosis of patients with haematological malignancies presenting with radiological abnormalities

Kosuke Makita; Yu Mikami; Hirotaka Matsuzaki; Osamu Narumoto; Daiya Takai; Yutaka Yatomi; Takahide Nagase

Patients with haematological malignancies usually have a plethora of respiratory complications. Bronchoscopy is one of the most important procedures used to diagnose respiratory complications. Despite enormous benefit, patients should be carefully selected for bronchoscopy as the process is invasive; however, there are only few reports evaluating the contributing factors of bronchoscopy that result in the definitive diagnosis of respiratory complications in these patients.


Respiratory medicine case reports | 2017

Successful treatment of pulmonary injury after nitrogen oxide exposure with corticosteroid therapy: A case report and review of the literature

Yasutoshi Kido; Akihisa Mitani; Hideaki Isago; Hideyuki Takeshima; Osamu Narumoto; Goh Tanaka; Yasuhiro Yamauchi; Daiya Takai; Nobuya Ohishi; Takahide Nagase

Nitrogen oxides are representative chemicals of occupational and environmental exposure, which can lead to fatal pulmonary injury. These oxides are also known to cause delayed occurrence of bronchiolitis obliterans (BO). Herein, we report a case of nitrogen oxide-induced lung injury. A 50-year-old man developed pulmonary edema after nitric acid exposure. Hypoxemia and respiratory failure were immediately improved after introduction of corticosteroid pulse therapy with supplemental oxygen. This was followed by administration of oral prednisolone, and delayed BO did not develop. This case supports the therapeutic efficacy of corticosteroids against pulmonary injury and late-onset BO after nitrogen oxide exposure. Key clinical message Prolonged oral prednisolone might be a potential therapy to prevent delayed onset of bronchiolitis obliterans after nitric acid exposure.

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