Koichiro Matsumoto

ORCID: 0000-0003-2242-8131
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About
Contact & Profiles
Research Areas
  • Asthma and respiratory diseases
  • Chronic Obstructive Pulmonary Disease (COPD) Research
  • Immune Cell Function and Interaction
  • IL-33, ST2, and ILC Pathways
  • Respiratory and Cough-Related Research
  • Lung Cancer Treatments and Mutations
  • Respiratory viral infections research
  • Neuropeptides and Animal Physiology
  • Cancer Immunotherapy and Biomarkers
  • RNA modifications and cancer
  • Immune Response and Inflammation
  • Respiratory Support and Mechanisms
  • Pediatric health and respiratory diseases
  • Lung Cancer Research Studies
  • interferon and immune responses
  • Inhalation and Respiratory Drug Delivery
  • Neuroscience of respiration and sleep
  • Allergic Rhinitis and Sensitization
  • Air Quality and Health Impacts
  • Tracheal and airway disorders
  • COVID-19 Clinical Research Studies
  • Cancer-related molecular mechanisms research
  • Olfactory and Sensory Function Studies
  • Wave and Wind Energy Systems
  • Sarcoidosis and Beryllium Toxicity Research

Kyushu University
2015-2025

Fukuoka Dental College
2023-2025

Samsung (Japan)
2024-2025

Fukuoka University Hospital
2024-2025

National Institute of Infectious Diseases
2022-2023

National Hospital Organization
2022-2023

Nishikyushu University
2022-2023

Fukuoka University
2022-2023

Nakanishi (Japan)
2022-2023

Nihon Kohden (Japan)
2022

Therapies targeted to the immune checkpoint mediated by PD-1 and PD-L1 show antitumor activity in a subset of patients with non-small cell lung cancer (NSCLC). We have now examined expression its regulation NSCLC positive for EML4-ALK fusion gene.The at protein mRNA levels lines was flow cytometry reverse transcription real-time PCR analysis, respectively. The 134 surgically resected specimens evaluated immunohistochemical analysis.The level higher than those negative gene. Forced Ba/F3...

10.1158/1078-0432.ccr-15-0016 article EN Clinical Cancer Research 2015-05-28

Abstract Background Airway epithelial barrier function is maintained by the formation of tight junctions (TJs) and adherens (AJs). Inhalation cigarette smoke causes airway dysfunction may contribute to pathogenesis chronic lung diseases such as asthma obstructive pulmonary disease (COPD). We assessed effects on expression multiple TJ AJ proteins in bronchial epithelium. also examined whether treatment with glucocorticosteroids (GCSs), long-acting β 2 -agonists (LABAs), human cathelicidin...

10.1186/s12931-019-1226-4 article EN cc-by Respiratory Research 2019-11-09

Although they are known to share pathophysiological processes, the relationship between periodontitis and chronic obstructive pulmonary disease (COPD) is not fully understood. The aim of present study was test hypothesis that associated with a greater risk development COPD, when smoking taken into account. analysis in 5-y follow-up population-based cohort based on 900 community-dwelling Japanese adults (age: 68.8 ± 6.3 [mean SD], 46.0% male) without COPD aged 60 or older at least 1 tooth....

10.1177/0022034519833630 article EN Journal of Dental Research 2019-03-08

Rationale: Several Western studies have reported that participants with preserved ratio impaired spirometry (PRISm) higher risks of airflow limitation (AFL) and death. However, evidence in East Asian populations is limited. Objectives: To investigate the relationship between PRISm death incident AFL a Japanese population. Methods: A total 3,032 community-dwelling aged ⩾40 years were seen follow-up for median 5.3 by annual examinations. Participants classified into lung function categories at...

10.1164/rccm.202110-2302oc article EN cc-by-nc-nd American Journal of Respiratory and Critical Care Medicine 2022-05-12

Abstract In the mucosal immune system, resident dendritic cells are specialized for priming Th2-polarized immunity, whereas Ag-presenting activity of macrophages has been linked with development Th1 phenotype. As an switch toward can protect against Th2-mediated allergic response, this study investigated capacity lung to stimulate responses during secondary exposure inhaled allergen, thereby suppressing airway inflammation in a murine model asthma. Following macrophage depletion...

10.4049/jimmunol.166.3.1471 article EN The Journal of Immunology 2001-02-01

Abstract B7-H1 (PD-L1) and B7-DC (PD-L2) are the ligands for programmed death-1 (PD-1), which is a member of CD28/CTLA-4 family has been implicated in peripheral tolerance. We investigated roles murine OVA-induced allergic asthma model. was constitutively expressed on dendritic cells, macrophages, B T cells lungs naive mice, its expression could be dramatically increased after allergen challenge. In contrast, scarcely but up-regulated challenge, although up-regulation macrophages minimal....

10.4049/jimmunol.172.4.2530 article EN The Journal of Immunology 2004-02-15

Abstract WSX-1 (IL-27R) is a class I cytokine receptor with homology to gp130 and IL-12 receptors typically expressed on CD4+ T lymphocytes. Although previous reports have clarified that IL-27/WSX-1 signaling plays critical roles in both Th1 differentiation attenuation of cell activation proinflammatory production during some bacterial or protozoan infections, little known about the importance cytokine-mediated diseases allergic origin. To this aim, we took advantage WSX-1-deficient...

10.4049/jimmunol.175.4.2401 article EN The Journal of Immunology 2005-08-15

T helper 2 cytokines, including interleukin (IL)-4, IL-5, and IL-13, play a critical role in allergic asthma. These cytokines transmit signals through the Janus kinase/signal transducer activator of transcription (STAT) Ras–extracellular signal-regulated kinase (ERK) signaling pathways. Although suppressor cytokine (SOCS) family proteins have been shown to regulate STAT pathway, mechanism regulating ERK pathway has not clarified. The Sprouty-related Ena/VASP homology 1–domain-containing...

10.1084/jem.20040616 article EN The Journal of Experimental Medicine 2005-01-03

Abstract Recent studies have demonstrated an important role for IL-5-dependent bone marrow eosinophil progenitors in allergic inflammation. However, using anti-IL-5 mAbs human asthmatics failed to suppress lower airway hyperresponsiveness despite suppression of eosinophilia; therefore, it is critical examine the IL-5 and responses pathogenesis disease. To do this, we studied effects deficiency (IL-5−/−) on function as well clinical local events, established experimental murine model...

10.4049/jimmunol.168.6.3017 article EN The Journal of Immunology 2002-03-15

Rationale: Chloride channels have been implicated in the regulation of mucus production epithelial cells. Expression hCLCA1, a calcium-activated chloride channel, has reported to be increased airway epithelium patients with asthma. Interleukin (IL)-13 induces cardinal features bronchial asthma, and glucocorticoids are not sufficient suppress IL-13–induced hyperresponsiveness or goblet cell hyperplasia.Objectives: We studied effects channel inhibitors asthma.Methods: The niflumic acid (NA),...

10.1164/rccm.200410-1420oc article EN American Journal of Respiratory and Critical Care Medicine 2006-03-10

Leukotriene B4 (LTB4) has been implicated in the pathogenesis of allergic diseases. BLT2, a low-affinity LTB4 receptor, is activated by and 12(S)-hydroxyheptadeca-5Z,8E,10E -trienoic acid (12-HHT). Although high-affinity receptor BLT1 shown to exert proinflammatory roles, role BLT2 inflammation not clarified. To study function development asthma, we used mice model ovalbumin (OVA)-induced airway disease. The 12-HHT levels were elevated bronchoalveolar lavage (BAL) fluids...

10.1096/fj.12-217000 article EN The FASEB Journal 2013-04-19

Immune-checkpoint inhibitors (ICIs) have improved clinical outcomes and are becoming a standard treatment for many cancer types. However, these drugs also induce immune-related adverse events, among which interstitial lung disease (ILD) is potentially fatal. The underlying mechanism of ILD induction by ICIs largely unknown. With the use flow cytometry, we determined expression levels immune-checkpoint proteins PD-1, TIM-3, TIGIT, LAG-3 PD-L1 in T cells bronchoalveolar lavage fluid (BALF)...

10.1093/intimm/dxaa022 article EN International Immunology 2020-04-03

Abstract Recent clinical studies have suggested that inhalation of incense smoke (IS) may result in impaired lung function and asthma. However, there is little experimental evidence to link IS with airway hyperresponsiveness (AHR) bronchial epithelial barrier function. Using mouse cell culture models, we evaluated the effects exposure on AHR, expression multiple tight junction (TJ)- adherens junction-associated mRNAs proteins lungs, cells assessed by transepithelial electronic resistance...

10.1038/s41598-021-86745-7 article EN cc-by Scientific Reports 2021-03-31

Interferon (IFN)-γ reduces airway responses after allergen challenge in mice. The mechanisms of this effect are not clear. These studies investigate whether IFN-γ can reverse prolonged IFN-γ–deficient (IFN-γKO) Sensitized mice (IFN-γKO and wild-type [WT]) were challenged with ovalbumin. Airway responsiveness, eosinophils bronchoalveolar lavage fluid, lung lymphocyte subsets (CD4+ CD8+) measured 24 hours 8 weeks challenge. In further experiments, we treated IFN-γKO recombinant starting 4 the...

10.1164/rccm.200202-095oc article EN American Journal of Respiratory and Critical Care Medicine 2002-08-15
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