Kyushu University Academic Staff Educational and Research Activities Database
Researcher information (To researchers) Need Help? How to update
Keiko Kan-o Last modified date:2023.06.21

Assistant Professor / Department of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu University
Respiratory Medicine
Kyushu University Hospital

Graduate School

E-Mail *Since the e-mail address is not displayed in Internet Explorer, please use another web browser:Google Chrome, safari.
 Reseacher Profiling Tool Kyushu University Pure
Academic Degree
Country of degree conferring institution (Overseas)
Field of Specialization
Respiratory Medicine
ORCID(Open Researcher and Contributor ID)
Total Priod of education and research career in the foreign country
Research Interests
  • Airway epithelial barrier funtion and expression of tight junction proteins
    keyword : airway epithelial barrier funtion・tight junction proteins
  • Virus-induced immune responses in lungs and bronchial epithelial cells
    keyword : virus infection・bronchial pithelial cells・lungs
  • exacerbations of asthma and chronic obstructive pulmonary disease
    keyword : asthma・COPD・exacerbations
Academic Activities
1. Yasuyoshi Washio, Satoko Sakata, Satoru Fukuyama, Takanori Honda, Keiko Kan-o, Mao Shibata, Jun Hata, Hiromasa Inoue, Takanari Kitazono, Koichiro Matsumoto, Toshiharu Ninomiya, Risks of Mortality and Airflow Limitation in Japanese Individuals with Preserved Ratio Impaired Spirometry, American Journal of Respiratory and Critical Care Medicine, 10.1164/rccm.202110-2302oc, 206, 5, 563-572, 2022.09, RATIONALE: Several Western studies have reported that participants with preserved ratio impaired spirometry (PRISm) have higher risks of airflow limitation (AFL) and death. However, evidence in East Asian populations is limited. OBJECTIVES: To investigate the relation between PRISm and the risks of death and incident AFL in a Japanese population. METHODS: A total of 3,032 community-dwelling Japanese participants aged ≥40 years were followed up for a median of 5.3 years by annual spirometry examinations. Participants were classified into lung function categories at baseline as follows: normal spirometry (forced expiratory volume in 1 second/forced vital capacity (FEV1/FVC) ≥0.70 and FEV1 ≥80% predicted), PRISm (≥0.70 and
2. Keiko Kan-o, Yasuyoshi Washio, Tsuguto Fujimoto, Natsuko Shiroyama, Takako Nakano, Kentaro Wakamatsu, Shohei Takata, Makoto Yoshida, Masaki Fujita, Koichiro Matsumoto, Differences in the spectrum of respiratory viruses and detection of human rhinovirus C in exacerbations of adult asthma and chronic obstructive pulmonary disease., Respiratory investigation, 10.1016/j.resinv.2021.08.009, 2021.09, BACKGROUND: Viral respiratory infections are a common cause of acute exacerbations of chronic obstructive pulmonary disease (AECOPD) and asthma. We conducted a multicenter prospective study to determine the differences in the spectrum of viruses between adults with asthma exacerbations and AECOPD and assessed the prevalence and impact of human rhinovirus (HRV)-C in adults, which is more pathogenic in children with asthma than other HRV species. METHODS: Nasopharyngeal and serum samples and clinical information were collected from 64 outpatients with adult asthma exacerbations and 44 outpatients with AECOPD between April 2018 and March 2020. Viral pathogens and HRV strains were identified from nasal samples by multiplex PCR and VP4/VP2 nested PCR. RESULTS: Viral pathogens were identified in 31 patients with asthma exacerbations (48.4%) and 17 patients with AECOPD (38.6%). The most commonly detected viruses were HRV/enterovirus followed by human metapneumovirus (hMPV) in patients with asthma exacerbations, and hMPV followed by parainfluenza virus in patients with AECOPD. HRV-C was the HRV species most commonly associated with both asthma exacerbations and AECOPD. Clinical characteristics, baseline lung function, serum inflammatory chemokines, hospitalization, and systemic steroid use did not differ between HRV-C-positive patients and those positive for other HRV species. CONCLUSIONS: Exacerbation-associated spectrum of viruses differed between adults with asthma exacerbations and AECOPD. HRV-C was the HRV species most often observed in adult asthma exacerbations and AECOPD, although it did not worsen patients' clinical outcomes relative to those of patients with other HRVs. Underlying disease-specific factors may be responsible for susceptibility to respiratory viruses. TRIAL REGISTRATION: UMIN-CTR UMIN000031934..
3. Yamamoto N, Kan-o K, Tatsuta M, Ishii Y, Ogawa T, Shinozaki S, Fukuyama S, Nakanishi Y, Matsumoto K, Incense smoke-induced oxidative stress disrupts tight junctions and bronchial epithelial barrier integrity and induces airway hyperresponsiveness in mouse lungs., Sci Rep. 2021; 11(1):7222., 10.1038/s41598-021-86745-7, 11, 1, 7222-7222, 2021.03.
4. Miyoko Tatsuta, Keiko Kan-o, Yumiko Ishii, Norio Yamamoto, Tomohiro Ogawa, Satoru Fukuyama, Aimi Ogawa, Akitaka Fujita, Yoichi Nakanishi, Koichiro Matsumoto, Effects of cigarette smoke on barrier function and tight junction proteins in the bronchial epithelium: protective role of cathelicidin LL-37, Respiratory Research, 10.1186/s12931-019-1226-4, 20, 1, 251-251, 2019.12, BACKGROUND: Airway epithelial barrier function is maintained by the formation of tight junctions (TJs) and adherens junctions (AJs). Inhalation of cigarette smoke causes airway epithelial barrier dysfunction and may contribute to the pathogenesis of chronic lung diseases such as asthma and chronic obstructive pulmonary disease (COPD). We assessed the effects of cigarette smoke on barrier function and expression of multiple TJ and AJ proteins in the bronchial epithelium. We also examined whether treatment with glucocorticosteroids (GCSs), long-acting β2-agonists (LABAs), and human cathelicidin LL-37 can protect against cigarette smoke extract (CSE)-induced barrier dysfunction. METHODS: Calu-3 cells cultured at the air-liquid interface were pretreated with or without GCSs, LABAs, GCSs plus LABAs, or LL-37, and subsequently exposed to CSE. Barrier function was assessed by transepithelial electronic resistance (TEER) measurements. Gene and protein expression levels of TJ and AJ proteins were analyzed by quantitative PCR and western blotting, respectively. Immunofluorescence staining of TJ and AJ proteins was performed. RESULTS: CSE decreased TEER and increased permeability in a concentration-dependent manner. CSE suppressed gene expression of claudin-1, claudin-3, claudin-4, claudin-7, claudin-15, occludin, E-cadherin, junctional adhesion molecule-A (JAM-A) and zonula occludens-1 (ZO-1) within 12 h post-CSE exposure, while suppressed protein expression levels of occludin at 12 h. CSE-treated cells exhibited discontinuous or attenuated immunostaining for claudin-1, claudin-3, claudin-4, occludin, ZO-1, and E-cadherin compared with untreated cells. GCS treatment partially restored CSE-induced TEER reduction, while LABA treatment had no effect. GCS and LABA combination treatment had no additive effect on CSE-induced TEER reduction and gene suppression of TJ and AJ proteins. Human cathelicidin LL-37 counteracted CSE-induced TEER reduction and prevented disruption of occludin and ZO-1. LL-37 also attenuated CSE-induced decreases in gene and protein expression levels of occludin. CONCLUSIONS: CSE caused airway epithelial barrier dysfunction and simultaneously downregulated multiple TJ and AJ proteins. GCS and LABA combination treatment had no additive effect on CSE-induced TEER reduction. LL-37 counteracted CSE-induced TEER reduction and prevented disruption of occludin and ZO-1. Use of LL-37 to counteract airway epithelial barrier dysfunction may have significant benefits for respiratory diseases such as asthma and COPD..