Masahiko Kato

Gunma Children's Medical Center, Shibukawa, Gunma Prefecture, Japan

Are you Masahiko Kato?

Claim your profile

Publications (115)332.82 Total impact

  • Journal of Allergy and Clinical Immunology 02/2015; 135(2):AB45. DOI:10.1016/j.jaci.2014.12.1074 · 11.25 Impact Factor
  • Journal of Allergy and Clinical Immunology 02/2015; 135(2):AB144. DOI:10.1016/j.jaci.2014.12.1408 · 11.25 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background: Epidemiological evidence indicates that the age at onset of asthma and allergen sensitization in early life is decreasing in people from Western countries. To explore latent trends, we conducted a retrospective examination of the age at onset of asthma and specific IgE antibodies against inhalant allergens in Japanese asthmatic children. Methods: We conducted a case series study of 103 consecutive children with atopic type of asthma (aged 2 years to 16 years, mean age 9.4 ± 3.4 years). Diagnoses of asthma and allergic rhinitis were defined according to Japanese guidelines. The onset of asthma and allergic rhinitis was also defined as any report of asthma and allergic rhinitis confirmed by a physician. Allergen sensitization was evaluated as specific serum IgE levels for 9 common inhalant allergens in peripheral blood. Atopic type of asthma was defined as a being positive for at least one aeroallergen. Results: Mean age at asthma onset was 2.3 ± 1.9 years, which is slightly lower than that of previous reports, including those published in Japan. A high prevalence rate of up to 80% was found for perennial antigens including Dermatophagoides spp. and house dust, as reported previously. Notably, some of the children aged at 1 year tested positive for these allergens. Conclusions: The age at onset of asthma seems to be decreasing in comparison with previous reports. Furthermore, the age at onset of allergen sensitization against inhalant allergens appears to follow this trend.
    Allergology International 05/2014; 63 Suppl 1(Supplement.1):23-8. DOI:10.2332/allergolint.13-OA-0631
  • Allergology International 05/2014; 63 Suppl 1(Supplement.1):53-6. DOI:10.2332/allergolint.13-LE-0633
  • Journal of Allergy and Clinical Immunology 02/2013; 131(2):AB190. DOI:10.1016/j.jaci.2012.12.1345 · 11.25 Impact Factor
  • International Archives of Allergy and Immunology 01/2013; 161(s2):159-163. DOI:10.1159/000350400 · 2.43 Impact Factor
  • International Archives of Allergy and Immunology 01/2013; 161(s2):129-137. DOI:10.1159/000350427 · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic mucocutaneous candidiasis (CMC) is a heterogeneous group of primary immunodeficiency diseases characterized by chronic and recurrent Candida infections of the skin, nails, and oropharynx. Gain-of-function mutations in STAT1 were very recently shown to be responsible for autosomal-dominant or sporadic cases of CMC. The reported mutations have been exclusively localized in the coiled-coil domain, resulting in impaired dephosphorylation of STAT1. However, recent crystallographic analysis and direct mutagenesis experiments indicate that mutations affecting the DNA-binding domain of STAT1 could also lead to persistent phosphorylation of STAT1. To our knowledge, this study shows for the first time that a DNA-binding domain mutation of c.1153C>T in exon 14 (p.T385M) is the genetic cause of sporadic CMC in two unrelated Japanese patients. The underlying mechanisms involve a gain of STAT1 function due to impaired dephosphorylation as observed in the coiled-coil domain mutations.
    The Journal of Immunology 06/2012; 189(3):1521-6. DOI:10.4049/jimmunol.1200926 · 5.36 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Respiratory syncytial (RS) virus infection is an important exacerbating factor in acute bronchial asthma. However, the precise mechanisms responsible for viral infection-induced exacerbations of asthma are uncertain. To elucidate the role of eosinophilic inflammation in the pathogenesis of virus-induced asthma, we investigated the effects of eosinophil granule proteins on bronchial epithelial cell infected with RS virus. Morphological changes and cytopathic effects in human type II pulmonary alveolar epithelial cells (A549) infected with RS virus and/or eosinophil granule proteins such as major basic protein (MBP), eosinophil peroxidase (EPO), eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN) were observed by microscopy. Apoptosis/necrosis was evaluated by trypan blue exclusion test. We also measured 8 types of phosphorylated proteins in MBP-treated A549 cells infected with RS virus. Although RS virus alone did not affect the cytopathic effects of A549 cells, high concentrations of MBP or a combination of 4 granule proteins resulted in cytopathic effects. MBP or EPO, but not ECP or EDN, induced cytotoxicity and necrosis of the infected A549 cells. Furthermore, MBP induced the phosphorylation of the extracellular signal-regulated kinase (ERK) 1/2, p38 mitogen-activated protein kinase (MAPK), Jun-N-terminal protein kinase (JNK), and signal transducer and activator of transcription (STAT)3 in the infected cells. These results suggest that eosinophil granule proteins, specifically MBP, damage bronchial epithelial cells infected with RS virus and that the MAPK family are involved in these responses, indicating that eosinophilic inflammation might be associated with the pathophysiology of RS virus-induced acute exacerbations of asthma.
    International Archives of Allergy and Immunology 02/2012; 158 Suppl 1(2):11-8. DOI:10.1159/000337752 · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Feeding dysfunction (FD) has recently been considered to comprise a prevalent set of symptoms in eosinophilic gastrointestinal disorders (EGIDs) in young children. We report the case of an 8-month-old girl with an EGID who visited our hospital due to vomiting, poor weight gain and feeding difficulties; her condition was discovered during the examination of the symptoms including FD. Tracheal aspiration and reduced esophageal clearance showed up in a barium swallow test and upper gastrointestinal contrast radiography, respectively. Delayed clearance from the stomach was also detected on gastrointestinal scintigraphy. Gastrointestinal endoscopy and biopsies revealed esophagitis with some eosinophils and duodenitis with eosinophilic inflammation. She was not a likely candidate for eosinophilic esophagitis. On administration of an elemental diet, the patient gained weight. Esophageal and stomach clearance subsequently improved, although the vomiting and FD persisted to some extent. We conclude that it is important to consider other EGIDs as well as eosinophilic esophagitis in the differential diagnosis of FD.
    International Archives of Allergy and Immunology 01/2012; 158 Suppl 1:83-6. DOI:10.1159/000337797 · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Because little information is available on eosinophil activation and cytokine response in virus-induced wheezing, we attempted to detect respiratory viruses and measure eosinophil cationic protein (ECP), and 27 types of cytokines/chemokines in both serum and nasal secretions from children with wheezing. This study was an observational, case-control investigation of 267 subjects, who were visited and/or hospitalized with acute respiratory symptoms (with wheezing: men, 115; women, 59; mean/median age, 3.6/3.0 years) or who were visited for regular physical examination and treatment (non-symptomatic wheezing: men, 48; women, 31; mean/median, 5.0/4.7 years), and 14 control subjects (controls: men, 9; women, 5; mean/median, 3.6/3.7 years). We detected viruses in nasal secretions from 174 patients with acute exacerbations of wheezing using antigen detection kits or reverse transcription-polymerase chain reaction, followed by direct DNA sequencing analysis. We measured peripheral eosinophil counts, and serum concentrations of ECP and 27 cytokines/chemokines using a multiplex bead-based assay in patients with wheezing or non-symptomatic wheezing. We also examined nasal ECP and 27 cytokines/chemokines in patients with wheezing. Of 174 samples from wheezing exacerbations, rhinovirus was detected in 59; respiratory syncytial (RS) virus in 44; enterovirus in 17; other viruses in 19; and no viruses in 35. Serum concentrations of ECP, IL-5, IL-6, IL-1ra, and IP-10 were significantly elevated in rhinovirus-induced wheezing compared with non-symptomatic wheezing. Similarly, serum ECP, IL-5, and IP-10 were significantly higher in rhinovirus-induced wheezing than in controls. On the other hand, IL-1ra and IP-10, but not ECP and IL-5 were significantly higher in RS virus-induced wheezing than in controls. Furthermore, only IL-5 was significantly elevated in the rhinovirus group compared with the RS virus group in both serum and nasal secretions. Different cytokine profile and eosinophil activation might be involved in rhinovirus- and RS virus-induced acute exacerbation of childhood wheezing.
    Pediatric Allergy and Immunology 02/2011; 22(1 Pt 2):e87-94. DOI:10.1111/j.1399-3038.2010.01026.x · 3.86 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Eosinophilic gastrointestinal disorders (EGIDs) are disorders characterized by primary eosinophil inflammation in the gastrointestinal tract. There are a small number of reports of eosinophil infiltration in gastrointestinal tracts presenting as EGIDs in infants. In this study, we present Japanese cases of EGIDs in infants. Five patients diagnosed with or strongly suspected to have EGIDs in our hospital from 2008 to 2010 were reviewed. Radiographic contrast enema examinations and/or endoscopies were performed in 4 and 3 patients, respectively. There were patients with eosinophilic colitis (1 suspected and 2 biopsy-proven), a patient who was suspected of having allergic eosinophilic enterocolitis, and a patient with eosinophilic gastroenteritis associated with pediatric hypereosinophilic syndrome. The causes and clinical findings of patients with intestinal eosinophil inflammation vary. Therefore, deliberate examination and observation are important for patients with infantile EGID.
    International Archives of Allergy and Immunology 01/2011; 155 Suppl 1:40-5. DOI:10.1159/000327264 · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Little information is available on eosinophil activation and the cytokine profile in virus-induced acute exacerbation of bronchial asthma; therefore, we examined the effects of treatments that included systemic corticosteroids on serum eosinophil cationic protein (ECP) and 17 cytokines/chemokines in rhinovirus- and respiratory syncytial (RS) virus-induced acute exacerbation of childhood asthma. We measured the peripheral eosinophil count, as well as the serum levels of ECP and 17 types of cytokines/chemokines (IL-1β, 2, 4, 5, 6, 7, 8, 10, 12, 13, and 17 and IFN-γ, TNF-α, GM-CSF, G-CSF, MCP-1, and MIP-1β), using a multiplex bead-based assay in 21 cases of rhinovirus- and 12 cases of RS virus-induced acute exacerbation of childhood asthma and 13 controls. We also compared the clinical data and the effects of systemic corticosteroids on these responses between rhinovirus and RS virus groups. The serum levels of ECP, IL-5, and IL-6 were significantly elevated in patients with rhinovirus-induced acute exacerbation of asthma compared with controls, while serum IL-1β and IFN-γ were significantly lower in patients with rhinovirus-induced acute exacerbation of asthma than in controls. On the other hand, in RS virus-induced acute exacerbation of asthma, only the peripheral eosinophil count was significantly decreased compared with that in rhinovirus-induced acute exacerbation of asthma and controls. Furthermore, the serum levels of ECP, IL-5, and IL-6 in rhinovirus-induced acute exacerbation of asthma and levels of G-CSF in RS virus-induced acute exacerbation of asthma were significantly reduced after treatments that included systemic corticosteroids, respectively. These results suggest that the effects of systemic corticosteroids on serum ECP and the cytokine profile are different between rhinovirus- and RS virus-induced acute exacerbation of childhood asthma.
    International Archives of Allergy and Immunology 01/2011; 155 Suppl 1:77-84. DOI:10.1159/000327434 · 2.43 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: RSV (respiratory syncytial virus)-induced pneumonia and bronchiolitis may be associated with hyperresponsive conditions, including asthma. Eosinophilic proteins such as MBP (major basic protein) may also be associated with the pathophysiology of asthma. To elucidate the roles of RSV infection and MBP in the pathogenesis of pneumonia with hyperresponsiveness, we investigated the effects of RSV infection and MBP on A549 (alveolar epithelial) cells. CPE (cytopathic effects) in A549 cells were observed by microscopy. Apoptosis and cell death was evaluated by flow cytometric analysis and modified MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] assay. We also measured 15 types of cytokines and chemokines in A549 cell supernatants. Although RSV alone did not affect the CPE of A549, high concentrations of MBP resulted in cell death within 24 h. Combinations of RSV and MBP synergistically induced cell death. In A549 cells infected with RSV alone, the release of GM-CSF (granulocyte-macrophage colony-stimulating factor) was significantly enhanced compared with control cells (no infection). In the cells treated with MBP alone, the production of IL (interleukin)-2, 4, 5, 7, 10, 12, 13, 17, IFN (interferon)-γ, GM-CSF, G-CSF (granulocyte colony-stimulating factor) and MIP (macrophage inflammatory protein)-1β was significantly increased compared with control cells. Notably, the levels of GM-CSF and IL-17 in RSV/MBP-treated cells were significantly higher than those treated with MBP alone. These results suggest that MBP synergistically enhanced the release of various cytokines/chemokines and the cell death of RSV-infected A549 cells, indicating that MBP may be closely associated with the pathophysiology of allergic reactions in bronchiolitis/pneumonia due to RSV.
    Cell Biology International 10/2010; 35(5):467-74. DOI:10.1042/CBI20100255 · 1.64 Impact Factor
  • Pediatrics International 08/2010; 52(4):e196-9. DOI:10.1111/j.1442-200X.2010.03135.x · 0.73 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Various pesticides are considered hazardous to human health. Of particular concern are potential problems of neurotoxicity associated with their use. Cellular toxicity may manifest as a variety of biological events, such as carcinogenesis (mutagenesis) and/or cell death. Recent reports indicate that signaling pathways regulate these cellular events. Thus, the toxicity of pesticides in cells may involve modulation of signaling pathways. In this review, we mainly focus on relationships between cellular events and signaling pathways in various pesticide-affected neural cells. Our data and those of related studies suggest that these pesticides affect both the viability and various signaling pathways of neural cells.
    Toxin Reviews 06/2010; 29(2):43-50. DOI:10.3109/15569543.2010.483533 · 0.84 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Little information is available on eosinophil activation and cytokine/chemokine responses in childhood asthma, thus we examined serum eosinophil cationic protein (ECP) and 27 types of cytokines/chemokines in acute exacerbation of asthma (acute asthma) and stable asthma. We determined peripheral eosinophil count, and the serum levels of ECP and 27 types of cytokines/chemokines (IL-1 beta, IL-1 ra, IL-2, -4, -5, -6, -7, -8, -9, -10, -12, -13, -15 and -17, IFN-gamma, IP-10, TNF-alpha, GM-CSF, G-CSF, MCP-1, MIP-1 alpha and -1 beta, eotaxin, RANTES, PDGF-bb, FGF basic and VEGF) using a multiplex bead-based assay in 85 acute and 79 stable asthma patients, and 14 controls. We also examined the effects of systemic corticosteroids on these responses in acute asthma. Results: The serum levels of ECP, IL-5, -6, -8 and -10, G-CSF, MCP-1, IL-1 ra and IP-10 were significantly elevated in acute compared with stable asthma. Similarly, serum levels of ECP, IL-5 and IP-10 were significantly higher in acute asthma than in controls. Furthermore, in the acute phase, elevated serum levels of ECP, IL-5, IL-6, IL-1 ra and IP-10, but not IL-8, IL-10, G-CSF and MCP-1 were significantly reduced after treatments that included systemic corticosteroids. Eosinophil activation could be induced by acute exacerbation of childhood asthma.
    International Archives of Allergy and Immunology 01/2010; 152 Suppl 1:62-6. DOI:10.1159/000312127 · 2.43 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: To clarify the immune pathophysiology of West syndrome (WS). We measured peripheral blood lymphocyte subset and serum cytokine profiles in 76 WS patients and 26 age-matched controls. Adrenocorticotropic hormone (ACTH) is one of the most effective therapy for WS and presumably immune-modulating; therefore, we compared the measured parameters between before ACTH (pre-ACTH) WS patients and controls, between cryptogenic and symptomatic WS patients before ACTH (pre-ACTH), and between before (pre-ACTH) and after (post-ACTH) ACTH WS patients. The post-ACTH group included those who received the last ACTH dose within 1 month of sampling. CD3+ CD25+, CD19+, and CD19+ CD95+ cells were found to be significantly lower in the pre-ACTH group than in the controls. Interleukin (IL)-1 receptor antagonist (RA), 5, 6, and 15; eotaxin; basic fibroblast growth factor (bFGF); and interferon gamma-inducible protein (IP)-10 levels were higher in pre-ACTH group than in the controls. No significant differences were found between the pre-ACTH cryptogenic and symptomatic groups. CD4+ cells, CD3+ cells, CD4+/8+ ratio, IL-1 beta, IL-12, and macrophage inflammatory protein (MIP)-1 beta were significantly higher in pre-ACTH group than in the post-ACTH group. Our study revealed immunological alterations in WS patients, and these responses were modified by ACTH therapy. Further study is needed to elucidate whether or how the immune system alteration is involved in the pathophysiology of WS.
    Brain & development 11/2009; 32(9):695-702. DOI:10.1016/j.braindev.2009.11.001 · 1.54 Impact Factor
  • Journal of Pediatric Hematology/Oncology 11/2008; 30(10):785-7. DOI:10.1097/MPH.0b013e318180bb33 · 0.96 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Although neutrophils are known to migrate in response to various chemokines and complement factors, the substances involved in the early stages of their transmigration and activation have been poorly characterized to date. Here we report the discovery of a peptide isolated from healthy porcine hearts that activated neutrophils. Its primary structure is H-Leu-Ser-Phe-Leu-Ile-Pro-Ala-Gly-Trp-Val-Leu-Ser-His-Leu-Asp-His-Tyr-Lys-Arg-Ser-Ser-Ala-Ala-OH, and it was indicated to originate from mitochondrial cytochrome c oxidase subunit VIII. This peptide caused chemotaxis at concentrations lower than that inducing beta-hexosaminidase release. Such responses were observed in neutrophilic/granulocytic differentiated HL-60 cells but not in undifferentiated cells, and G(i2)-type G proteins were suggested to be involved in the peptide signaling. Moreover the peptide activated human neutrophils to induce beta-hexosaminidase secretion. A number of other amphipathic neutrophil-activating peptides presumably originating from mitochondrial proteins were also found. The present results suggest that neutrophils monitor such amphipathic peptides including the identified peptide as an initiation signal for inflammation at injury sites.
    Journal of Biological Chemistry 10/2008; 283(45):30596-605. DOI:10.1074/jbc.M803913200 · 4.60 Impact Factor

Publication Stats

1k Citations
332.82 Total Impact Points

Institutions

  • 2004–2012
    • Gunma Children's Medical Center
      Shibukawa, Gunma Prefecture, Japan
  • 2008
    • Tokyo Metropolitan Children's Medical Center
      Edo, Tōkyō, Japan
  • 2006
    • Toho University
      Edo, Tōkyō, Japan
  • 1991–2005
    • Gunma University
      • Department of Pediatrics
      Maebashi, Gunma, Japan
  • 1998
    • Mayo Clinic - Rochester
      Rochester, Minnesota, United States
  • 1993
    • The Heart Lung Center
      Londinium, England, United Kingdom