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ABSTRACT: Airway inflammation is a fundamental feature of bronchial asthma. We examined whether educational guidance using a text on pathophysiology and management of asthma modify airway inflammation of severe asthma.
Eighteen severe persistent asthmatics were enrolled in this study. Evaluation on asthma control using Asthma Control Test (ACT), Asthma Health Questionnaire (AHQ)-Japan), FEV1, percentages of eosinophils and neutrophils in induced sputum were analyzed before and 4 weeks after patient education process.
Following educational guidance, ACT and FEV1 did not improve, but AHQ score significantly improved. Furthermore, percentage of eosinophils in sputum significantly reduced. On the contrary, the percentage of neutrophils in sputum was not changed. In accordance with this lack of the change in neutrophil numbers, neutrophil chemoattractants including IL-8 or CXCR3 in the induced sputum did not change before and after patient guidance.
Educational guidance using a text on pathophysiology and management of asthma provides some effects on quality of life in asthmatic patients and eosinophilic inflammation, however, this procedure does not modify the control status of asthma and neutrophilic inflammation seen with severe asthma.
Arerugī = [Allergy] 02/2012; 61(2):194-203.
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ABSTRACT: Based on clinical and radiological findings, Cottin defined combined pulmonary fibrosis and emphysema (CPFE) as pulmonary emphysema in the upper lungs and interstitial pneumonia in the lower lungs with various radiological patterns. Pathologic findings of CPFE probably corresponded with diffuse interstitial pneumonia with pulmonary emphysema, emphysema with fibrosis, and the combination of both. We described reported radiological findings of CPFE.
Pulmonary medicine. 01/2012; 2012:816541.
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Kazuyuki Nakagome,
Mitsuru Imamura,
Hirokazu Okada,
Kimito Kawahata,
Tsutomu Inoue,
Kumiko Hashimoto,
Hiroaki Harada,
Takehiro Higashi,
Rie Takagi,
Kazuhisa Nakano,
Koichi Hagiwara, Minoru Kanazawa,
Makoto Dohi,
Makoto Nagata,
Sho Matsushita
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ABSTRACT: Allergic airway inflammation is generally considered a Th2-type immune response. Recent studies, however, demonstrated that Th17-type immune responses also play important roles in this process, especially in the pathogenesis of neutrophilic airway inflammation, a hallmark of severe asthma. We previously reported that dendritic cells release dopamine to naive CD4(+) T cells in Ag-specific cell-cell interaction, in turn inducing Th17 differentiation through dopamine D1-like receptor (D1-like-R). D1-like-R antagonist attenuates Th17-mediated diseases such as experimental autoimmune encephalomyelitis and autoimmune diabetes. However, the effect of antagonizing D1-like-R on Th17-mediated airway inflammation has yet to be studied. In this study, we examined whether D1-like-R antagonist suppresses OVA-induced neutrophilic airway inflammation in OVA TCR-transgenic DO11.10 mice and then elucidated the mechanism of action. DO11.10 mice were nebulized with OVA or PBS, and some mice received D1-like-R antagonist orally before OVA nebulization. D1-like-R antagonist significantly suppressed OVA-induced neutrophilic airway inflammation in DO11.10 mice. It also inhibited the production of IL-17 and infiltration of Th17 cells in the lung. Further, D1-like-R antagonist suppressed the production of IL-23 by lung CD11c(+) APCs. In contrast, D1-like-R antagonist did not increase Foxp3(+) regulatory T cells in the lung. D1-like-R antagonist neither suppressed nonspecific LPS-induced neutrophilic airway inflammation nor OVA-induced eosinophilic airway inflammation. These results indicate that D1-like-R antagonist could suppress Th17-mediated neutrophilic airway inflammation, raising the possibility that antagonizing D1-like-R serves as a promising new strategy for treating neutrophil-dominant severe asthma.
The Journal of Immunology 04/2011; 186(10):5975-82. · 5.79 Impact Factor
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Rie Hoshi,
Kazuyuki Nakagome,
Hirotoshi Aoki,
Yotaro Takaku,
Takefumi Yamaguchi,
Tomoyuki Soma,
Fuyumi Nishihara,
Kenichiro Komiyama,
Kouichi Hagiwara, Minoru Kanazawa,
Makoto Nagata
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ABSTRACT: A case involved a 39-year-old female nurse in a health-care facility for elderly individuals requiring long-term care, who presented with insufficient control of bronchial asthma. Although she did not have tinea, she had opportunities for contact with patients who did. Careful interview of history suggested a relationship between asthma exacerbation and workplace, so we measured the specific IgE antibody to Trichophyton and confirmed a positive result. As occupational exposure to Trichophyton was considered as a cause of asthma exacerbations, avoidance of Trichophyton as well as anti-asthma treatment was conducted and symptoms improved. Identification and avoidance of specific allergens is essential for successful long-term management of asthma. However, measurement of specific IgE antibody to Trichophyton is not routinely performed, although this fungus could induce not only tinea, but also asthma. The possibility that occupational exposure to trichophyton could exacerbate asthma symptoms needs to be kept in mind, particularly in the case of nurses who may be in contact with elderly individuals with tinea.
Arerugī = [Allergy] 02/2011; 60(2):207-13.
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Takashi Hirama,
Takefumi Yamaguchi,
Hitoshi Miyazawa,
Tomoaki Tanaka,
Giichi Hashikita,
Etsuko Kishi,
Yoshimi Tachi,
Shun Takahashi,
Keiji Kodama,
Hiroshi Egashira,
Akemi Yokote,
Kunihiko Kobayashi,
Makoto Nagata,
Toshiaki Ishii,
Manabu Nemoto,
Masahiko Tanaka,
Koichi Fukunaga,
Satoshi Morita, Minoru Kanazawa,
Koichi Hagiwara
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ABSTRACT: Commensal organisms are frequent causes of pneumonia. However, the detection of these organisms in the airway does not mean that they are the causative pathogens; they may exist merely as colonizers. In up to 50% cases of pneumonia, the causative pathogens remain unidentified, thereby hampering targeting therapies. In speculating on the role of a commensal organism in pneumonia, we devised the battlefield hypothesis. In the "pneumonia battlefield," the organism-to-human cell number ratio may be an index for the pathogenic role of the organism. Using real-time PCR reactions for sputum samples, we tested whether the hypothesis predicts the results of bacteriological clinical tests for 4 representative commensal organisms: Streptococcus pneumoniae, Haemophilus influenzae, Pseudomonas spp., and Moraxella catarrhalis. The cutoff value for the organism-to-human cell number ratio, above which the pathogenic role of the organism was suspected, was set up for each organism using 224 sputum samples. The validity of the cutoff value was then tested in a prospective study that included 153 samples; the samples were classified into 3 groups, and each group contained 93%, 7%, and 0% of the samples from pneumonia, in which the pathogenic role of Streptococcus pneumoniae was suggested by the clinical tests. The results for Haemophilus influenzae, Pseudomonas spp., and Moraxella catarrhalis were 100%, 0%, and 0%, respectively. The battlefield hypothesis enabled legitimate interpretation of the PCR results and predicted pneumonia in which the pathogenic role of the organism was suggested by the clinical test. The PCR reactions based on the battlefield hypothesis may help to promote targeted therapies for pneumonia. The prospective observatory study described in the current report had been registered to the University Hospital Medical Information Network (UMIN) registry before its initiation, where the UMIN is a registry approved by the International Committee of Medical Journal Editors (ICMJE). The UMIN registry number was UMIN000001118: A prospective study for the investigation of the validity of cutoff values established for the HIRA-TAN system (April 9, 2008).
PLoS ONE 01/2011; 6(9):e24474. · 4.09 Impact Factor
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ABSTRACT: Eosinophils play an important role in the pathogenesis of bronchial asthma and its exacerbation. Recent reports suggest the involvement of IFN-γ-inducible protein of 10 kDa (IP-10) in virus-induced asthma exacerbation. The objective of this study was to examine whether CXCR3 ligands including IP-10 modify the effector functions of eosinophils.
Eosinophils isolated from the blood of healthy donors were stimulated with CXCR3 ligands and their adhesion to rh-ICAM-1 was then measured using eosinophil peroxidase assays. The generation of eosinophil superoxide anion (O2-) was examined based on the superoxide dismutase-inhibitable reduction of cytochrome C. Eosinophil-derived neurotoxin (EDN) release was evaluated to determine whether CXCR3 ligands induced eosinophil degranulation. Cytokine and chemokine production by eosinophils was examined using a Bio-plex assay.
Eosinophil adhesion to ICAM-1 was significantly enhanced by IP-10, which also significantly induced eosinophil O2- generation in the presence of ICAM-1. Both the enhanced adhesion and O2- generation were inhibited by an anti-β2 integrin mAb or an anti-CXCR3 mAb. Other CXCR3 ligands, such as monokine induced by IFN-γ (Mig) and IFN-inducible T cell α chemoattractant (I-TAC), also induced eosinophil adhesion and O2- generation in the presence of ICAM-1. IP-10, but not Mig or I-TAC, increased the release of EDN. IP-10 increased the production of a number of cytokines and chemokines by eosinophils.
These findings suggest that CXCR3 ligands such as IP-10 can directly upregulate the effector functions of eosinophils. These effects might be involved in the activation and infiltration of eosinophils in the airway of asthma, especially in virus-induced asthma exacerbation.
Respiratory research 01/2011; 12:138. · 3.36 Impact Factor
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ABSTRACT: The interaction between allergic rhinitis and bronchial asthma is well known. However, there is little epidemiological data on the relationship between nasal diseases and asthma, especially in Japan.
We administered a questionnaire to 126 patients to examine the frequency of associations between nasal and asthma symptoms in patients with both nasal disease and asthma. We also investigated in which type of patients the asthma symptoms were affected by changes in nasal symptoms.
Thirty-eight patients (30%) were aware that their asthma was worsened by exacerbated nasal disease, and nasal treatment improved asthma in 28 patients (22%). The influence of changes in nasal symptoms on asthma symptoms was stronger in patients lacking good asthma control. The relationship between nasal and asthma symptoms tended to be stronger in patients with sinusitis.
About 30% of patients with nasal disease and asthma reported an association between their nasal and asthma symptoms. Nasal treatment is considered to be important for asthma control, especially in patients with asthma symptoms. These results suggested the important role of comprehensive allergy care in controlling both nasal disease and asthma.
Arerugī = [Allergy] 06/2010; 59(6):688-98.
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ABSTRACT: There is evidence that excessive use of inhalational beta(2)-agonists induces the deterioration of asthma. Although the exact mechanism of this remains to be elucidated, overuse of beta(2)-agonists may impair the Th1/Th2 balance in asthmatic airways. The aim of the present study was to evaluate whether salbutamol, a representative inhalational beta(2)-agonist, modifies the production of Th1- and Th2-type cytokines by mononuclear cells separated from patients with asthma and healthy volunteers.
Peripheral blood mononuclear cells (PBMCs) obtained from 8 healthy volunteers and 10 patients with mild persistent asthma allergic to house dust mites were treated with either salbutamol or medium alone. PBMCs were then stimulated with either medium alone, house dust mite (Dermatophagoides farina, Df) allergen or a combination of ionomycin plus phorbol 12-myristate 13-acetate ester (PMA). Concentrations of IFN-gamma, IL-13, TNF-alpha and RANTES in the cell supernatants were measured using ELISA.
In PBMCs from healthy volunteers, salbutamol did not modify IFN-gamma production, but increased the spontaneous production of IL-13. In contrast, salbutamol significantly inhibited the spontaneous and ionomycin- plus PMA-stimulated production of IFN-gamma by PBMCs from asthmatics. Salbutamol significantly enhanced both spontaneous and Df-induced production of IL-13 by PBMCs from asthmatics. Salbutamol did not modify the production of TNF-alpha. Finally, salbutamol enhanced the production of RANTES induced by Df allergen in asthmatics.
Salbutamol inhibits IFN-gamma and enhances IL-13 production by PBMCs from asthmatics. These effects would promote a Th1/Th2 imbalance in the airways and may therefore contribute to the deterioration of asthma.
International Archives of Allergy and Immunology 01/2010; 152 Suppl 1:32-40. · 2.40 Impact Factor
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ABSTRACT: Most patients with asthma are currently controlled by pharmacotherapeutic means such as inhaled corticosteroid (ICS). However, whether ICS actually induces remission of asthma remains unknown. The present study evaluates changes in airway inflammation and hyperresponsiveness in adult patients with asthma after stopping ICS.
We enrolled 11 patients with allergic asthma (7 males and 4 females; mean age, 52.3 years) who had been asymptomatic and had no exacerbation by low-dose ICS. Airway hyperresponsiveness (AHR) was assessed using methacholine challenge, and induced sputum was evaluated before and every 3 months after ICS cessation during the 1-year follow-up.
Among the 11 asthmatics, AHR increased in 10 (90.9%) and asthma clinically relapsed in 4 (36.4%) within 1 year of ICS cessation. AHR increased in all 7 asthmatics that were sensitized to Dermatophagoides farinae and asthma clinically relapsed in 4 (57.1%) of them. Furthermore, eosinophil numbers and IL-4 concentrations in the sputum significantly increased after ICS cessation.
Remission with normal airway response to methacholine (no AHR) might be rare in adult patients with allergic asthma, and sensitization to house dust mites appears to play an important role in relapse. Therefore, ICS cessation should be carefully considered in patients sensitive to house dust mites. Serial determination of eosinophil counts or IL-4 concentrations in sputum might be appropriate for monitoring and preventing asthma relapse in adults.
International Archives of Allergy and Immunology 01/2010; 152 Suppl 1:41-6. · 2.40 Impact Factor
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Rinako Sadakata,
Atsushi Hatamochi,
Keiji Kodama,
Akiko Kaga,
Takefumi Yamaguchi,
Tomoyuki Soma,
Yutaka Usui,
Makoto Nagata,
Akira Ohtake,
Koichi Hagiwara, Minoru Kanazawa
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ABSTRACT: Ehlers-Danlos syndrome type IV (EDS type IV), vascular type, an autosomal dominant disorder caused by a mutation of the type III procollagen gene (COL3A1) is the most severe form of EDS and often presents with aortic hemorrhage or organ perforation. This report discusses a male patient with EDS type IV with dyspnea due to hemopneumothorax. He had thin skin and hypermobile joints and was clinically confirmed as having EDS type IV. The diagnosis was genetically confirmed by a mutation c.2528 G>A (p.Gly843Glu) in the COL3A1 gene. The position of the mutation has never been reported.
Internal Medicine 01/2010; 49(16):1797-800. · 0.94 Impact Factor
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ABSTRACT: Although adverse reactions to local anesthetics are often diagnosed as local anesthetic allergy, there is evidence that most of these reactions occur via non-allergic mechanisms.
To evaluate allergic reactions to local anesthetics, challenge tests were performed in 20 patients who had a history of adverse events to local anesthetics for whom dental treatment was planned. The diagnostic protocol of this challenge test consisted of skin prick and intracutaneous tests, as well as subsequent incremental subcutaneous challenge tests with local anesthetics such as lidocaine.
17 patients (85%) showed no immediate allergic response to lidocaine, which could then be used for dental treatment. Three patients (15%) reacted positively to lidocaine: one had local erythema at the site of the skin prick, and two reacted to subcutaneous challenge.
The proportion of immediate-type reactions to local anesthetics is small but not rare in patients suspected of having local anesthetic allergy. This result suggests that the diagnostic approach to confirm allergy to local anesthetics is clinically important and requires further study in a larger population.
Arerugī = [Allergy] 07/2009; 58(6):657-64.
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Takashi Ishiguro,
Noboru Takayanagi, Minoru Kanazawa,
Kazuyoshi Kurashima,
Yutaka Yoshii,
Koichiro Yoneda,
Yousuke Miyahara,
Naho Kagiyama,
Daidou Tokunaga,
Hiroo Saito,
Fumiaki Aoki,
Mikio Ubukata,
Tsutomu Yanagisawa,
Yutaka Sugita
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ABSTRACT: We describe the case of a 40-year-old woman who was admitted for dyspnea and pitting edema of the lower extremities. Severe type II respiratory failure and right ventricular heart failure were present. Non-invasive positive pressure ventilation (NIPPV) improved the symptoms and blood gas values. Since the results of respiratory function tests and computed tomography indicated neuromuscular disease, muscle biopsy was performed and nemaline myopathy was diagnosed. NIPPV was necessary due to severe hypoxia and hypercapnia caused by severe hypoventilation during sleep; however, daytime NIPPV was stopped within a few days, and the patient was discharged with instructions to continue NIPPV at night only. Since discharge, she has been followed-up on an outpatient basis for 8 years. Adult-onset nemaline myopathy with respiratory failure and right ventricular heart failure as presenting features is rare, and NIPPV can be useful in such cases.
Nihon Kokyūki Gakkai zasshi = the journal of the Japanese Respiratory Society. 03/2009; 47(2):163-7.
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ABSTRACT: Eosinophils preferentially accumulate at sites of inflammation in the asthmatic airway. Participation of circulating eosinophils in the airway inflammation in asthma involves their interaction with adhesion molecules expressed on the endothelial cell surface and exposure to inflammatory mediators, such as cysteinyl leukotrienes (cysLTs).
To investigate whether interaction of eosinophils with adhesion molecules modifies the functions of these cells induced by cysLTs. Methods: Eosinophils were isolated from the blood of healthy donors, incubated in the EIA plates coated with adhesion proteins, and then exposed to LTD4. The generation of superoxide anion (O2-), adhesion to the plates, and release of eosinophil-derived neutrotoxin (EDN) were evaluated.
Neither VCAM-1 nor LTD4 (100 nM) independently induced eosinophil O2- generation, however, combined exposure to the two molecules synergistically induced eosinophil O2- generation. ICAM-1 by itself induced eosinophil O2- generation, which was enhanced by LTD4. On the contrary, P-selectin did not induce O2- generation, either in the presence or absence of LTD4. LTD4 significantly enhanced eosinophil adhesion to rh-VCAM-1 and rh-ICAM-1, but not to rh-P-selectin. Finally, we observed that combined exposure of eosinophils to LTD4 and VCAM-1 induced the release of EDN.
Combined exposure to VCAM-1 or ICAM-1 and cysLT effectively induces the effector functions of eosinophils. Eosinophil adhesion to and migration across endothelial cells via these specific adhesion proteins and subsequent exposure to cysLTs may be mechanisms underlying activation of the effector functions of eosinophils in the asthmatic airway.
International Archives of Allergy and Immunology 02/2009; 149 Suppl 1:31-8. · 2.40 Impact Factor
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ABSTRACT: There is evidence that eosinophils and neutrophils are simultaneously increased in the airways of some patients with chronic refractory asthma. The mechanisms by which neutrophils accumulate in the airways of asthmatics remain to be elucidated, however, chemoattractants for neutrophils such as CXC chemokines may affect either the accumulation or functional status of neutrophils in such patients. The objective of the present study was to identify the CXC chemokine responsible for the neutrophilic and possibly eosinophilic inflammation observed in the airways of patients with refractory asthma.
Following the inhalation of hypertonic saline, induced sputum was obtained from 14 healthy controls, 16 patients with mild well-controlled nonrefractory asthma, and 14 patients with refractory asthma. Concentrations of CXC chemokines and differential inflammatory cell counts were determined.
The percentages of induced sputum eosinophils were significantly higher both in patients with nonrefractory asthma and in patients with refractory asthma. On the other hand, the percentages of neutrophils were increased only in sputum from patients with refractory asthma. The concentration of IL-8, but not ENA-78 or GRO-alpha, was also significantly increased in induced sputum from patients with refractory asthma. The concentration of IL-8 correlated significantly with the percentages of neutrophils.
The results of the present study suggest that IL-8, but not ENA-78 or GRO-alpha, may contribute to the observation of neutrophilic inflammation in patients with refractory asthma.
International Archives of Allergy and Immunology 02/2009; 149 Suppl 1:87-93. · 2.40 Impact Factor
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Case Reports 01/2009; 2009.
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ABSTRACT: Mucormycosis is an uncommon fungal infection, which generally develops in immunosuppressed hosts. In particular, pulmonary infection by Cunninghamella bertholletiae, a rare species of Mucor, is characterized by invasiveness and high mortality. Herein a case of pulmonary mucormycosis due to C. bertholletiae in a female patient with chronic renal insufficiency, secondary to microscopic polyarteritis, is reported. The patient survived after successful treatment with a cumulative dose of 1508 mg of amphotericin B, phased reduction of glucocorticoid therapy and chest tube drainage of a pneumothorax, without the necessity for surgical intervention. This case demonstrates that conservative therapy may be effective in patients for whom surgical intervention is not an option.
Respirology 04/2008; 13(2):309-11. · 2.42 Impact Factor
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Hitoshi Miyazawa,
Tomoaki Tanaka,
Yoshiaki Nagai,
Masaru Matsuoka,
Akihisa Sutani,
Kiyoshi Udagawa,
Jialing Zhang,
Takashi Hirama,
Yoshitake Murayama,
Nobuyuki Koyama,
Kenji Ikebuchi,
Makoto Nagata, Minoru Kanazawa,
Toshihiro Nukiwa,
Seiichi Takenoshita,
Kunihiko Kobayashi,
Koichi Hagiwara
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ABSTRACT: Mutations in the epidermal growth factor receptor (EGFR) are observed in a fraction of non-small-cell lung cancers (NSCLS). EGFR mutation-positive NSCLS responds to gefitinib. Secondary T790M mutation confers gefitinib resistance to NSCLS. A detection test for the T790M mutation was designed based on the peptide nucleic acid-locked nucleic acid polymerase chain reaction clamp method. The specificity and sensitivity of the test were both greater than 0.99. The test revealed that only a small population of the PC-13 cells carried the T790M mutation. The test also revealed that the T790M mutation was found in none of 151 NSCLC specimens obtained before gefitinib treatment, whereas it was found in four of four specimens obtained from NSCLS that had become refractory to gefitinib. In one patient in whom the L858R-positive EGFR allele was amplified to multiple copies, an L858R-T790M double-mutant allele emerged during the gefitinib therapy. This allele was expressed highly. The T790M mutation detection test based on the peptide nucleic acid-locked nucleic acid polymerase chain reaction clamp method is sensitive and specific, and is applicable to clinical practice. It detects T790M-positive cells in the course of gefitinib treatment, and thus will help to devise therapies effective for T790M-positive NSCLS.
Cancer Science 04/2008; 99(3):595-600. · 3.33 Impact Factor
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ABSTRACT: The use of a budesonide (BUD)/formoterol (FOR) combination (Symbicort) for both maintenance and reliever therapy reduces the exacerbation of asthma better than the traditional fixed-dose regimens. In the early stage of exacerbation, the combination therapy could intervene with the development of subsequent airway inflammation. The objective of the study was to evaluate whether in the early stage of cell activation the use of BUD/FOR combination would modify the adhesion of eosinophils or production of cytokines from mononuclear cells.
Human peripheral blood eosinophils, pretreated with BUD (0.1 microM), FOR (0.1 microM) or BUD/FOR combination for 30 min at 37 degrees C, were stimulated with IL-5, leukotriene D4 or phorbol myristate acetate, and eosinophil adhesion was evaluated using an eosinophil peroxidase assay. BUD (0.1 microM), FOR (0.1 microM) or BUD/FOR combination was added to the peripheral blood mononuclear cells stimulated with ionomycin plus phorbol myristate acetate. Concentrations of IL-5 and RANTES in the cell supernatant were measured using ELISA.
BUD, FOR or BUD/FOR combination did not modify the eosinophil adhesion induced by any stimulators. In contrast, BUD or BUD/FOR combination significantly reduced the productions of IL-5 and RANTES in peripheral blood mononuclear cells (BUD: p < 0.0001, p = 0.027 vs. control; BUD/FOR: p < 0.0001, p = 0.031 vs. control) when the drugs were added 15 min, but not 4 h, following cell stimulation.
In the early stage of exacerbation of asthma, inhaled BUD may suppress the progression of the allergic inflammatory cascade by inhibiting the mononuclear cells. These results also underline the importance of using BUD in rescue inhaler.
International Archives of Allergy and Immunology 01/2008; 146 Suppl 1:22-7. · 2.40 Impact Factor
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Minoru Kanazawa
Nippon rinsho. Japanese journal of clinical medicine 11/2007; 65 Suppl 8:119-25.
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Minoru Kanazawa
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ABSTRACT: Differential diagnosis of chronic obstructive pulmonary disease (COPD) from asthma is not a difficult task for many clinicians. Patients with COPD have a history of heavy smoking and show a slowly progressive dyspnea on exertion and there is little variability in symptoms, and they show a poor response to bronchodilators and corticosteroids. Asthma usually begins in early childhood with atopy, shows episodic dyspnea with wheezing, especially during night and early morning. Some patients, however, show adult onset, irreversible airflow limitation, and neutrophilic airway inflammation. The airway remodeling in asthma may be the cause of confusing pathophysiology. Other diseases showing airway hyperresponsiveness, such as allergic bronchopulmonary aspergillosis, Churg-Strauss syndrome, and left heart failure presenting cardiac asthma, may sometimes show similar clinical pictures to COPD. Chronic airway diseases are also possible candidates for differential diagnosis of COPD. Bronchiectasis, sinobronchial syndrome, diffuse panbronchiolitis, obliterative bronchiolitis, and other chronic airway diseases should be considered. Some interstitial lung diseases, such as smoking-related interstitial lung diseases and lymphangioleiomyomatosis, often show obstructive ventilatory impairment, and therefore should be considered in differential diagnosis of COPD.
Nippon rinsho. Japanese journal of clinical medicine 05/2007; 65(4):675-81.