• Tuberculosis and Respiratory Diseases
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• v.85 no.4
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• pp.283-288
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• 2022

Asthma is a chronic inflammatory disease of the airways characterized by varying and recurrent symptoms, reversible airway obstruction, and bronchospasm. In this paper, clinical important studies on asthma published between March 2021 and February 2022 were reviewed. A study on the relationship between asthma and chronic rhinosinusitis, bronchiectasis, and hormone replacement therapy was published. A journal on the usefulness of fractional exhaled nitric oxide for the prediction of severe acute exacerbation was also introduced. Studies on the effect of inhaler, one of the most important treatments for asthma, were published. Studies on the control of severe asthma continued. Phase 2 and 3 studies of new biologics were also published. As the coronavirus disease 2019 (COVID-19) pandemic has been prolonged, many studies have explored the prevalence and mortality of COVID-19 infection in asthma patients.

• Genomics & Informatics
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• v.4 no.3
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• pp.103-109
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• 2006

IL-28RA is one of the important candidate genes for complex trait of genetic diseases, but there are only a few published results for this gene. Previously, we identified eighteen SNPs and two variation sites in the entire coding regions of IL-28RA including promoter regions, and suggested that the g.32349G>A polymorphism of IL-28RA might be associated with susceptibility to allergic rhinitis. In this study, we chose seven SNPs (g.-1193A>C, g.-30C>T, g.17654C>T, g.27798A>G, g.31265C>T, g.31911C>T and g.32349G>A) of IL-28RA, and attempted to find out whether these polymorphisms were furtherassociated with genetic predisposition of asthma. We analyzed the genotype and allele frequencies of IL-28RA polymorph isms between the asthma patients and healthy controls. We also investigated the frequencies of haplotype constructed by these SNPs between asthma patients and controls. Our results suggest that the polymorphisms of IL-28RA gene were not associated with susceptibility to asthma, and not with IgE production and eosinophil recruitment. The haplotype frequencies by these SNPs also not significantly associated between the healthy controls and asthma patients. This result indicates that the IL -2BRA polymorphisms might be not associated withasthma susceptibility.

• Journal of Pharmacopuncture
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• v.7 no.3
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• pp.123-129
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• 2004

Nowadays Asthma is considered to be an inflamatory disease characterized by airway hyperresponsiveness and pulmonary eosinophilia. Hominis Placenta is the dried placenta of a healthy women. It has correspondence to the meridians of lung and kindey. Hominis Placenta acupuncture therapy has effect on invigoration of vital energy nourishing blood and tonifying the essence. It can be applied to the disease as Asthma, pulmonary tuberculosis, chronic hepatitis, liver cirrhosis, degenerative change and cerebrovascular disease. We treated two patients of Asthma with CVA by Homins Placenta Aqua-Acupuncture. The effect of Homins Placenta Aqua-Acupuncture was assessed by analyzing the pulmonary function test(PFT) and Quality of Life Questionnaire for adult Korean Asthmatics(QLQAKA) in patients before and after treatment. Total score was increased. The patients are satisfied our treatment. But further research concerning this is still necessary.

• Biomolecules & Therapeutics
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• v.8 no.2
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• pp.107-112
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• 2000

To investigate the alteration of airway mucin in airway disease patients, immunoassay procedures were employed using monoclonal antibodies HM02 and HM03 (Hybridoma, 18,457-463, 1999). Alteration of mucin release was determined by ELISA and the integrity of mucin was determined by Western blot. In ELISA, it was found that mucin release increased from pneumonia, chronic cough, bronchiectasis, eosinophilic pneumonia, lung cancer and bronchial asthma patients. In Western blot, the increase in immunoreactivity was observed in case of pneumonia, chronic cough, bronchiectasis and bronchial asthma. In bronchial asthma, there was no obvious degradation of mucin while in other diseases, varying degree of mucin degradation was observed. The data from the present study implicate that HMO2 and HM03 are suitable for the immunological analysis of mucin in airway disease patients. The role of increased mucin release and varying degree of mucin degradation on airway diseases should be further investigated in the future.

• IMMUNE NETWORK
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• v.21 no.4
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• pp.25.1-25.16
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• 2021

Asthma is a heterogeneous disease whose development is shaped by a variety of environmental and genetic factors. While several recent studies suggest that microbial dysbiosis in the gut may promote asthma, little is known about the relationship between the recently discovered lung microbiome and asthma. Innate lymphoid cells (ILCs) have also been shown recently to participate in asthma. To investigate the relationship between the lung microbiome, ILCs, and asthma, we recruited 23 healthy controls (HC), 42 patients with non-severe asthma, and 32 patients with severe asthma. Flow cytometry analysis showed severe asthma associated with fewer natural cytotoxicity receptor (NCR)⁺ILC3s in the lung. Similar changes in other ILC subsets, macrophages, and monocytes were not observed. The asthma patients did not differ from the HC in terms of the alpha and beta-diversity of the lung and gut microbiomes. However, lung function correlated positively with both NCR⁺ILC3 frequencies and microbial diversity in the lung. Sputum NCR⁺ILC3 frequencies correlated positively with lung microbiome diversity in the HC, but this relationship was inversed in severe asthma. Together, these data suggest that airway NCR⁺ILC3s may contribute to a healthy commensal diversity and normal lung function.

• Environmental Analysis Health and Toxicology
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• v.20 no.3 s.50
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• pp.209-213
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• 2005

Due to steady increase of childhood asthma, exposure to air toxics including PAHs have been thought as an etiology for the asthma. PAHs -involvement in airway inflammation, such as IgE production, is the potential mechanism of the PAHs-induced asthma. Cytochrome P450s (CYPs), particularly CYP1A1 is known enzyme to metabolite PAHs and to be induced by PAHs. The CYP1A1 expression has been emphasized as an biomarker for PAHs - exposure. The present study was performed to clarify the etiology of childhood asthma with PAHs-exposure using mRNA expression of CYP1A1 . The study Objects were Korean children who were asthma patients (cases) or other hospital controls (N=20; age,3 $\~$ 16; boys,56$\%$). As result, we detected expression of the CYP1A1 in all peripheral blood specimens which were collected from the subjects. Moreover, we found approx. 300 fold-higher expression of the CYP1A1 in the cases than that in the controls (p(<)0.01). When we considered age which was related to Asthma, the above significant trend was somewhat diluted, however, the relation between asthma and the Cypih i expression waL stronger than that between asthma and age (chi square,7.99 vs. 3.34). Therefore, our study supports that PAHs induce or worse childhood asthma and suggests application of expression of the CYP1A1 as an initiation or progress biomarker for PAHs - induced childhood asthma.

• Clinical and Experimental Pediatrics
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• v.59 no.6
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• pp.276-279
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• 2016

Sjogren-Larsson syndrome (SLS) is a rare autosomal recessive neurocutaneous disorder with worldwide incidence of 0.4 per 100,000 people. It is characterized by the triad of congenital ichthyosis, spastic diplegia or quadriplegia, and mental retardation. Herein we report a 2-year-old male child with SLS, asthma, and recurrent pneumonia. SLS was confirmed by a molecular genetics study that revealed a deletion mutation in the ALDH3A2 gene. An ALDH3A2 gene mutation results in dysfunction of the microsomal enzyme fatty aldehyde dehydrogenase and impaired metabolism and accumulation of leukotriene B4, which is a key molecule and a pro-inflammatory mediator in developing allergic diseases, especially asthma. An increased level of leukotriene B4 has been reported in SLS patients. As far as we are aware, this is the first report of SLS associated with asthma and recurrent pneumonia. In conclusion, pediatricians should be aware of and evaluate patients with SLS for possible associated asthma and allergic disorders.

• YAKHAK HOEJI
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• v.54 no.6
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• pp.507-521
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• 2010

Training for asthma patients by professionals has been highly emphasized for patients' self-management. In the present study, three standardized training sessions targeting hospital pharmacists were performed. On the basis of the number of training sessions taken, a non-educated group (CG), an once-educated group (NG), and a twice more-educated group (IG) were allocated. The most frequent errors of using an inhalant were shaking before the use in MDI while taking breathe out before inhaling in the case of DPI, and the total average number of errors were the biggest for CG and the smallest in IG. On comparison in the number of the four symptoms of asthma according to the level of seriousness, it was revealed that the total average number was the biggest in CG and the smallest in IG. In the level of awareness regarding the contents of training for patients, patients over 50 tended to answer that they were aware of education contents, and particularly in mouth rinsing and the use before/after a meal, significant similarity was examined. Regular asthma patient training performed by hospital pharmacists appeared to reduce errors in the inhaler usage, increase the quality of life of an patient, and help a patient remember the contents of the training. Especially among patients over 50, it was found to be more effective and retraining of more than two sessions was requisite.

• Tuberculosis and Respiratory Diseases
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• v.83 no.3
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• pp.234-241
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• 2020

Background: The fractional exhaled nitric oxide (FENO) test is useful in asthma patients. However, a few studies on its usefulness in chronic obstructive pulmonary disease (COPD) patients have been reported. We analyzed the FENO level distribution and clinical characteristics according to the FENO level in COPD patients. Methods: From December 2014 to June 2019, COPD patients who underwent pulmonary function and FENO tests at Chonnam National University Hospital were retrospectively evaluated for FENO, comorbidities, asthma history, blood eosinophil, and pulmonary function test. The high FENO group was defined as those with FENO level>25 parts per billion (ppb). Results: A total of 849 COPD patients (mean age, 70.3±9.4 years) were included. The mean forced expiratory volume at 1 second was 66.5±21.7% and the mean FENO level was 24.3±20.5 ppb. Patients with FENO ≤25 ppb were 572 (67.4%) and those with FENO >25 ppb were 277 (32.6%). Blood eosinophil percentage was significantly higher (4.2±4.8 vs. 2.7±2.5, p<0.001) in patients with the high FENO group than the low FENO group. The high FENO group revealed a significantly higher frequency of patients with blood eosinophil percentage >3% (46.9% vs. 34.8%, p=0.001) and asthma history (25.6% vs. 8.6%, p<0.001) than the lower FENO group. Asthma history, blood eosinophil percentage >3%, and positive bronchodilator response (BDR) were independent risk factors for the high FENO level (adjusted odds ratio [aOR], 3.85; p<0.001; aOR, 1.46; p=0.017; and aOR, 1.57, p=0.034, respectively) in the multivariable analysis. Conclusion: The FENO level distribution varied in COPD patients and the mean FENO value was slightly elevated. Asthma history, eosinophil percent, and positive BDR were independent risk factors for the high FENO level.

• IMMUNE NETWORK
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• v.7 no.1
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• pp.18-25
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• 2007

Background: Although glucocorticoids (GCs) are effective in controlling asthma in the majority of patients, a subset of asthmatics fails to demonstrate a satisfactory response, even to systemic GC therapy. This population is referred to as being "steroid-resistant". The actual mechanism underlying steroid resistance in asthma remains to be elucidated. Methods: We have investigated how dexamethasone (DEX) regulates asthmatic phenotypes in a murine model of asthma, in which mice received i.p. immunization twice, followed by two bronchoprovocations with aerosolized OVA with a one-week interval, which we have recently described. Results: Pretreatment with DEX resulted in an inhibition of NF-${\kappa}B$ activation in asthmatic lungs, and also inhibited bronchoalveolar lavage (BAL) levels of NF-${\kappa}B$-dependent cytokines such as TNF-${\alpha}$ and CC chemokines [eotaxin and monocyte chemotactic protein (MCP)-1]. DEX was effective in suppressing airway hyperresponsiveness (AHR) at 10 h, Th2-dependent asthmatic phenotypes such as airway eosinophilia, BAL levels of Th2 cytokines (IL-5 and IL-13), and mucin production. However, DEX failed to suppress BAL levels of CXC chemokines [macrophage inflammatory protein-2 (MIP-2) and keratinocyte-derived chemokine (KC)] and airway neutrophilia. Conclusion: Airway neutrophilia is among the phenomena observed in patients with severe GC-resistant asthma. This study will provide insight into the molecular basis for airway neutrophila seen in steroid-resistant asthma. Further studies are required to delineate the underlying mechanism of CXC chemokine expression in asthma.