A novel synthetic mycolic Acid inhibits bronchial hyperresponsiveness and allergic inflammation in a mouse model of asthma
Recognition of microbes is important to trigger the innate immune system. Mycolic acid (MA) is a component of the cell walls of mycobacteria such as Mycobacterium bovis Bacillus Calmette-Guerin. MA has immunogenic properties, which may modulate the innate and adaptive immune response. This study aim...
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| Published in: | Allergy, asthma & immunology research Vol. 6; no. 1; pp. 83 - 88 |
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| Language: | English |
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Korea (South)
The Korean Academy of Asthma, Allergy and Clinical Immunology; The Korean Academy of Pediatric Allergy and Respiratory Disease
01-01-2014
대한천식알레르기학회 |
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| Abstract | Recognition of microbes is important to trigger the innate immune system. Mycolic acid (MA) is a component of the cell walls of mycobacteria such as Mycobacterium bovis Bacillus Calmette-Guerin. MA has immunogenic properties, which may modulate the innate and adaptive immune response. This study aimed to investigate whether a novel synthetic MA (sMA) inhibits allergic inflammatory responses in a mouse model of asthma.
BALB/c mice were injected intraperitoneally with sMA followed by sensitization and challenge with ovalbumin (OVA). Mice were examined for bronchial hyperresponsiveness (BHR), the influx of inflammatory cells into the lung tissues, histopathological changes in the lungs and CD4(+)CD25(+)Foxp3(+) T cells in the spleen, and examined the response after the depleting regulatory T cells (Tregs) with an anti-CD25mAb.
Treatment of mice with sMA suppressed the asthmatic response, including BHR, bronchoalveolar inflammation, and pulmonary eosinophilic inflammation. Anti-CD25mAb treatment abrogated the suppressive effects of sMA in this mouse model of asthma and totally depleted CD4(+)CD25(+)Foxp3(+) T cells in the spleen.
sMA attenuated allergic inflammation in a mouse model of asthma, which might be related with CD4(+)CD25(+)Foxp3(+) T cell. |
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| AbstractList | Recognition of microbes is important to trigger the innate immune system. Mycolic acid (MA) is a component of the cell walls of mycobacteria such as Mycobacterium bovis Bacillus Calmette-Guerin. MA has immunogenic properties, which may modulate the innate and adaptive immune response. This study aimed to investigate whether a novel synthetic MA (sMA) inhibits allergic inflammatory responses in a mouse model of asthma.
BALB/c mice were injected intraperitoneally with sMA followed by sensitization and challenge with ovalbumin (OVA). Mice were examined for bronchial hyperresponsiveness (BHR), the influx of inflammatory cells into the lung tissues, histopathological changes in the lungs and CD4(+)CD25(+)Foxp3(+) T cells in the spleen, and examined the response after the depleting regulatory T cells (Tregs) with an anti-CD25mAb.
Treatment of mice with sMA suppressed the asthmatic response, including BHR, bronchoalveolar inflammation, and pulmonary eosinophilic inflammation. Anti-CD25mAb treatment abrogated the suppressive effects of sMA in this mouse model of asthma and totally depleted CD4(+)CD25(+)Foxp3(+) T cells in the spleen.
sMA attenuated allergic inflammation in a mouse model of asthma, which might be related with CD4(+)CD25(+)Foxp3(+) T cell. Purpose: Recognition of microbes is important to trigger the innate immune system. Mycolic acid (MA) is a component of the cell walls of mycobacteria such as Mycobacterium bovis Bacillus Calmette-Guerin. MA has immunogenic properties, which may modulate the innate and adaptive immune response. This study aimed to investigate whether a novel synthetic MA (sMA) inhibits allergic inflammatory responses in a mouse model of asthma. Methods: BALB/c mice were injected intraperitoneally with sMA followed by sensitization and challenge with ovalbumin (OVA). Mice were examined for bronchial hyperresponsiveness (BHR), the influx of inflammatory cells into the lung tissues, histopathological changes in the lungs and CD4+CD25+Foxp3+ T cells in the spleen, and examined the response after the depleting regulatory T cells (Tregs) with an anti-CD25mAb. Results: Treatment of mice with sMA suppressed the asthmatic response, including BHR, bronchoalveolar inflammation, and pulmonary eosinophilic inflammation. Anti-CD25mAb treatment abrogated the suppressive effects of sMA in this mouse model of asthma and totally depleted CD4+CD25+Foxp3+ T cells in the spleen. Conclusions: sMA attenuated allergic inflammation in a mouse model of asthma, which might be related with CD4+CD25+Foxp3+ T cell. KCI Citation Count: 5 PURPOSERecognition of microbes is important to trigger the innate immune system. Mycolic acid (MA) is a component of the cell walls of mycobacteria such as Mycobacterium bovis Bacillus Calmette-Guerin. MA has immunogenic properties, which may modulate the innate and adaptive immune response. This study aimed to investigate whether a novel synthetic MA (sMA) inhibits allergic inflammatory responses in a mouse model of asthma. METHODSBALB/c mice were injected intraperitoneally with sMA followed by sensitization and challenge with ovalbumin (OVA). Mice were examined for bronchial hyperresponsiveness (BHR), the influx of inflammatory cells into the lung tissues, histopathological changes in the lungs and CD4(+)CD25(+)Foxp3(+) T cells in the spleen, and examined the response after the depleting regulatory T cells (Tregs) with an anti-CD25mAb. RESULTSTreatment of mice with sMA suppressed the asthmatic response, including BHR, bronchoalveolar inflammation, and pulmonary eosinophilic inflammation. Anti-CD25mAb treatment abrogated the suppressive effects of sMA in this mouse model of asthma and totally depleted CD4(+)CD25(+)Foxp3(+) T cells in the spleen. CONCLUSIONSsMA attenuated allergic inflammation in a mouse model of asthma, which might be related with CD4(+)CD25(+)Foxp3(+) T cell. |
| Author | Yu, Jinho Seo, Ju-Hee Kang, Mi-Jin Park, Seoung-Ju Kim, Young-Joon Lee, Yong-Chul Jeong, Se Kyoo Jung, Young-Ho Lee, Seung-Hwa Yu, Ho-Sung Kim, Byoung-Ju Kim, Ha-Jung Hong, Soo-Jong |
| AuthorAffiliation | 2 Applied Research Division Neopharm Co., Ltd., Daejeon, Korea 4 Research Center for Standardization of Allergic Diseases, University of Ulsan College of Medicine, Seoul, Korea 7 Research Center for Pulmonary Disorders, Chonbuk National University Medical School, Jeonju, Korea 3 Department of Pediatrics, Childhood Asthma Atopy Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea 6 Department of Pediatrics, Inje University Haeundae Paik Hospital, Busan, Korea 5 Department of Pediatrics, Korea Cancer Center Hospital, Seoul, Korea 1 Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea |
| AuthorAffiliation_xml | – name: 6 Department of Pediatrics, Inje University Haeundae Paik Hospital, Busan, Korea – name: 1 Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea – name: 4 Research Center for Standardization of Allergic Diseases, University of Ulsan College of Medicine, Seoul, Korea – name: 3 Department of Pediatrics, Childhood Asthma Atopy Center, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea – name: 7 Research Center for Pulmonary Disorders, Chonbuk National University Medical School, Jeonju, Korea – name: 5 Department of Pediatrics, Korea Cancer Center Hospital, Seoul, Korea – name: 2 Applied Research Division Neopharm Co., Ltd., Daejeon, Korea |
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| CitedBy_id | crossref_primary_10_1016_j_micpath_2019_103628 crossref_primary_10_14202_vetworld_2017_655_661 crossref_primary_10_4168_aair_2018_10_4_406 crossref_primary_10_3389_fmicb_2022_1009440 crossref_primary_10_4168_aair_2014_6_3_187 crossref_primary_10_1002_celc_201800455 crossref_primary_10_1038_s41598_024_63356_6 |
| Cites_doi | 10.1002/eji.201040719 10.1111/j.1398-9995.2005.00834.x 10.3345/kjp.2008.51.4.343 10.1016/S0140-6736(01)06252-3 10.1016/j.jaci.2004.03.057 10.1128/IAI.68.12.6883-6890.2000 10.1056/NEJMra054308 10.4168/aair.2010.2.2.61 10.1002/eji.200425332 10.1093/intimm/dxn043 10.1164/ajrccm/146.1.109 10.1136/bmj.299.6710.1259 10.3858/emm.2011.43.5.028 10.1164/rccm.200507-1175OC 10.1046/j.1365-2222.2000.00772.x 10.4168/aair.2010.2.3.199 10.1263/jbb.100.429 10.1056/NEJMoa1007302 10.1016/j.coi.2004.01.004 |
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| Copyright | Copyright © 2014 The Korean Academy of Asthma, Allergy and Clinical Immunology • The Korean Academy of Pediatric Allergy and Respiratory Disease 2014 |
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| Keywords | regulatory T cells Mycolic acid allergic inflammation asthma mice |
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| Title | A novel synthetic mycolic Acid inhibits bronchial hyperresponsiveness and allergic inflammation in a mouse model of asthma |
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