Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking
Background. IRAK-M, negatively regulating Toll-like receptor, is shown the dual properties in the varied disease contexts. We studied the effect of IRAK-M deficiency on cigarette smoking- (CS-) induced airway inflammation under acute or subacute conditions in a mouse model. Methods. A number of cell...
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| Format: | Article |
| Language: | English |
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Wiley
2017-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/6506953 |
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| author | Haihong Gong Tao Liu Wei Chen Weixun Zhou Jinming Gao |
| author_facet | Haihong Gong Tao Liu Wei Chen Weixun Zhou Jinming Gao |
| author_sort | Haihong Gong |
| collection | DOAJ |
| description | Background. IRAK-M, negatively regulating Toll-like receptor, is shown the dual properties in the varied disease contexts. We studied the effect of IRAK-M deficiency on cigarette smoking- (CS-) induced airway inflammation under acute or subacute conditions in a mouse model. Methods. A number of cellular and molecular techniques were used to detect the differences between IRAK-M knockout (KO) and wild type (WT) mice exposed to 3-day or 7-week CS. Results. Airway inflammation was comparable between IRAK-M KO and WT mice under 3-day CS exposure. Upon short-term CS exposure and lipopolysaccharide (LPS) inhalation, IRAK-M KO mice demonstrated worse airway inflammation, significantly higher percentage of Th17 cells and concentrations of proinflammatory cytokines in the lungs, and significantly elevated expression of costimulatory molecules CD40 and CD86 by lung dendritic cells (DCs) or macrophages. Conversely, 7-week CS exposed IRAK-M KO mice demonstrated significantly attenuated airway inflammation, significantly lower concentrations of proinflammatory cytokines in the lungs, significantly increased percentage of Tregs, and lower expression of CD11b and CD86 by lung DCs or macrophages. Conclusions. IRAK-M plays distinctive effect on CS-induced airway inflammation, and influences Treg/Th17 balance and expression of costimulatory molecules by DCs and macrophages, depending on duration and intensity of stimulus. |
| format | Article |
| id | doaj-art-7ce988d3007b410d9ee7edbed112a09c |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-7ce988d3007b410d9ee7edbed112a09c2025-02-03T05:57:37ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/65069536506953Effect of IRAK-M on Airway Inflammation Induced by Cigarette SmokingHaihong Gong0Tao Liu1Wei Chen2Weixun Zhou3Jinming Gao4Department of Respiratory Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, ChinaDepartment of Respiratory Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, ChinaDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, ChinaDepartment of Pathology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, ChinaDepartment of Respiratory Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100730, ChinaBackground. IRAK-M, negatively regulating Toll-like receptor, is shown the dual properties in the varied disease contexts. We studied the effect of IRAK-M deficiency on cigarette smoking- (CS-) induced airway inflammation under acute or subacute conditions in a mouse model. Methods. A number of cellular and molecular techniques were used to detect the differences between IRAK-M knockout (KO) and wild type (WT) mice exposed to 3-day or 7-week CS. Results. Airway inflammation was comparable between IRAK-M KO and WT mice under 3-day CS exposure. Upon short-term CS exposure and lipopolysaccharide (LPS) inhalation, IRAK-M KO mice demonstrated worse airway inflammation, significantly higher percentage of Th17 cells and concentrations of proinflammatory cytokines in the lungs, and significantly elevated expression of costimulatory molecules CD40 and CD86 by lung dendritic cells (DCs) or macrophages. Conversely, 7-week CS exposed IRAK-M KO mice demonstrated significantly attenuated airway inflammation, significantly lower concentrations of proinflammatory cytokines in the lungs, significantly increased percentage of Tregs, and lower expression of CD11b and CD86 by lung DCs or macrophages. Conclusions. IRAK-M plays distinctive effect on CS-induced airway inflammation, and influences Treg/Th17 balance and expression of costimulatory molecules by DCs and macrophages, depending on duration and intensity of stimulus.http://dx.doi.org/10.1155/2017/6506953 |
| spellingShingle | Haihong Gong Tao Liu Wei Chen Weixun Zhou Jinming Gao Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking Mediators of Inflammation |
| title | Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking |
| title_full | Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking |
| title_fullStr | Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking |
| title_full_unstemmed | Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking |
| title_short | Effect of IRAK-M on Airway Inflammation Induced by Cigarette Smoking |
| title_sort | effect of irak m on airway inflammation induced by cigarette smoking |
| url | http://dx.doi.org/10.1155/2017/6506953 |
| work_keys_str_mv | AT haihonggong effectofirakmonairwayinflammationinducedbycigarettesmoking AT taoliu effectofirakmonairwayinflammationinducedbycigarettesmoking AT weichen effectofirakmonairwayinflammationinducedbycigarettesmoking AT weixunzhou effectofirakmonairwayinflammationinducedbycigarettesmoking AT jinminggao effectofirakmonairwayinflammationinducedbycigarettesmoking |