Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring
Abstract The root of asthma can be linked to early life, with prenatal environments influencing risk. We investigate the effects of maternal asthma on the offspring’s lungs during fetal and adult life. Adult offspring of asthmatic mothers show an increase in lung group 2 innate lymphoid cell (ILC2)...
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| Format: | Article |
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Nature Portfolio
2025-01-01
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| Series: | Nature Communications |
| Online Access: | https://doi.org/10.1038/s41467-025-55941-8 |
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| author | Tomoaki Takao Ako Matsui Chie Kikutake Keiko Kan-o Azusa Inoue Mikita Suyama Isamu Okamoto Minako Ito |
| author_facet | Tomoaki Takao Ako Matsui Chie Kikutake Keiko Kan-o Azusa Inoue Mikita Suyama Isamu Okamoto Minako Ito |
| author_sort | Tomoaki Takao |
| collection | DOAJ |
| description | Abstract The root of asthma can be linked to early life, with prenatal environments influencing risk. We investigate the effects of maternal asthma on the offspring’s lungs during fetal and adult life. Adult offspring of asthmatic mothers show an increase in lung group 2 innate lymphoid cell (ILC2) number and function with allergen-induced lung inflammation. Offspring of asthmatic mothers show phenotypic alteration of their lung ILC2s during fetal life, with increased expression of genes related to activation and glucocorticoid signaling. Furthermore, these offspring carry overlapping chromatin-accessible altered regions, including glucocorticoid receptor-binding regions in their lung ILC2s both at the fetal stage and adulthood, suggesting persistent prenatal epigenetic changes. Moreover, maternal exposure to glucocorticoids has similar effects on fetal lung ILC2s and contributes to allergen-induced lung inflammation during adulthood. Thus, asthma during pregnancy may have long-term effects on lung ILC2s in the offspring from the embryonic period, contributing to an increased risk of developing asthma. |
| format | Article |
| id | doaj-art-de4f43cbaf4d4d91b480983530c7a0c4 |
| institution | Kabale University |
| issn | 2041-1723 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Nature Portfolio |
| record_format | Article |
| series | Nature Communications |
| spelling | doaj-art-de4f43cbaf4d4d91b480983530c7a0c42025-01-19T12:31:37ZengNature PortfolioNature Communications2041-17232025-01-0116111610.1038/s41467-025-55941-8Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspringTomoaki Takao0Ako Matsui1Chie Kikutake2Keiko Kan-o3Azusa Inoue4Mikita Suyama5Isamu Okamoto6Minako Ito7Division of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu UniversityDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu UniversityDivision of Bioinformatics, Medical Institute of Bioregulation, Kyushu UniversityDepartment of Respiratory Medicine, Tokyo Women’s Medical UniversityLaboratory for Epigenome Inheritance, RIKEN Center for Integrative Medical SciencesDivision of Bioinformatics, Medical Institute of Bioregulation, Kyushu UniversityDepartment of Respiratory Medicine, Graduate School of Medical Sciences, Kyushu UniversityDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu UniversityAbstract The root of asthma can be linked to early life, with prenatal environments influencing risk. We investigate the effects of maternal asthma on the offspring’s lungs during fetal and adult life. Adult offspring of asthmatic mothers show an increase in lung group 2 innate lymphoid cell (ILC2) number and function with allergen-induced lung inflammation. Offspring of asthmatic mothers show phenotypic alteration of their lung ILC2s during fetal life, with increased expression of genes related to activation and glucocorticoid signaling. Furthermore, these offspring carry overlapping chromatin-accessible altered regions, including glucocorticoid receptor-binding regions in their lung ILC2s both at the fetal stage and adulthood, suggesting persistent prenatal epigenetic changes. Moreover, maternal exposure to glucocorticoids has similar effects on fetal lung ILC2s and contributes to allergen-induced lung inflammation during adulthood. Thus, asthma during pregnancy may have long-term effects on lung ILC2s in the offspring from the embryonic period, contributing to an increased risk of developing asthma.https://doi.org/10.1038/s41467-025-55941-8 |
| spellingShingle | Tomoaki Takao Ako Matsui Chie Kikutake Keiko Kan-o Azusa Inoue Mikita Suyama Isamu Okamoto Minako Ito Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring Nature Communications |
| title | Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring |
| title_full | Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring |
| title_fullStr | Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring |
| title_full_unstemmed | Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring |
| title_short | Maternal asthma imprints fetal lung ILC2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring |
| title_sort | maternal asthma imprints fetal lung ilc2s via glucocorticoid signaling leading to worsened allergic airway inflammation in murine adult offspring |
| url | https://doi.org/10.1038/s41467-025-55941-8 |
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