A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach
Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R.
BMJ Publishing Group
Published 2018
BMJ Publishing Group
Published 2018
| Publication Date: |
2018-04-07
|
|---|---|
| Publisher: |
BMJ Publishing Group
|
| Print ISSN: |
0017-5749
|
| Electronic ISSN: |
1468-3288
|
| Topics: |
Medicine
|
| Published by: |
| _version_ | 1836398880741130240 |
|---|---|
| autor | Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. |
| beschreibung | Objective Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown. Design To determine candidate genes important in these processes, macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced SPEM (L635-treated) were isolated and RNA sequenced. Effects on metaplasia development after acute parietal cell loss induced by L635 were evaluated in interleukin (IL)-33, IL-33 receptor (ST2) and IL-13 knockout (KO) mice. Results Profiling of metaplasia-associated macrophages in the stomach identified an M2a-polarised macrophage population. Expression of IL-33 was significantly upregulated in macrophages associated with advanced SPEM. L635 induced metaplasia in the stomachs of wild-type mice, but not in the stomachs of IL-33 and ST2 KO mice. While IL-5 and IL-9 were not required for metaplasia induction, IL-13 KO mice did not develop metaplasia in response to L635. Administration of IL-13 to ST2 KO mice re-established the induction of metaplasia following acute parietal cell loss. Conclusions Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages. |
| citation_standardnr | 6228090 |
| datenlieferant | ipn_articles |
| feed_id | 3103 |
| feed_publisher | BMJ Publishing Group |
| feed_publisher_url | http://www.bmj.com/ |
| insertion_date | 2018-04-07 |
| journaleissn | 1468-3288 |
| journalissn | 0017-5749 |
| publikationsjahr_anzeige | 2018 |
| publikationsjahr_facette | 2018 |
| publikationsjahr_intervall | 7984:2015-2019 |
| publikationsjahr_sort | 2018 |
| publisher | BMJ Publishing Group |
| quelle | Gut |
| relation | http://gut.bmj.com/cgi/content/short/67/5/805?rss=1 |
| search_space | articles |
| shingle_author_1 | Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. |
| shingle_author_2 | Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. |
| shingle_author_3 | Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. |
| shingle_author_4 | Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. |
| shingle_catch_all_1 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach Objective Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown. Design To determine candidate genes important in these processes, macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced SPEM (L635-treated) were isolated and RNA sequenced. Effects on metaplasia development after acute parietal cell loss induced by L635 were evaluated in interleukin (IL)-33, IL-33 receptor (ST2) and IL-13 knockout (KO) mice. Results Profiling of metaplasia-associated macrophages in the stomach identified an M2a-polarised macrophage population. Expression of IL-33 was significantly upregulated in macrophages associated with advanced SPEM. L635 induced metaplasia in the stomachs of wild-type mice, but not in the stomachs of IL-33 and ST2 KO mice. While IL-5 and IL-9 were not required for metaplasia induction, IL-13 KO mice did not develop metaplasia in response to L635. Administration of IL-13 to ST2 KO mice re-established the induction of metaplasia following acute parietal cell loss. Conclusions Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages. Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. BMJ Publishing Group 0017-5749 00175749 1468-3288 14683288 |
| shingle_catch_all_2 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach Objective Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown. Design To determine candidate genes important in these processes, macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced SPEM (L635-treated) were isolated and RNA sequenced. Effects on metaplasia development after acute parietal cell loss induced by L635 were evaluated in interleukin (IL)-33, IL-33 receptor (ST2) and IL-13 knockout (KO) mice. Results Profiling of metaplasia-associated macrophages in the stomach identified an M2a-polarised macrophage population. Expression of IL-33 was significantly upregulated in macrophages associated with advanced SPEM. L635 induced metaplasia in the stomachs of wild-type mice, but not in the stomachs of IL-33 and ST2 KO mice. While IL-5 and IL-9 were not required for metaplasia induction, IL-13 KO mice did not develop metaplasia in response to L635. Administration of IL-13 to ST2 KO mice re-established the induction of metaplasia following acute parietal cell loss. Conclusions Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages. Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. BMJ Publishing Group 0017-5749 00175749 1468-3288 14683288 |
| shingle_catch_all_3 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach Objective Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown. Design To determine candidate genes important in these processes, macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced SPEM (L635-treated) were isolated and RNA sequenced. Effects on metaplasia development after acute parietal cell loss induced by L635 were evaluated in interleukin (IL)-33, IL-33 receptor (ST2) and IL-13 knockout (KO) mice. Results Profiling of metaplasia-associated macrophages in the stomach identified an M2a-polarised macrophage population. Expression of IL-33 was significantly upregulated in macrophages associated with advanced SPEM. L635 induced metaplasia in the stomachs of wild-type mice, but not in the stomachs of IL-33 and ST2 KO mice. While IL-5 and IL-9 were not required for metaplasia induction, IL-13 KO mice did not develop metaplasia in response to L635. Administration of IL-13 to ST2 KO mice re-established the induction of metaplasia following acute parietal cell loss. Conclusions Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages. Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. BMJ Publishing Group 0017-5749 00175749 1468-3288 14683288 |
| shingle_catch_all_4 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach Objective Alternatively activated macrophages (M2) are associated with the progression of spasmolytic polypeptide-expressing metaplasia (SPEM) in the stomach. However, the precise mechanism(s) and critical mediators that induce SPEM are unknown. Design To determine candidate genes important in these processes, macrophages from the stomach corpus of mice with SPEM (DMP-777-treated) or advanced SPEM (L635-treated) were isolated and RNA sequenced. Effects on metaplasia development after acute parietal cell loss induced by L635 were evaluated in interleukin (IL)-33, IL-33 receptor (ST2) and IL-13 knockout (KO) mice. Results Profiling of metaplasia-associated macrophages in the stomach identified an M2a-polarised macrophage population. Expression of IL-33 was significantly upregulated in macrophages associated with advanced SPEM. L635 induced metaplasia in the stomachs of wild-type mice, but not in the stomachs of IL-33 and ST2 KO mice. While IL-5 and IL-9 were not required for metaplasia induction, IL-13 KO mice did not develop metaplasia in response to L635. Administration of IL-13 to ST2 KO mice re-established the induction of metaplasia following acute parietal cell loss. Conclusions Metaplasia induction and macrophage polarisation after parietal cell loss is coordinated through a cytokine signalling network of IL-33 and IL-13, linking a combined response to injury by both intrinsic mucosal mechanisms and infiltrating M2 macrophages. Petersen, C. P., Meyer, A. R., De Salvo, C., Choi, E., Schlegel, C., Petersen, A., Engevik, A. C., Prasad, N., Levy, S. E., Peebles, R. S., Pizarro, T. T., Goldenring, J. R. BMJ Publishing Group 0017-5749 00175749 1468-3288 14683288 |
| shingle_title_1 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach |
| shingle_title_2 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach |
| shingle_title_3 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach |
| shingle_title_4 | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach |
| timestamp | 2025-06-30T23:34:06.980Z |
| titel | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach |
| titel_suche | A signalling cascade of IL-33 to IL-13 regulates metaplasia in the mouse stomach |
| topic | WW-YZ |
| uid | ipn_articles_6228090 |