IL-36 Regulates Neutrophil Chemotaxis and Bone Loss at the Oral Barrier
Tissue-specific mechanisms regulate neutrophil immunity at the oral barrier, which plays a key role in periodontitis. Although it has been proposed that fibroblasts emit a powerful neutrophil chemotactic signal, how this chemotactic signal is driven has not been clear. The objective of this study was to investigate the site-specific regulatory mechanisms by which fibroblasts drive powerful neutrophil chemotactic signals within the oral barrier, with particular emphasis on the role of the IL-36 family. The present study found that IL-36γ, agonist of IL-36R, could promote neutrophil chemotaxis via fibroblast. Single-cell RNA sequencing data disclosed that IL36G is primarily expressed in human and mouse gingival epithelial cells and mouse neutrophils. Notably, there was a substantial increase in IL-36γ levels during periodontitis. In vitro experiments demonstrated that IL-36γ specifically activates gingival fibroblasts, leading to chemotaxis of neutrophils. In vivo experiments revealed that IL-36Ra inhibited the infiltration of neutrophils and bone resorption, while IL-36γ promoted their progression in the ligature-induced periodontitis mouse model. In summary, these data elucidate the function of the site-enriched IL-36γ in regulating neutrophil immunity and bone resorption at the oral barrier. These findings provide new insights into the tissue-specific pathophysiology of periodontitis and offer a promising avenue for prevention and treatment through targeted intervention of the IL-36 family.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:103 |
|---|---|
| Enthalten in: |
Journal of dental research - 103(2024), 4 vom: 27. März, Seite 442-451 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Liu, J [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Cytokines |
|---|
| Anmerkungen: |
Date Completed 28.03.2024 Date Revised 28.03.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1177/00220345231225413 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM369042166 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM369042166 | ||
| 003 | DE-627 | ||
| 005 | 20240329000621.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 240229s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1177/00220345231225413 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1353.xml |
| 035 | |a (DE-627)NLM369042166 | ||
| 035 | |a (NLM)38414292 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Liu, J |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a IL-36 Regulates Neutrophil Chemotaxis and Bone Loss at the Oral Barrier |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 28.03.2024 | ||
| 500 | |a Date Revised 28.03.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Tissue-specific mechanisms regulate neutrophil immunity at the oral barrier, which plays a key role in periodontitis. Although it has been proposed that fibroblasts emit a powerful neutrophil chemotactic signal, how this chemotactic signal is driven has not been clear. The objective of this study was to investigate the site-specific regulatory mechanisms by which fibroblasts drive powerful neutrophil chemotactic signals within the oral barrier, with particular emphasis on the role of the IL-36 family. The present study found that IL-36γ, agonist of IL-36R, could promote neutrophil chemotaxis via fibroblast. Single-cell RNA sequencing data disclosed that IL36G is primarily expressed in human and mouse gingival epithelial cells and mouse neutrophils. Notably, there was a substantial increase in IL-36γ levels during periodontitis. In vitro experiments demonstrated that IL-36γ specifically activates gingival fibroblasts, leading to chemotaxis of neutrophils. In vivo experiments revealed that IL-36Ra inhibited the infiltration of neutrophils and bone resorption, while IL-36γ promoted their progression in the ligature-induced periodontitis mouse model. In summary, these data elucidate the function of the site-enriched IL-36γ in regulating neutrophil immunity and bone resorption at the oral barrier. These findings provide new insights into the tissue-specific pathophysiology of periodontitis and offer a promising avenue for prevention and treatment through targeted intervention of the IL-36 family | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a cytokines | |
| 650 | 4 | |a inflammation | |
| 650 | 4 | |a innate immunity | |
| 650 | 4 | |a neutrophil biology | |
| 650 | 4 | |a pathology | |
| 650 | 4 | |a periodontitis | |
| 650 | 7 | |a Interleukin-1 |2 NLM | |
| 700 | 1 | |a Meng, H |e verfasserin |4 aut | |
| 700 | 1 | |a Mao, Y |e verfasserin |4 aut | |
| 700 | 1 | |a Zhong, L |e verfasserin |4 aut | |
| 700 | 1 | |a Pan, W |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Q |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Journal of dental research |d 1945 |g 103(2024), 4 vom: 27. März, Seite 442-451 |w (DE-627)NLM000005630 |x 1544-0591 |7 nnns |
| 773 | 1 | 8 | |g volume:103 |g year:2024 |g number:4 |g day:27 |g month:03 |g pages:442-451 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1177/00220345231225413 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 103 |j 2024 |e 4 |b 27 |c 03 |h 442-451 | ||