IL-36γ regulates mediators of tissue homeostasis in epithelial cells
| Autor: | Glen M. Scholz, Paul D. Veith, Eric C. Reynolds, Jacqueline E Heath |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Virulence Factors Immunology Gingiva Inflammation Biology Biochemistry Proinflammatory cytokine 03 medical and health sciences 0302 clinical medicine Lipocalin-2 medicine Bacteroidaceae Infections Immunology and Allergy Homeostasis Humans Molecular Biology Porphyromonas gingivalis Tissue homeostasis Cells Cultured Innate immune system Interleukin-17 Mouth Mucosa Epithelial Cells Hematology biology.organism_classification Cell biology body regions Gingipain 030104 developmental biology Matrix Metalloproteinase 9 030220 oncology & carcinogenesis Interleukin 17 medicine.symptom Interleukin-1 |
| Zdroj: | Cytokine. 119 |
| ISSN: | 1096-0023 |
| Popis: | IL-36 cytokines are critical regulators of mucosal inflammation and homeostasis. IL-36γ regulates the expression of inflammatory cytokines and antimicrobial proteins by gingival epithelial cells (e.g. TIGK cells). Here, we show that IL-36γ also regulates the expression of matrix metalloproteinase 9 (MMP9) and neutrophil gelatinase-associated lipocalin (NGAL), important mediators of antimicrobial immunity and tissue homeostasis in mucosal epithelia. MMP9 and NGAL were not similarly induced by IL-17 or IL-22, thus indicating the importance of IL-36γ in the regulation of MMP9 and NGAL. Mechanistically, MMP9 and NGAL expression was demonstrated to be induced in an IRAK1- and NF-κB-dependent manner. Furthermore, signaling by p38 MAP kinase may enable their expression to be independently regulated by IL-36γ. The stronger IL-36γ-inducible expression of MMP9 and NGAL in terminally differentiating TIGK cells suggests that control of their expression is associated with the maturation of the gingival epithelium. Although MMP9 and NGAL expression in epithelial cells can also be induced by bacteria, their expression in TIGK cells was not induced by the periodontal pathogen Porphyromonas gingivalis, most likely due to antagonism by the gingipain proteinase virulence factors. This study advances our understanding of how IL-36γ may promote oral mucosal immunity and tissue homeostasis, and how this may be dysregulated by bacterial pathogens. |
| Databáze: | OpenAIRE |
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