The Effects of Interleukin‐10 Depletion In Vivo on the Immune Response to <i>Porphyromonas gingivalis</i> in a Murine Model

Herminajeng, Endang; Sosroseno, Wihaskoro; Bird, P. S.; Seymour, G. J.

doi:10.1902/jop.2001.72.11.1527

Cited by 19 publications

(18 citation statements)

References 39 publications

(53 reference statements)

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“…Also, IL-10 was involved in local B cell response and detected in inflamed gingival tissues [19]. IL-10 could be secreted by T cells, B cells and other periodontal cells [10, 26, 28]. Studies demonstrated that miR-146a inhibition did not change IL-10 production in human gingival fibroblasts [10].…”

Section: Discussionmentioning

confidence: 99%

miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6

Jiang

Deng

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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It has been suggested that microRNAs (miRs) are involved in the immune regulation of periodontitis. However, it is unclear whether and how miRs regulate the function of B cells in the context of periodontitis. This study is to explore the role of miR-146a on the inflammatory cytokine production of B cells challenged by Porphyromonas gingivalis (P. gingivalis) lipopolysaccharide (LPS). Primary B cells were harvested from mouse spleen. Quantitative real-time polymerase chain reaction (qPCR), enzyme-linked immunosorbent assay (ELISA) were used to detect the expression of inflammatory cytokines in B cells in the presence or absence of P. gingivalis LPS and/or miR-146a. Bioinformatics, luciferase reporter assay and overexpression assay were used to explore the binding target of miR-146a. Our results showed that miR-146a level in B cells was elevated by P. gingivalis LPS stimulation, and the mRNA expressions of interleukin (IL)-1β, 6 and 10, and IL-1 receptor associated kinase-1 (IRAK1), but not TNF receptor associated factor 6 (TRAF6), were also upregulated. The expression levels of IL-1β, 6, 10 and IRAK1 were reduced in the presence of miR-146a mimic, but were elevated by the addition of miR-146a inhibitor. MiR-146a could bind with IRAK1 3' untranslated region (UTR) but not TRAF6 3'-UTR. Overexpression of IRAK1 reversed the inhibitory effects of miR-146a on IL-1β, 6 and 10. In summary, miR-146a inhibits inflammatory cytokine production in B cells through directly targeting IRAK1, suggesting a regulatory role of miR-146a in B cell-mediated periodontal inflammation.

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Section: Discussionmentioning

confidence: 99%

miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6

Jiang

Deng

et al. 2018

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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“…Together, these results indicated that the cooperative response to IL-10 and CD27/CD70 interactions appeared to regulate B-cell immunoglobulin production Nagumo and Agematsu, 1998;Agematsu et al, 1999). IL-10 is known to augment antibody production in activated B cells in some in vivo systems (Stein et al 1997;Herminajeng et al 2001;Finnegan et al 2003) as well as in some in vitro systems (Kindler and Zubler, 1997;Choe and Choi, 1998;Xu et al 2004).…”

Section: Fig 2 Continuedmentioning

confidence: 91%

IL-10 controls Th2-type cytokine production and eosinophil infiltration in a mouse model of allergic airway inflammation

Kosaka

Tamauchi

Terashima³

et al. 2011

Immunobiology

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“…To investigate the survival rate of the diabetic mice with LPS, Porphyromonas gingivalis LPS (3 mg/kg, LD50 = 30 mg/kg body weight)(Wako) was administered repeatedly intraperitoneally once a week to the STZ-induced diabetic mice which had shown blood glucose levels above 600 mg/dl for four months [26], [27]. The injection was conducted under inhalation anesthesia with 2% isoflurane.…”

Section: Methodsmentioning

confidence: 99%

Expression of Toll-Like Receptor 2 in Glomerular Endothelial Cells and Promotion of Diabetic Nephropathy by Porphyromonas gingivalis Lipopolysaccharide

et al. 2014

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The toll-like receptor (TLR) has been suggested as a candidate cause for diabetic nephropathy. Recently, we have reported the TLR4 expression in diabetic mouse glomerular endothelium. The study here investigates the effects of the periodontal pathogen Porphyromonas gingivalis lipopolysaccharide (LPS) which is a ligand for TLR2 and TLR4 in diabetic nephropathy. In laser-scanning microscopy of glomeruli of streptozotocin- and a high fat diet feed-induced type I and type II diabetic mice, TLR2 localized on the glomerular endothelium and proximal tubule epithelium. The TLR2 mRNA was detected in diabetic mouse glomeruli by in situ hybridization and in real-time PCR of the renal cortex, the TLR2 mRNA amounts were larger in diabetic mice than in non-diabetic mice. All diabetic mice subjected to repeated LPS administrations died within the survival period of all of the diabetic mice not administered LPS and of all of the non-diabetic LPS-administered mice. The LPS administration promoted the production of urinary protein, the accumulation of type I collagen in the glomeruli, and the increases in IL-6, TNF-α, and TGF-β in the renal cortex of the glomeruli of the diabetic mice. It is thought that blood TLR ligands like Porphyromonas gingivalis LPS induce the glomerular endothelium to produce cytokines which aid glomerulosclerosis. Periodontitis may promote diabetic nephropathy.

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The Effects of Interleukin‐10 Depletion In Vivo on the Immune Response to Porphyromonas gingivalis in a Murine Model

Cited by 19 publications

References 39 publications

miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6

miR-146a regulates inflammatory cytokine production in Porphyromonas gingivalis lipopolysaccharide-stimulated B cells by targeting IRAK1 but not TRAF6

IL-10 controls Th2-type cytokine production and eosinophil infiltration in a mouse model of allergic airway inflammation

Expression of Toll-Like Receptor 2 in Glomerular Endothelial Cells and Promotion of Diabetic Nephropathy by Porphyromonas gingivalis Lipopolysaccharide

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