IL-18 Receptor Expression on Epithelial Cells is Upregulated by TNF Alpha

Krasna, Eliska; Kolesár, Libor; Slavčev, Antonij; Valhova, Sarka; Kronosova, Bohumira; Jaresova, Marcela; Striz, Ilja

doi:10.1007/s10753-006-8967-1

Cited by 16 publications

(12 citation statements)

References 26 publications

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“…IL-18Rα expression has been demonstrated in renal tubular epithelial cells in vitro, and shown to be upregulated in response to stimulation with TNF-α and other proinflammatory cytokines [12]. Our study has shown that while appreciable levels of IL-18Rα are expressed in glomeruli, IL-18Rα mRNA and protein are undetectable in untreated and stimulated wild-type primary MCs.…”

Section: Discussionmentioning

confidence: 47%

“…IL-18 is also known to induce the production of IL-2, granulocyte-macrophage colony-stimulating factor and IL-2 receptor (α-chain). IL-18 is involved in the pathophysiology of autoimmune disorders such as LN, as well as crescentic glomerulonephritis, diabetic nephropathy and allograft rejection [12,13,14,15,16]. …”

Section: Introductionmentioning

confidence: 99%

“…IL-18 and IL-18 receptor (IL-18R) expression is not restricted to cells of the immune system, but also includes vascular smooth muscle cells [17,18,19], renal tubular epithelial cells [12], podocytes [20] and vascular endothelial cells [18]. A recent study showed that LPS can enhance IL-18 production in mouse MCs [21].…”

Section: Introductionmentioning

confidence: 99%

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Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

Hardy

Hambly²,

Ko³

et al. 2010

Nephron Exp Nephrol

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Background/Aims: Mesangial cell (MC) hyperplasia is associated with several kidney diseases. Experimental studies confirm upregulation of IL-18 in glomerular disease and renal allograft rejection. We evaluated whether MCs express IL-18 and IL-18 receptor-α (IL-18Rα) with and without stimulation by LPS, AngII and PDGF. Methods: Glomeruli were isolated using Dynabeads perfusion. MCs were cultured by glomerular explantation. IL-18 and IL-18Rα expression were detected by RT-PCR, ELISA and flow cytometry. Results: Significantly higher levels of IL-18 expression were detected in isolated glomeruli, compared to cortical tissue devoid of glomeruli, and in MCs, compared to tubular cells (both p < 0.01). Increased IL-18 expression was detected in MCs, but not podocytes, endothelial cells or tubular cells in response to LPS stimulation. IL-18 mRNA and protein expression were significantly upregulated by AngII (p < 0.05) and LPS (p < 0.01), but not PDGF-BB, in primary MCs and a MC line (MES13). IL-18Rα mRNA was almost undetectable in MCs treated with or without LPS, AngII and PDGF-BB. IL-18Rα protein was not detected by flow cytometry. Conclusions: MCs express IL-18, which was significantly increased after LPS and AngII stimulation, but do not express appreciable levels of IL-18Rα. MC-derived IL-18 is unlikely to be an autocrine mediator in glomerular disease given the lack of IL-18Rα.

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Section: Discussionmentioning

confidence: 47%

Section: Introductionmentioning

confidence: 99%

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Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

Hardy

Hambly²,

Ko³

et al. 2010

Nephron Exp Nephrol

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“…Thus, an explanation could be that low levels of IL-18 may be due to the presence of IL-18R in gingival epithelia. It has been reported that the expression of IL-18R on renal and epithelial cell lines can be induced in response to TNF alpha and other proinflammatory cytokines [30]. Another important aspect which may explain the low levels of IL-18 in diabetic patients with PD, is the neutrophils' function in the inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

IL-18 and Anti- <i>P. gingivalis</i> Antibodies in Patients with Diabetes and Chronic Periodontitis

Coralia¹

2016

IJI

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Periodontitis is an important complication in patients with diabetes mellitus. Chronic periodontitis is caused mostly by Porphyromonas gingivalis in Mexico, and by proinflammatory cytokines like IL-1, IL-6, TNFa, and IL-18. The aim of our study was to quantify IL-18 and to detect antibodies against P. gingivalis in gingival crevicular fluid of type 2 diabetes mellitus (T2DM) patients with chronic periodontal disease (PD). We studied a total of 40 patients divided in four groups: group 1 T2DM patients with PD, group 2 T2DM patients without PD, group 3 non-diabetic patients with PD, and a control group of healthy individuals. IL-18 was quantified using a commercial ELISA kit. Detection of IgG and IgM antibodies in gingival crevicular fluid was carried out through ELISA using P. gingivalis semi-purified proteins. Our results showed T2DM patients with chronic PD had low levels of IL-18, whereas non-diabetic patients with chronic PD had the highest. IgM antibodies were detected in diabetic and non-diabetic with chronic PD. IgG antibodies were detected in patients with T2DM and chronic PD, non-diabetic patients with chronic PD, and healthy individuals. In conclusion, IL-18 was detected in low concentrations in gingival crevicular fluid of patients with T2DM and chronic PD. This could be due to a dysregulation of immune-inflammatory responses secondary to diabetes, or by the presence of IL-18 binding protein in gingival fluid. Low levels of IgG antibodies in T2DM patients with PD could be due to the formation of immune complexes, which would explain the greater periodontal damage these patients present.

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“…This cytokine binds to its receptor IL‐18R1 and activates inflammatory signalling pathway (Azam et al, ). The pro‐inflammatory cytokines such as TNF and IL‐1 upregulate IL‐18R1 expression in epithelial cells and enhance IL‐8 secretion (Krásná et al, ).…”

Section: Introductionmentioning

confidence: 99%

Epigenetic and inflammatory events in experimental periodontitis following systemic microbial challenge

Palioto

Finoti

Kinane

et al. 2019

J Clinic Periodontology

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Aim The purpose of this study was to determine inflammatory and epigenetic features following induction of oral and gut dysbiosis in experimental periodontitis in order to examine the interplay between oral and systemic infection. Materials and Methods Periodontitis was induced in 6‐ to 8‐week‐old C57BL/6 mice by (a) Ligature placement (Lig group) (oral challenge); (b) P. gingivalis gavage (Pg group) (systemic challenge); and (c) the combination of the two models oral and systemic challenge (Pg + Lig). The duration of the experiment was 60 days, and the animals were then sacrificed for analyses. Alveolar bone loss was assessed, and a multiplex immunoassay was performed. Maxillae and gut tissues were immunostained for DNMT3b (de novo methylation marker), B and T lymphocyte attenuator (BTLA) and IL‐18R1 (inflammation markers). Results Pg and Pg + Lig groups exhibited higher bone loss when compared to Sham. BAFF, VEGF, RANKL, RANTES and IP‐10 were significantly higher with Pg gavage. Likewise, DNMT3b was overexpressed in both gut and maxilla after the Pg administration. The same pattern was observed for BTLA and IL‐18R1 in gut tissues. Conclusions The systemic microbial challenge either alone or in combination with local challenge leads to distinct patterns of inflammatory and epigenetic features when compared to simply locally induced experimental periodontitis.

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IL-18 Receptor Expression on Epithelial Cells is Upregulated by TNF Alpha

Cited by 16 publications

References 26 publications

Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

IL-18 and Anti- <i>P. gingivalis</i> Antibodies in Patients with Diabetes and Chronic Periodontitis

Epigenetic and inflammatory events in experimental periodontitis following systemic microbial challenge

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IL-18 Receptor Expression on Epithelial Cells is Upregulated by TNF Alpha

Cited by 16 publications

References 26 publications

Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

Stimulation of Mesangial Cells by Angiotensin II and Lipopolysaccharide Increases Expression of Interleukin-18, but Not IL-18 Receptor

IL-18 and Anti- &lt;i&gt;P. gingivalis&lt;/i&gt; Antibodies in Patients with Diabetes and Chronic Periodontitis

Epigenetic and inflammatory events in experimental periodontitis following systemic microbial challenge

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IL-18 and Anti- <i>P. gingivalis</i> Antibodies in Patients with Diabetes and Chronic Periodontitis