&lt;b&gt;Increases in IL-33 production by fimbriae and lipopeptide from &lt;/b&gt;&lt;i&gt;&lt;b&gt;Porphyromonas gingivalis&lt;/b&gt;&lt;/i&gt;&lt;b&gt; in mouse bone marrow-derived dendritic cells via Toll-like receptor &lt;/b&gt;&lt;b&gt;2 &lt;/b&gt;

Tada, Hiroyuki; Suzuki, Ryuichi; Nemoto, Eiji; Shimauchi, Hidetoshi; Matsushita, Kazunobu; Takada, Haruhiko

doi:10.2220/biomedres.38.189

“…43 However, whether the amount of IL-33 is increased in the GCF of chronic periodontitis patients is controversial. [44][45][46][47] According to in vitro and in vivo animal experiments, the expression of IL-33 can be induced by gingipain, fimbriae and lipopeptide from P. gingivalis 48,49 and might lead to alveolar bone destruction through a receptor activator of nuclear factor-κB ligand (RANKL)-dependent pathway. 50,51 IL-18 was first recognized as an interferon (IFN)-γ-inducing factor and an activator of NK (natural killer) cells and Th1 cells, which are closely related to type 1 immunity.…”

Section: Pro-inflammatory Cytokines Involved In Periodontitismentioning

confidence: 99%

The cytokine network involved in the host immune response to periodontitis

Pan

¹

,

Wang

²

,

Chen

³

2019

View full text Add to dashboard Cite

Periodontitis is an inflammatory disease involving the destruction of both soft and hard tissue in the periodontal region. Although dysbiosis of the local microbial community initiates local inflammation, over-activation of the host immune response directly activates osteoclastic activity and alveolar bone loss. Many studies have reported on the cytokine network involved in periodontitis and its crucial and pleiotropic effect on the recruitment of specific immunocytes, control of pathobionts and induction or suppression of osteoclastic activity. Nonetheless, particularities in the stimulation of pathogens in the oral cavity that lead to the specific and complex periodontal cytokine network are far from clarified. Thus, in this review, we begin with an up-to-date aetiological hypothesis of periodontal disease and summarize the roles of cytokines in the host immune response. In addition, we also summarize the latest cytokine-related therapeutic measures for periodontal disease.

show abstract

“…demonstrated that TLR4-agonistic LPS derived from Porphyromonas gingivalis did not induce IL-33 expression in dendritic cells, but live P. gingivalis cells induced IL-33 [37], suggesting that P. gingivalis LPS inhibits IL-33-inducing activity in P.…”

Section: Discussionmentioning

confidence: 99%

“…They proposed that LPS recognition by TLR4 inhibits NF-κB and IRF3, the activation of which is known to mediate IL-33 expression. Additionally, Tada et al demonstrated that TLR4agonistic LPS derived from Porphyromonas gingivalis did not induce IL-33 expression in dendritic cells, but live P. gingivalis cells induced IL-33 [37], suggesting that P. gingivalis LPS inhibits IL-33-inducing activity in P. gingivalis cells. These observations suggest that TLR4 signalling inhibits IL-33 expression.…”

Section: Discussionmentioning

confidence: 99%

Citrobacter koseri stimulates dendritic cells to induce IL-33 expression via abundant ATP production

Kataoka

¹

,

Mori

²

,

Into

³

2021

Journal of Medical Microbiology

View full text Add to dashboard Cite

Introduction. Food allergies (FAs) occur due to intestinal immune dysfunction elicited by dysbiotic conditions. It was previously determined by us that Citrobacter species propagate in the faeces of mice with FAs and worsen allergic symptoms by inducing the allergenic cytokine IL-33. Dendritic cells can play important roles in regulation of FA responses. Hypothesis. Citrobacter species propagating in intestines of mice worsen allergic symptoms by stimulating dendritic cells to induce IL-33 expression. Aim. The aim of the present study was to analyse whether C. koseri stimulates dendritic cells to induce IL-33 expression. Methodology. IL-33 expression was evaluated in a DC2.4 mouse dendritic cell line stimulated by live or heat-inactivated C. koseri JCM1658, ATP, LPS extracted from C. koseri JCM1658 or other enterobacteria by real-time PCR. The ATP concentration and number of live bacteria in the culture supernatant were measured simultaneously. Results. Live C. koseri JCM1658 induced higher levels of IL-33 expression than other enterobacteria tested, but such a response was not elicited by heat-inactivated C. koseri JCM1658. LPS extracted from C. koseri JCM1658 did not induce IL-33 expression and suppressed live C. koseri JCM1658-induced IL-33 expression via the activation of Toll-like receptor 4 signalling. Furthermore, ATP produced by C. koseri JCM1658 stimulated dendritic cells to induce IL-33 expression by stimulating the P2X7 receptor, and LPS attenuated extracellular ATP-induced IL-33 expression. C. koseri JCM1658 was observed to proliferate more vigorously and produce more ATP than other enterobacteria. Conclusion. C. koseri acts as an allergenic bacterium through ATP production, stimulating dendritic cells to induce IL-33 expression, while LPS released from inactivated C. koseri JCM1658 attenuates this allergenicity.

show abstract

“…The role of IL-33 in periodontitis remains controversial. IL-33 and ST2 expression are increased in periodontic regions in both humans and mice (Malcolm et al, 2015;Lapérine et al, 2016;Tada et al, 2016), apparently reflecting enhanced expression by oral epithelial cells (Tada et al, 2017;Papathanasiou et al, 2020). In vitro, IL-33 promotes osteoclast (OC) differentiation from human monocytes and peripheral blood mononuclear cells, even in the absence of receptor activator of nuclear factor kappa-B ligand (RANKL) (an OC differentiation factor) (Mun et al, 2010;Eeles et al, 2015).…”

Section: Introductionmentioning

confidence: 99%

IL-33 deficiency suppresses alveolar bone loss in a ligature-induced periodontitis model

Aida

¹

,

Takeda

²

,

Nakae

³

et al. 2023

Biomed. Res.

1

0

View full text Add to dashboard Cite

Interleukin-33 (IL-33) is a member of the IL-1 cytokine family that has been studied primarily in the context of type 2 immune responses. Recent reports suggest that IL-33 also enhances the functions of various immune cells and contributes to the development of different inflammatory diseases. Interestingly, IL-33 and its receptor ST2 axis exerted either inhibitory or promotional effects on alveolar bone loss in various periodontitis models. Using a mouse model of ligature-induced periodontitis, we found that the levels of mRNAs encoding IL-33 and other inflammatory cytokines (IL-1α, IL-1β, IL-6, and TNFα) were augmented in gingival tissues of wild-type (WT) mice, and that the alveolar bone loss amount was lower in IL-33-deficient than WT mice. The numbers and proportions of IFN-γ-producing CD8 + T and regulatory T cells were decreased while those of Th17 cells were increased in the draining lymph nodes of IL-33-deficient mice compared to WT mice. Additionally, the level of RNA encoding an osteoclastogenic molecule, i.e., receptor activator of nuclear factor kappa-B ligand (RANKL), in ligated gingival tissue was higher in IL-33-deficient than WT mice. These results suggest that IL-33 is involved in alveolar bone loss in the ligature-induced periodontitis model, although IL-33 may inhibit osteoclast differentiation.

show abstract

<b>Increases in IL-33 production by fimbriae and lipopeptide from </b><i><b>Porphyromonas gingivalis</b></i><b> in mouse bone marrow-derived dendritic cells via Toll-like receptor </b><b>2 </b>

Cited by 10 publications

References 25 publications

The cytokine network involved in the host immune response to periodontitis

The cytokine network involved in the host immune response to periodontitis

Citrobacter koseri stimulates dendritic cells to induce IL-33 expression via abundant ATP production

IL-33 deficiency suppresses alveolar bone loss in a ligature-induced periodontitis model

Contact Info

Product

Resources

About