ST2 Deletion Increases Inflammatory Bone Destruction in Experimentally Induced Periapical Lesions in Mice

Velickovic, Milena; Pejnović, Nada; Mitrović, Slobodanka; Radosavljević, Gordana; Jovanović, Ivan; Kanjevac, Tatjana; Jovičić, Nemanja; Lukić, Aleksandra

doi:10.1016/j.joen.2014.11.017

Cited by 14 publications

(17 citation statements)

References 29 publications

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“…The data on the role of IL‐33/ST2 signaling in the pathogenesis of periapical lesions are lacking. Our recent results show that IL‐33/ST2 pathway negatively regulates inflammatory bone destruction in experimentally induced periapical lesions in mice by preventing Th1/Th17 cell‐mediated immune responses . Therefore, IL‐33/ST2 signaling might be important for the restriction of proinflammatory immune response in the periapical lesions, which remains to be further elucidated.…”

Section: Discussionmentioning

confidence: 92%

Expression of interleukin‐33 and its receptorST2 in periapical granulomas and radicular cysts

Velickovic¹,

Pejnović²,

Petrović

et al. 2015

J Oral Pathology Medicine

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Section: Discussionmentioning

confidence: 92%

Expression of interleukin‐33 and its receptorST2 in periapical granulomas and radicular cysts

Velickovic¹,

Pejnović²,

Petrović

et al. 2015

J Oral Pathology Medicine

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“…The relationship between the inhibitory characteristic of FoxP3 and the proinflammatory feature of IL-17 in the periapical lesions was also highlighted. However, some of the existing articles 33,34 addressing this issue were excluded from this systematic review because they used animal experiments in their methodology, which limits the extension of the results to humans.…”

Section: Limitationsmentioning

confidence: 99%

Treg and Th17 cells in inflammatory periapical disease: a systematic review

et al. 2017

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The process involved in periapical lesions, which occur as an outcome of pulpal necrosis, is regulated by the immune system including regulatory T cells (Treg) and T helper 17 cell (Th17) responses. The objective of this study was to conduct a frequency systematic review to determine the presence of Treg/Th17 responses and the influence of these cells in the progression of chronic inflammatory periapical lesions in humans. A systematic computerized search was carried out in Pubmed, Medline, Web of Science and Scopus electronic databases from their date of inception through the first week of May 2017. In addition, the reference lists of the included articles and the grey literature were hand-searched. Articles that evaluated the presence and influence of Treg/Th17 in the progression of human periapical lesions were included. Study selection and the quality assessment of the included articles (using the Newcastle-Ottawa scale) were carried out by two authors. Fifty-seven titles/abstracts were screened and eight studies met the eligibility criteria and were included in this systematic review. The included studies showed large variation in the type of periapical lesion assessed, mean age, age range, type of experiment and findings regarding the participation of Th17 and Treg in the status of inflammatory periapical lesions. The studies showed the involvement of Treg in the modulation of the inflammatory response in radicular cysts and periapical granulomas. This systematic review highlights the relationship between Treg and Th17 acting in a subtle balance inhibiting or promoting the progression of human periapical lesions.

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“…On the contrary, we have recently shown that ST2 deletion increases inflammatory bone destruction in experimentally induced periapical lesions in mice. Increased bone loss in ST2-deficient mice was related to increased RANKL/OPG NKL expression and the extent of alveolar ratio, the key indicator of bone resorption, as well as increased number of TRAP-positive osteo-clasts 40 . In addition, in the human model we were the first to demonstrate the expression of IL-33 and ST2 receptor in periapical granulomas and radicular cysts.…”

Section: Significance Of the Obtained Results In Relation To The Avaimentioning

confidence: 92%

“…Nasuprot tome, mi smo nedavno pokazali da delecija ST2 gena povećava inflamatornu destrukciju alveolarne kosti u eksperimentalno indukovanim periapeksnim lezijama kod miševa. Povećani gubitak koštanog tkiva kod ST2 deficijentnih miševa povezan je sa povećanjem RANKL / OPG odnosa, ključnog pokazatelja resorpcije kosti, kao i sa povećanjem broja TRAPpozitivnih osteoklasta 40 . Pored toga, u humanom modelu prvi smo pokazali ekspresiju IL-33 i ST2 receptora u periapeksnim granulomima i radiksnim cistama.…”

Section: Značaj Dobijenih Rezultata U Okviru Dostupnih Naučnih čInjenicaunclassified

Potential effect of IL-33/ST2 signal pathway on alveolar bone loss

Aleksic¹,

Lukić²

2016

Acta stomatologica Naissi

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SažetakUvod: ST2 je član IL-1R familije receptora, dok je interleukin-33 (IL-33) njegov prirodni ligand. Kako se u ekstracelularni prostor oslobađa iz nekrotičnih ćelija, IL-33 može da ima ulogu "alarmina" koji obaveštava imunski sistem o postojanju destrukcije tkiva. S obzirom da je ST2 receptor eksprimiran na gotovo svim ćelijama imunskog sistema, IL-33/ST2 signalni put ima važnu ulogu u patogenezi brojnih bolesti u kojima uglavnom aktivacija ovog puta podstiče razvoj Th2 imunskog odgovora. Protektivna ili proinflamatorna uloga IL-33/ST2 signalne osovine direktno je zavisna od dominantnog imunskog odgovora koji je u osnovi ovih oboljenja. Podaci iz literature o uticaju IL-33/ST2 signalnog puta na resorpciju alveolarne kosti su veoma oskudni. Mi smo ispitali uticaj delecije ST2 gena i administracije IL-33 na periapeksnu inflamatornu destrukciju kosti kod BALB/c miševa. Periapeksne lezije ST2-/miševa sadržale su veći procenat CD4+ T limfocita, CD3+CCR6+ T limfocita, IFN-γ-, IL-17-, TNF-α-i IL-6produkujućih ćelija u okviru gejtovanih CD4+ T limfocita u poređenju sa lezijama WT miševa. Nasuprot tome, administracija IL-33 kod WT miševa prouzrokovala je smanjenje procenta CD4+ T limfocita koji produkuju proinflamatorne citokine i povećanje procenta IL-4-produkujućih ćelija. Zaključak: IL-33/ST2 signalni put negativno reguliše intenzitet periapeksne destrukcije alveolarne kosti prevencijom razvoja Th1/Th17 imunskog odgovora i ukazuju na moguću protektivnu ulogu IL-33 u terapiji gubitka alveolarne kosti. Buduća istraživanja implementiraće novu strategiju lečenja u stomatološku praksu. Klјučne reči: IL-33/ST2 signalni put, alveolarna kost, gubitakAbstract Introduction: ST2 is a member of IL-1R receptor family and interleukin-33 (IL-33) is its natural ligand. IL-33 functions as an "alarmin" released upon necrotic cell death to alert the immune system to tissue damage. As ST2 receptor is expressed on many immune cells, IL-33/ST2 signal pathway has important proinflammatory or protective role in the pathogenesis of numerous diseases. IL-33/ST2 signaling promotes Th2 immune response in allergy, autoimmunity and chronic inflammatory disorders, but its role in the pathogenesis of alveolar bone loss is still unclear. We have investigated the effects of ST2 gene deletion and IL-33 administration on the periapical inflammatory bone destruction in BALB/c mice. We found that periapical lesions in ST2-/-mice are characterized by increased frequencies of CD4+ T cells, CD3+CCR6+ T cells and IFN-γ+, IL-17+, TNF-α+ and IL-6+ cells in gated CD4+ T cells compared with lesions in WT mice. A significant decrease in the percentage of CD4+ T cells producing proinflammatory cytokines and an increase in the percentage of IL-4 producing cells was observed in the periapical lesions in WT mice after IL-33 administration. Conclusion: IL-33/ST2 signaling negatively regulates severity of periapical inflammatory bone destruction by preventing Th1/Th17 cell-mediated immune responses and indicate a possible protective role of IL-33 in the therapy of al...

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ST2 Deletion Increases Inflammatory Bone Destruction in Experimentally Induced Periapical Lesions in Mice

Cited by 14 publications

References 29 publications

Expression of interleukin‐33 and its receptorST2 in periapical granulomas and radicular cysts

Expression of interleukin‐33 and its receptorST2 in periapical granulomas and radicular cysts

Treg and Th17 cells in inflammatory periapical disease: a systematic review

Potential effect of IL-33/ST2 signal pathway on alveolar bone loss

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