Autologous Meatal Skin Graft Implantation and Intratympanic Injection of &lt;b&gt;&lt;i&gt;Pseudomonas aeruginosa&lt;/i&gt;&lt;/b&gt;: A New Experimental Mouse Model of Acquired Middle Ear Cholesteatoma

Yu, Shaohua; Chen, Yu Bin; Chen, Qia Xin; Liu, Yi; Jiang, Huai; Zhang, Zhi Gang; Huang, Xi

doi:10.1159/000354348

Cited by 3 publications

(2 citation statements)

References 38 publications

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“…According to the method published by Wolfman et al 37,. Yu Si et al 38. (co-first author) implanted the normal auricle skin into the middle ear of mice and injected 5 μl of Pseudomonas aeruginosa around the implant to mimic the pathogenic process.…”

Section: Discussionmentioning

confidence: 99%

TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation

Jiang

et al. 2016

Sci Rep

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Triggering receptor expressed on myeloid cells (TREM) has been broadly studied in inflammatory disease. However, the expression and function of TREM-2 remain undiscovered in acquired cholesteatoma. The expression of TREM-2 was significantly higher in human acquired cholesteatoma than in normal skin from the external auditory canal, and its expression level was positively correlated with the severity of bone destruction. Furthermore, TREM-2 was mainly expressed on dendritic cells (DCs). In human acquired cholesteatoma, the expression of proinflammatory cytokines (IL-1β, TNF-α and IL-6) and matrix metalloproteinases (MMP-2, MMP-8 and MMP-9) were up-regulated, and their expression levels were positively correlated with TREM-2 expression. Osteoclasts were activated in human acquired cholesteatoma. In an animal model, TREM-2 was up-regulated in mice with experimentally acquired cholesteatoma. TREM-2 deficiency impaired the maturation of experimentally acquired cholesteatoma and protected against bone destruction induced by experimentally acquired cholesteatoma. Additional data showed that TREM-2 up-regulated IL-1β and IL-6 expression via TLR4 instead of the TLR2 signaling pathway and promoted MMP-2 and MMP-8 secretion and osteoclast activation in experimentally acquired cholesteatoma. Therefore, TREM-2 might enhance acquired cholesteatoma-induced bone destruction by amplifying the inflammatory response via TLR4 signaling pathways and promoting MMP secretion and osteoclast activation.

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Section: Discussionmentioning

confidence: 99%

TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation

Jiang

et al. 2016

Sci Rep

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“…Experimental models of acquired cholesteatoma have been previously described 47 . Briefly, the right tympanic membrane was laterally incised at the pars tensa with a sterile 25-gauge needle, andthe free margin of the tympanic membrane was then rolled into the tympanic cavity.…”

Section: Methodsmentioning

confidence: 99%

TLR4 drives the pathogenesis of acquired cholesteatoma by promoting local inflammation and bone destruction

Chen

et al. 2015

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Acquired cholesteatoma is a chronic inflammatory disease characterized by both hyperkeratinized squamous epithelial overgrowth and bone destruction. Toll-like receptor (TLR) activation and subsequent inflammatory cytokine production are closely associated with inflammatory bone disease. However, the expression and function of TLRs in cholesteatoma remain unclear.We observed inflammatory cell infiltration of the matrix and prematrix of human acquired cholesteatoma, as well as dramatically increased expression of TLR4 and the pro-inflammatory cytokines TNF-α and IL-1β. TLR2 exhibited an up-regulation that was not statistically significant. TLR4 expression in human acquired cholesteatoma correlated with disease severity; the number of TLR4-positive cells increased with an increased degree of cholesteatoma, invasion, bone destruction, and hearing loss. Moreover, TLR4 deficiency was protective against experimental acquired cholesteatoma-driven bone destruction and hearing loss, as it reduced local TNF-α and IL-1β expression and impaired osteoclast formation by decreasing expression of the osteoclast effectors receptor activator of nuclear factor (NF)-κB ligand (RANKL) and tartrate-resistant acid phosphatase (TRAP). TLR2 deficiency did not relieve disease severity, inflammatory responses, or osteoclast formation. Moreover, neither TLR2 nor TLR4 deficiency had an effect on antimicrobial peptides, inducible iNOS,BD-2 expression or bacterial clearance. Therefore, TLR4 may promote cholesteatoma-induced bone destruction and deafness by enhancing inflammatory responses and osteoclastogenesis.

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Bacterial Infections and Osteoclastogenesis Regulators in Men and Women with Cholesteatoma

Likus

Siemianowicz

Markowski

et al. 2015

Arch. Immunol. Ther. Exp.

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One of the most distinct features of middle ear cholesteatoma is bone destruction. Aetiology of cholesteatoma is thought to be multifactorial. Endotoxins produced by bacteria are thought to initiate the inflammation process in the middle ear leading to cholesteatoma. There are physiological differences in bone metabolism between men and women. The aim of our study was the immunohistochemical evaluation of the contents of two key components of the OPG/RANK/RANKL triad-RANKL and OPG in cholesteatoma, to analyse if there are any differences between the sexes and to evaluate the bacteria species isolated from cholesteatoma just before surgical treatment and to evaluate their plausible influence on the expression of OPG and RANKL in cholesteatoma. Twenty-one adult patients with acquired cholesteatoma who underwent surgery were analysed. There were no statistically significant differences in the expression of both regulators of osteoclastogenesis between the sexes. In 38.1 % patients cholesteatoma was not infected, whereas in 61.9 % patients various bacterial infections or mycosis were found. The most frequently isolated species was Pseudomonas aeruginosa (14.29 % infections) followed by Staphylococcus aureus (9.52 % infections). There were no statistically significant differences in expression of both OPG and RANKL between uninfected and infected cholesteatomas.

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Autologous Meatal Skin Graft Implantation and Intratympanic Injection of <b><i>Pseudomonas aeruginosa</i></b>: A New Experimental Mouse Model of Acquired Middle Ear Cholesteatoma

Cited by 3 publications

References 38 publications

TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation

TREM-2 promotes acquired cholesteatoma-induced bone destruction by modulating TLR4 signaling pathway and osteoclasts activation

TLR4 drives the pathogenesis of acquired cholesteatoma by promoting local inflammation and bone destruction

Bacterial Infections and Osteoclastogenesis Regulators in Men and Women with Cholesteatoma

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