Glucocorticoids reduce nitric oxide concentration in middle ear effusion from lipopolysaccharide induced otitis media

Pudrith, Charles; Martin, Dusan; Kim, You Hyun; Jahng, Patrick; Kim, Biblia S.; Wall, Michael; Jung, Timothy T. K.

doi:10.1016/j.ijporl.2010.01.008

Cited by 8 publications

(6 citation statements)

References 22 publications

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“…The OME in the present study was induced by LPS, which might represent a different entity. However, it has been reported that LPS-induced experimental OME had symptoms similar to clinical OME (8, 9). …”

Section: Animal Modelsmentioning

confidence: 97%

Comparison of Eardrum Mobility in Acute Otitis Media and Otitis Media With Effusion Models

Guan

Li²,

Gan³

2013

Otology &Amp; Neurotology

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Objective To investigate the eardrum mobility difference between acute otitis media (AOM) and experimental otitis media with effusion (OME). Animal models Thirty-three Hartley guinea pigs were included in this study. The AOM and OME were created by transbullar injection of Streptococcus pneumoniae and lipopolysaccharide into the middle ear, respectively. Main Outcome Measures Three days post inoculation, the morphological changes of the middle ear were assessed with otoscopy and histological sections. Vibrations of the tympanic membrane (TM) at umbo in response to pure tone sound were measured using laser Doppler vibrometry. Results The purulent effusion, ossicular adhesion, and thickened TM and middle ear mucosa were observed in the AOM ears, and the OME ears had serous effusion and less thickened TM and mucosa in the middle ear. The displacement of TM in AOM was lower than that in OME ears, especially at 0.2–4 kHz. Conclusion The TM mobility difference between the AOM and OME ears were mainly caused by the middle ear ossicular structure changes during the bacterial infection in AOM.

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Section: Animal Modelsmentioning

confidence: 97%

Comparison of Eardrum Mobility in Acute Otitis Media and Otitis Media With Effusion Models

Guan

Li²,

Gan³

2013

Otology &Amp; Neurotology

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“…In this context, dexamethasone emerges as an attractive candidate because of its pleiotropic protective properties. In various cell types and animal models it inhibits the induction of MMPs, prostaglandins, inflammatory cytokines, nitric oxide, and other oxygen‐derived radicals . The literature is inconsistent on whether dexamethasone inhibits or promotes apoptosis in different types of cells but, as described below, it protects the viability of chondrocytes exposed to IL‐1.…”

Section: Dexamethasonementioning

confidence: 99%

Intra‐articular dexamethasone to inhibit the development of post‐traumatic osteoarthritis

Grodzinsky

Wang

Kakar

et al. 2017

Journal Orthopaedic Research

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Injury to the joint provokes a number of local pathophysiological changes, including synthesis of inflammatory cytokines, death of chondrocytes, breakdown of the extra-cellular matrix of cartilage and reduced synthesis of matrix macromolecules. These processes combine to engender the subsequent development of post-traumatic osteoarthritis (PTOA). To prevent this from happening, it is necessary to inhibit these disparate responses to injury; given their heterogeneity, this is challenging. However, dexamethasone has the necessary pleiotropic properties required of a drug for this purpose. Using in vitro models, we have shown that low doses of dexamethasone sustain the synthesis of cartilage proteoglycans while inhibiting their breakdown after injurious compression in the presence or absence of inflammatory cytokines. Under these conditions, dexamethasone is non-toxic and maintains the viability of chondrocytes exposed chronically to such cytokines as interleukin (IL)-1, IL-6 and tumor necrosis factor-α. Moreover, the anti-inflammatory properties of dexamethasone have been appreciated for decades. In view of this information, we have initiated a pilot clinical study to determine whether a single, intra-articular injection of dexamethasone into the wrist shows promise in preventing PTOA after intra-articular fracture of the distal radius.

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“…LPS has been shown to produce IL-1β, IL-6, TNFα, COX-1, and COX-2 in the middle ear [27,55,56]. As such, it has been used in numerous studies to induce experimental otitis media [57][58][59]. What is not known is how LPS induces inflammation.…”

Section: Cytokine Production Due To Lipopolysaccharide (Lps)-induced mentioning

confidence: 99%

Cytokine Responses in the Common Cold and Otitis Media

Wine

Alper

2012

Curr Allergy Asthma Rep

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Cytokines are a group of diverse molecules that influence the function of every organ system. They are most well studied in their effects on the immune system and their integral role in mediating inflammation. The common cold and otitis media are two such disease states, and much has been learned about the various effects of cytokines in each disease. Most often the viruses isolated include rhinovirus (RV), respiratory syncytial virus (RSV), adenovirus, coronavirus, and picornavirus. Otitis media, sinusitis, bronchiolitis, pneumonia, and asthma exacerbation are commonly accepted as complications of viral upper respiratory tract infections. Furthermore, otitis media and upper respiratory infections are inextricably linked in that the majority (>70 %) of cases of acute otitis media occur as complications of the common cold. Cytokine polymorphisms have been associated with the severity of colds as well as the frequency of otitis media. This article attempts to update the reader on various studies that have recently been published regarding the role of cytokines in these two disease entities.

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Glucocorticoids reduce nitric oxide concentration in middle ear effusion from lipopolysaccharide induced otitis media

Cited by 8 publications

References 22 publications

Comparison of Eardrum Mobility in Acute Otitis Media and Otitis Media With Effusion Models

Comparison of Eardrum Mobility in Acute Otitis Media and Otitis Media With Effusion Models

Intra‐articular dexamethasone to inhibit the development of post‐traumatic osteoarthritis

Cytokine Responses in the Common Cold and Otitis Media

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