Experimental Otitis Media following Middle Ear Inoculation of Nonviable<i>Streptococcus Pneumoniae</i>

Lowell, Seth H.; Juhn, Steven K.; Giebink, G. Scott

doi:10.1177/000348948008900523

Cited by 27 publications

(11 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Further work with the same animal model showed that lipoperoxidation was increased in middle ears injected with heat‐killed pneumococcus 34 . Other authors have demonstrated that inflammatory changes occur in the middle ear after injection with heat‐killed bacteria 35,36 ; this is apparently caused by the products of bacterial cell death. Because lipid peroxidation is known to occur under these conditions, oxygen radicals are further implicated as a contributor to inflammation.…”

Section: Discussionmentioning

confidence: 99%

Lipoperoxidation As a Measure of Free Radical Injury in Otitis Media

Haddad

1998

The Laryngoscope

View full text Add to dashboard Cite

Free radical damage, as evidenced by lipoperoxidation, has previously been demonstrated to contribute to the inflammatory changes associated with acute otitis media. The present study was undertaken to evaluate whether lipoperoxidation continues to be present for a period of time after middle ear infection. Eighty-two 300- to 400-g guinea pigs were injected with Streptococcus pneumoniae in the left ear and sterile saline in the right ear as a control. Animals were examined and sacrificed on day 5, 10, 20, or 30; middle ear mucosa was harvested and assayed for lipid hydroperoxide content. A statistically significant increase in lipoperoxidation was seen at each time point studied, compared with controls. Lipoperoxidation was highest at days 5 and 10; a significant decrease was seen at days 20 and 30. Histologic sections of middle ear mucosa of two animals per group were prepared and evaluated for inflammation. These results demonstrate that lipoperoxidation may contribute to middle ear inflammation for a significant period of time after acute infection; the findings are discussed in light of other work on the role of free radicals in otitis media.

show abstract

Section: Discussionmentioning

confidence: 99%

Lipoperoxidation As a Measure of Free Radical Injury in Otitis Media

Haddad

1998

The Laryngoscope

View full text Add to dashboard Cite

show abstract

“…Influenza virus inoculated into the nose causes an increase in the frequency of goblet cells in the nasopharyngeal portion of the eustachian tube (185). Increased frequency of goblet cells was also induced by pneumococcal antigens in the bulla of guinea pigs (186). It has also been observed that the ratio of albumin to immunoglobulin can shed light on the stage of infection and further deduce the pathomechanics of infection (187).…”

Section: Inflammation and Ommentioning

confidence: 99%

The Role of Inflammatory Mediators in the Pathogenesis of Otitis Media and Sequelae

Juhn

Jung

Hoffman

et al. 2008

Clin Exp Otorhinolaryngol

140

148

View full text Add to dashboard Cite

This review deals with the characteristics of various inflammatory mediators identified in the middle ear during otitis media and in cholesteatoma. The role of each inflammatory mediator in the pathogenesis of otitis media and cholesteatoma has been discussed. Further, the relation of each inflammatory mediator to the pathophysiology of the middle and inner ear along with its mechanisms of pathological change has been described. The mechanisms of hearing loss including sensorineural hearing loss (SNHL) as a sequela of otitis media are also discussed. The passage of inflammatory mediators through the round window membrane into the scala tympani is indicated. In an experimental animal model, an application of cytokines and lipopolysaccharide (LPS), a bacterial toxin, on the round window membrane induced sensorineural hearing loss as identified through auditory brainstem response threshold shifts. An increase in permeability of the blood-labyrinth barrier (BLB) was observed following application of these inflammatory mediators and LPS. The leakage of the blood components into the lateral wall of the cochlea through an increase in BLB permeability appears to be related to the sensorineural hearing loss by hindering K+ recycling through the lateral wall disrupting the ion homeostasis of the endolymph. Further studies on the roles of various inflammatory mediators and bacterial toxins in inducing the sensorineumral hearing loss in otitis media should be pursued.

show abstract

“…Einige Studien konnten ein modifiziertes Proliferations-, Differenzierungs-und Migrationsverhalten der Keratinozyten der Cholesteatommatrix belegen [3-5, 27, 28]. Das "aggressive" Verhalten der Cholesteatommatrix scheint durch die Freisetzung von Zytokinen und Wachstumsfaktoren aus Zellen des entzündlichen Infiltrats beeinflußt zu werden [1,10,15,18,22,34]. …”

unclassified

Immunhistochemische Untersuchungen von Mittelohrschleimhautresten im Cholesteatom

Sudhoff

Borkowski

Bujía

et al. 1997

HNO

View full text Add to dashboard Cite

The development of a middle ear cholesteatoma is usually associated with chronic inflammation and displacement of the mucosa present by the invading squamous epithelium. To analyze the clinically different behaviors of both epithelia, we used immunohistochemical methods to study the distribution and expression of interleukin-1 (Il-1), transforming growth factor-alpha (TGF-alpha), epidermal growth factor (EGF), epidermal growth factor-receptor (EGF-R), the proliferation marker MIB 1, c-myc proto-oncogene product and activation marker 4F2. Results stromal that keratinocytes in a cholesteatoma exhibited a much higher activation and proliferation rate when compared to middle ear mucosa cells. Middle ear epithelial cells showed no immunoreactivity for TGF-alpha, EGF-R, Il-1 and c-myc in contrast to the markedly positive immunoreactivity found in cholesteatoma matrix. The local release of cytokines and growth factors, such as TGF-alpha, EGF and Il-1 by inflammatory cells seems to be an important factor for the hyper-proliferative behavior of cholesteatoma epithelium. Our findings could contribute to the pathogenesis of middle ear cholesteatoma and give a possible explanation for the sustained progression of its growth leading to displacement of the middle ear mucosa.

show abstract

Experimental Otitis Media following Middle Ear Inoculation of NonviableStreptococcus Pneumoniae

Cited by 27 publications

References 15 publications

Lipoperoxidation As a Measure of Free Radical Injury in Otitis Media

Lipoperoxidation As a Measure of Free Radical Injury in Otitis Media

The Role of Inflammatory Mediators in the Pathogenesis of Otitis Media and Sequelae

Immunhistochemische Untersuchungen von Mittelohrschleimhautresten im Cholesteatom

Contact Info

Product

Resources

About