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[The influence of medicine to the expression of cell adhesion molecule in experimental otitis media with effusion]

Shengzi Wang1, Yuehua Yan, Shuyi Wang

  • 1Department of Radiotherapy, EENT Hospital, Shanghai Fudan University, Shanghai 200031.

Lin Chuang Er Bi Yan Hou Ke Za Zhi = Journal of Clinical Otorhinolaryngology
|November 2, 2004
PubMed
Abstract

Insights

Cefaclor and Prednisonum reduce cell adhesion molecules in experimental otitis media with effusion (OME). These drugs may improve OME by decreasing Mac-1 and L-Selectin expression, key in the inflammatory response.

Area of Science:

  • Immunology
  • Otolaryngology
  • Pharmacology

Context:

  • Otitis media with effusion (OME) is a common condition often associated with inflammation and fluid accumulation in the middle ear.
  • The role of cell adhesion molecules, such as Mac-1 and L-Selectin, in the pathogenesis of OME is not fully understood.
  • Bacterial antigens, like those from nontypeable *Hemophilus influenzae*, can trigger inflammatory responses in the middle ear.

Purpose:

  • To investigate the influence of Cefaclor and Prednisonum on the expression of cell adhesion molecules (Mac-1 and L-Selectin) in a rat model of experimental otitis media with effusion (OME).
  • To explore the relationship between the expression of these adhesion molecules and the pathological changes in the middle ear mucosa during OME.

Summary:

  • Experimental OME was induced in Sprague-Dawley rats using formalin-killed nontypeable *Hemophilus influenzae*.
  • Flow cytometry analysis revealed increased expression of Mac-1 and L-Selectin in the bacterial group, correlating with middle ear mucosal pathology.
  • Treatment with Cefaclor and Prednisonum led to decreased expression of these adhesion molecules and reduced leukocyte accumulation in the middle ear.

Impact:

  • The findings suggest that dead bacteria can act as antigens, initiating inflammatory responses and effusion in OME.
  • Expression of Mac-1 and L-Selectin is strongly linked to the inflammatory processes in OME.
  • Cefaclor and Prednisonum show potential therapeutic benefits for OME, possibly by modulating the expression of Mac-1 and L-Selectin and mitigating leukocyte infiltration.

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