The immune response of the adenoid and middle ear in otitis media

The immune response of the adenoid and middle ear in otitis media

Otolaryngology Head and Neck Surgery Volume 117 Number 2 tic-embedded 10 lam sections. The findings were correlated with the initial and final ABR th...

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Otolaryngology Head and Neck Surgery Volume 117 Number 2

tic-embedded 10 lam sections. The findings were correlated with the initial and final ABR thresholds. It was observed that, as previously reported, ABR thresholds were preserved after surgical occlusion of one or more semicircular canals. Suctioning of inner ear fluid led to transient loss of thresholds with recovery. Amputlectomy produced dichotomous results, with some subjects preserving and others losing auditory function. Wide vestibulotomy resulted in permanent loss of auditory function in most cases. Histologically there was intraluminal fibrosis and inflammation near the site of surgical entry. Most specimens showed normal cochlear architecture and hair cell counts, irrespective of the degree of hearing loss. Vestibular hair cells were also well preserved, even when they were close to the site of surgical injury. These findings suggest that electromechanical changes, rather than cell death, are responsible for changes in auditory and vestibular function after partial labyrinthectomy. (Supported by the National Institute for Deafness and Other Communicative Disorders.)

Research Forum - - Tuesday

P 125

10:45 AM

Immune Pathogenesis and Therapy of Head and Neck Cancer CARTER VAN WAES, MD, PhD

11:00 AM Immunology of Inner Ear Disease JEFFREY P, HARRIS, MD, PhD

11:15 AM

The Immune Response of the Adenoid and Middle Ear in Otitis Media JOEL BERNSTEIN, MD, PhD

P O S T E R S (SESSION C)

Authors will b e present at their posters Tuesday, Sept. 9, 1997, 9:05 to 9:35 A M

9i00 AM

Poster I

Discussion

Development of a Murine Oral Squamous Cell Carcin o m a Cell Line Model for the Study of the Genetic and Immunologic Steps Involved in Tumor Progression of

9:05 t o 9:35 AM

Posters (Session C) See pages P125 to P146

9:35 to 10:10 AM Room 103--SFMC

Neel Distinguished Research Lecturer Where W e Stand with G e n e Therapy R, MICHAEL BLAESE, M D

I0:I0 to 11:30 A M R o o m 103--SFMC

SESSION A/B: Presidential Research Symposia 10:10 AM The Basis of the Immunologic Response: Differentiating Self From Non-self

WI .LIAM J. RICHTSMEIER,MD, PhD 10:30 AM

Allergy and Immunology RCBERT M. NACLERIO, MD

Head and Neck Cancer GIOVANA R. THOMAS, MD (presenter), FRED J. HENDLER, MD, PhD, ZHONG CHEN, MD, PhD, and CARTER VAN WAES, MD, PhD, Bethesda, Md., and LouisviLle, Ky.

A multi-step model of squamous cell carcinoma (SCC) of the upper aerodigestive tract in inbred mice has been needed to facilitate identification of changes in gene expression and immune recognition that are necessary for tumor development and progression of head and neck carcinoma. Five clonal oral keratinocyte lines with an immortalized phenotype were obtained following two cycles of exposure to carcinogen 4NQO and cloning of transformants in soft agar. The cell lines were inoculated into Balb/c SCID mice to determine whether they were immediately tumorigenic or required an extended time interval for adaptation and progression in vivo. Appearance of palpable tumor was delayed and required from 5 to 32 weeks, consistent with the possibility that additional genetic or phenotypic changes were necessary for adaptation of the transformed cells in the host environment. Five tumors arising from the different keratinocyte clones that grew were re-isolated and designated B6C3-4 scid, B7E11-4 scid, B4B84 scid, B6D8-4 scid, and B7E3-4 scid. The histologic origin of the tumors and re-isolated cell lines was characterized including immunostainingfor pancytokeratin and ct6[~4 surface integrin. Four of five tumors were well-differentiated SCC and the lines derived from them were positive for epithelial pancytokeratin and cc6~4 surface integrin markers. Histology of B6D8-4 scid tumor was consistent with a spindle variant and expressed no markers of epithelial differentiation. When the growth rate of the original and re-isolated cell lines was