Biomedical subjects

Jizhen Lin

Publications and source records attributed to Jizhen Lin.

21 records · Page 2Linked to original sources

PubMed2002

Feline immunodeficiency virus-mediated gene therapy of middle ear mucosa cells.

HYPOTHESIS: To investigate the feasibility of gene therapy of the middle ear mucosa using a novel vector. BACKGROUND: Given present medications are unable to affect chronic otitis media, cholesteatoma, or tympanic membrane perforation, newer methods of treatment like gene therapy for these diseases must be explored. These genes can then be used to alter cytokines in the middle ear, slow or stop cholesteatoma growth, or improve tympanic membrane perforation healing. Feline immunodeficiency virus (FIV), a new lentiviral vector has been found to have greater than 90% efficiency in transfecting epithelial cells. Therefore, in vivo gene therapy of middle ear mucosa cells was attempted. METHODS: Twenty microliter of 5x10(5) vectors per ml FIV carrying the gene for green fluorescence protein (GFP) was introduced into the middle ears of Sprague-Dawley rats via a bulla approach. RESULTS: Expression of the GFP gene was observed in the middle ear mucosa cells at 1 week post-inoculation indicating transfection. CONCLUSION: Gene therapy of the middle ear is feasible with a FIV-based vector.

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PubMed2002

Induction of mucous cell metaplasia in the middle ear of rats using a three-step method: an improved model for otitis media with mucoid effusion.

Otitis media with mucoid effusion, characterized by mucous cell metaplasia in the middle ear cleft and thick fluid accumulation in the middle ear cavity, is a common otological disease that frequently affects young children. Multiple factors are involved in the development of this disease, especially middle ear infection and Eustachian tube dysfunction. In this study, in order to induce otitis media with effusion in rats, we introduced a three-step method, namely inoculation of Streptococcus pneumoniae at 10(7) colony-forming units (CFU)/ear or Haemophilus influenzae at 5 x 10(7) CFU/ear into the middle ear cavity twice at 2-week intervals, followed by Eustachian tube obstruction (ETO) for 4 and 8 weeks. Animals inoculated with phosphate-buffered saline (PBS) twice in the same manner followed by ETO served as controls. Middle ear effusion and mucosa were harvested for evaluation of carbohydrate concentrations and mucous cell density, respectively. We found that rats inoculated with S. pneumoniae twice, followed by ETO at 8 weeks, yielded the highest carbohydrate concentration in middle ear effusion and the highest goblet cell density in the middle ear cavity compared to the H. influenzae and PBS groups. It is tentatively concluded that inoculation of S. pneumoniae at 10(7) CFU/ear into the middle ear cavity of rats twice at 2-week intervals, followed by ETO for 8 weeks, is a promising animal model for otitis media with mucoid effusion which may be valuable for studying the human counterpart.

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PubMed2002

Induction of mucous cell metaplasia by tumor necrosis factor alpha in rat middle ear: the pathological basis for mucin hyperproduction in mucoid otitis media.

Mucoid otitis media (MOM), one of the leading causes of acquired hearing loss in children, is characterized by mucous cell hyperplasia in the middle ear cleft associated with mucin accumulation in the middle ear cavity. The factors that stimulate mucous cell metaplasia-hyperplasia and mucin hyperproduction are poorly understood. Recent studies demonstrated that tumor necrosis factor alpha (TNF-alpha), present in human middle ear effusion, stimulated mucin production in vitro and up-regulated mucin gene expression in vivo. These findings suggest that TNF-alpha is important in the development of mucous cell metaplasia-hyperplasia. This study demonstrated that inoculation of TNF-alpha into the middle ear cavity followed by eustachian tube obstruction stimulated mucous cell metaplasia-hyperplasia in the middle ear cleft, accompanied by abundant mucin or mucin-like glycoproteins in the middle ear effusion--a phenotype of MOM in humans. This finding suggests that TNF-alpha plays a key role in the pathogenesis of MOM through induction of mucous cell metaplasia-hyperplasia and mucin production.

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