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A M Carpenter

Publications and source records attributed to A M Carpenter.

41 records · Page 3Linked to original sources
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Cells involved in the middle ear defense system.

Despite the high incidence and prevalence of otitis media, its pathogenesis is not thoroughly understood. In the last decade, many efforts have been made to provide a better understanding, and abundant information has become available. At the same time the field of immunology has advanced at an extremely rapid pace. We have followed the gradual cellular events in the defense reaction of the middle ear, utilizing eustachian tube obstruction to induce otitis. Seventy-five cats were divided in groups and sacrificed at intervals between one day and six months, and their temporal bones were studied. During an initial phase of inflammation, polymorphonuclears appear at three days in connective tissue; at the same time active fibroblasts synthesize tropocollagen and ground substance while epithelial cells secrete mucus and lysozymes. These cells, together with those involved in the mucociliary transport system and a patent functional eustachian tube, constitute the nonspecific system of defense. The transition cells are the macrophages which appear at one week to interact with T and B cells to produce the specific immune response. Plasma cells appear at two weeks to peak at one month with synthesis of immunoglobulins A, G and M. A secretory immune system is observed. At three and six months, lymphocytes are the predominant cells and occasional accumulations of mononuclears are observed. The reaction involves the entire middle ear, including mucoperiosteum, middle ear muscles and round window membrane. We believe that a better understanding of the middle ear defense system will lead in time to a practical clinical assessment of the immunological status during the evolution of each particular process or disease involving the middle ear, and a more rational approach to the treatment and, hopefully, prevention of chronic ear disease.

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A longitudinal study of cellular changes in experimental otitis media.

A longitudinal sequential study of otitis media in an experimental animal (cat) using eustachian tube obstruction was done. Fifty animals were used. The continuum of mucoperiosteal changes from one day to six months after obstruction revealed gradual changes that were similar for each animal. Stages were defined, and by using different staining techniques, including immunocytochemistry, an overall middle ear defense system was postulated and documented. Nonspecific as well as specific defense systems, including localized immunity, were described. Effusions were studied in a continuum, and their pathogenesis was discussed.

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PubMedDate not supplied

FSH does not directly influence testicular macrophages.

We have previously demonstrated that conditioned medium from testicular macrophages stimulates testosterone production by Leydig cells. It was also reported that conditioned medium from macrophages treated with follicle-stimulating hormone (FSH) had an even greater amount of Leydig cell-stimulating activity than medium from untreated macrophages, indicating that this factor is under the regulation of FSH. However, most other laboratories have been unable to reproduce this effect of FSH. We have recently purified and partially characterized the stimulatory factor from macrophage-conditioned medium that stimulates Leydig cells. The purpose of the present investigation was to reinvestigate the effect of FSH by determining whether it regulates the production of this purified factor and by determining whether macrophages have mRNA for the FSH receptor. Testicular macrophages were isolated from adult rats and incubated 24 hours with human recombinant FSH (20 units/ml), ovine FSH (200 ng/ml), fetal bovine serum (2%), or dibutyryl cyclic adenosine monophosphate (1 mM). The macrophage-derived factor (MDF) was then purified from conditioned medium of the various treatment groups and added to Leydig cells. The concentration of testosterone in the Leydig cell medium was then measured after 16 hours. It was found that serum significantly stimulated production of the MDF. However, FSH had no effect on production of the MDF in the presence or absence of serum. Dibutyryl cyclic adenosine monophosphate exerted a slight inhibitory effect on production of the macrophage-derived factor. Most importantly, testicular macrophages did not express detectable levels of FSH receptor mRNA, either in vivo or in vitro, when evaluated using either in situ hybridization or northern analysis, under identical conditions that clearly demonstrated FSH receptor mRNA in Sertoli cells. We conclude that testicular macrophages are not a direct target for FSH.

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