Further experimental observations of transplantation of canine larynx.
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Biomedical subjects
Publications and source records attributed to G Mogi.
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In order to clarify the role of the microflora of the nasopharynx and adenoids as causative factors of otitis media with effusion (OME), bacteriologic species in middle ear effusions (MEEs), nasopharyngeal smears, and adenoid tissues of children with OME were cultured. The change in the microflora of the nasopharynx after adenoidectomy, and the degree of bacterial agreement between the microflora of the nasopharynx and adenoid tissue were investigated. Nasopharyngeal bacterial flora were investigated in 259 children with OME from November 1984 to November 1987. The patients were divided into two groups: group A (43 patients) underwent adenoidectomy, and group B (216 patients) had no adenoidectomy. Hemophilus influenzae, Streptococcus pneumoniae, Branhamella catarrhalis, and Staphylococcus aureus were cultured in 66.7% of nasopharyngeal smears from group B, and in 46.5% from group A. Adenoid specimens for bacteriologic investigation were obtained from 38 adenoidectomy patients at surgery. Of these, H influenzae were cultured from adenoid specimens taken from 16 of the 26 patients with OME (group C), while only three of the 12 adenoidectomy patients without OME (group D) were found to have H influenzae in their adenoid specimens. The findings of this study suggest that adenoid vegetation plays an important role in the etiology of OME.
The exact architecture of the normal nasopharyngeal tonsil remains obscure because most histopathologic investigations have been based on surgically removed adenoids. We compared enlarged adenoids and normal nasopharyngeal tonsils under both light and electron microscopes. The marked features of clinically enlarged adenoids were a large extension of the reticular epithelium and increased germinal centers. A tendency toward increased stratified squamous epithelium and decreased ciliated epithelium was apparent in enlarged adenoids, possibly due to inflammatory conditions. One type of nonciliated cell seemed to transport foreign material into underlying lymphocytes, as do the M cells of gut-associated lymphoid tissue. This type of nonciliated cell was rarely found in the extended reticular epithelium of enlarged adenoids. These findings suggest a disturbance of the antigen-trapping system and surface protections in adenoidal enlargement.
Previously the authors proposed that the perilymphatic inner ear immune system is independent of that of the cerebrospinal fluid. In the present study, the effect of dilatation of blood vessels surrounding the cochlea of chinchillas on the transfer of serum antibodies to the perilymph was tested. The possibility of local production of antibodies in the perilymphatic space was also investigated by antigen introduction into the inner ear through the facial nerve canal. The dilatation of blood vessels accelerated the transfer of serum antibodies to the perilymph, even though this transfer activity was limited. Results of the study, showing the effect of antibody production in the perilymphatic space upon introduction of antigen into the inner ear through the facial nerve canal, would deny local antibody production in the inner ear, particularly in the perilymphatic space.
This study was designed to clarify the role of immune reaction in otitis media with effusion (OME). Immune-mediated OME was induced in chinchillas, and characteristics of the disease were evaluated biochemically, cytologically, and histologically. OME was induced by a single intratympanic inoculation of keyhole limpet hemocyanin (KLH) in animals which had a high serum anti-KLH IgG titer. In addition, OME was maintained for 3 weeks in seven of 17 chinchillas, boosted by intradermal and intratympanic injections at 1-week intervals. Cells in the middle ear effusion (MEE) consisted substantially of neutrophils, a few macrophages, and other cells. The mean histamine and prostaglandin E2 levels in the MEE significantly exceeded the levels in corresponding sera. The lining membrane of the bullae was edematous and thickened due to dilatation and rupture of blood capillaries and cell infiltration. Next, the animals were inoculated with immune complex into the tympanic cavity. MEE appeared in all treated ears within three days after injection. Biochemical, cytologic, and histologic findings of the immune complex-induced OME resembled those of immune-mediated OME. An immune peroxidase method demonstrated that neutrophils in MEE phagocytose immune complexes. Our findings suggest that a perpetual cycle of inflammatory substances may maintain an inflammatory condition in the middle ear.
PURPOSE: The immunological potential of the murine tympanic membrane was studied under normal and inflammatory conditions. MATERIALS AND METHODS: Experimental otitis media was induced by injecting keyhole limpet hemocyanin into the tympanic cavity of systemically sensitized mice. The animals were killed from 1 day to 2 weeks after the injection, and the distribution of the immunocompetent cells in the tympanic membrane was compared with those in normal animals, by immunohistochemical and toluidine blue staining. RESULTS: Tympanic membranes under normal conditions showed few immunocompetent cells, except mast cells and la-positive dendritic cells (presumably Langerhans' cells) in the pars flaccida and in the annular and manubrial regions of the pars tensa. After the induction of otitis media, lymphocytes migrated into these regions, although the other regions of the pars tensa showed few of these cells. la-positive cells migrated into both pars tensa and pars flaccida. Mast cells did not show obvious changes between the normal and inflammatory conditions. CONCLUSION: The pars flaccida and the annular and manubrial regions of the pars tensa are considered to be the immunologically potential sites, responsible for the immune responses. The remaining greater part of the tympanic membrane can recognize antigens by the migrated Langerhans' cells.
PURPOSE: The adenoid has long been recognized as an important factor in the pathogenesis of otitis media with effusion (OME). However, there is still considerable debate concerning how the condition of the adenoid tissue is involved in the cause of OME. The purpose of this study is to investigate whether the adenoid is an active agent of OME. PATIENTS AND METHODS: One hundred forty-six patients aged from 3 to 6 years who underwent adenoidectomy at Oita Medical University (Japan) were retrospectively compared with patients with and without OME regarding macroscopic size of the adenoid, adenoidal-nasopharyngeal ratio (AN ratio), incidence of sinusitis and nasal allergy, bacteriological examination of adenoid tissues, reticular formation of the epithelium, and the percent of ciliated epithelium. RESULTS: There was no significant difference in the size of adenoids. Haemophilus influenzae (HI) was cultured more frequently in adenoid specimens from patients with OME. A tendency toward increased stratified squamous epithelium and decreased ciliated epithelium was apparent in patients with OME. Reticular epithelium extension was greater in patients with than without OME. CONCLUSION: Adenoid inflammation is implicated in the pathogenesis of OME and the adenoids have an important role in the cause of OME by being a reservoir for HI.
PURPOSE: The relationship between chronic sinusitis and allergy has been discussed for many years. Type I allergies are believed to be involved in chronic sinusitis. However, there is not enough evidence to allow allergic sinusitis to be distinguished as an exact entity. This study was designed to examine the role of immunoglobulin E-mediated allergic reactions in allergic sinusitis. PATIENTS AND METHODS: We investigated the differences between 31 patients with allergic rhinitis and chronic sinusitis (allergic sinusitis) and 48 control subjects with nonallergic chronic sinusitis (chronic sinusitis). The pathological features of paranasal sinus effusion and mucosa were examined and compared in these two groups. RESULTS: The number of eosinophils, activated eosinophils, and neutrophils was higher in paranasal sinus effusion from patients with allergic sinusitis. The concentration of interleukin-5 was higher in the effusion of allergic sinusitis patients. In addition, more eosinophils and activated eosinophils infiltrated into the sinus mucosa of patients with allergic sinusitis. CONCLUSION: The type I allergic reaction has a significant role in the pathogenesis of sinusitis arising in patients with allergic rhinitis.
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Secretory IgA (SIgA) is the predominant immunoglobulin in certain external secretions and may have an important role in immunological mucosal resistance. SIgA differs in chemical and immunological properties from serum IgA. The present study was undertaken to investigate the antigenic relationship between SIgA, free secretory component (FSC) and serum IgA and the localization of SIgA as well as other immunological classes in tissues of oral and respiratory passages by use of immunofluorescence technique. SIgA and FSC were highly purified from human colostrum and rabbit anti-SIgA and anti-SC antisera were prepared. On the basis of antigenic relationships between SIgA, FSC and serum IgA, it was emphasized that individual specific antisera for SC and IgA and/or SIgA should be used in immunochemical or immunohistological investigations for SIgA. The present study failed to detect SC determinants in palatine and lingual tonsils. However, it was evident that cells present in the pharyngeal tonsillar epithelium contain SC determinants. SC molecules may be synthesized in certain secretory cells of mucous membrane and glandular epithelium and the combining of SC with IgA could occur in the cytoplasm of epithelial cells, the intercellular spaces and/or in the lumens of glandular acini and ductules.
Secretory IgA (SIgA) was isolated from pooled middle ear effusions (MEE) and its antigenicity and subunit structure were found to be identical to those of SIgA in saliva, nasal secretion and colostrum. The calculated percentage of SIgA in the total IgA of effusions was approximately 11%. Although the SIgA antibodies against streptolysin and staphylolysin were very low when compared to that of IgG class in effusion, this finding confirmed that MEE is at least partially a result of local immunologic reactions. The IgE concentration did not become elevated in both the MEE and serum obtained from patients with otitis media with effusion. Specific reaginic activity against mites was found in 5 of 56 (8.9%) MEE. Our findings would not suggest the significant role of atopic allergy in the formation of MEE.
Forty-two fetal and 90 developing young rats were studied electron microscopically to obtain a normal cellular distribution pattern of middle ear mucosa. The results showed that while ciliated columnar or cuboidal cells interspersed with secretory cells were predominantly distributed around the tympanic orifice and transitional zone, cuboidal or squamous nonciliated cells without secretory granules were numerous in the remaining part of the bulla. Development of ciliated cells started at the 17th or 18 th fetal day,paralleling that of secretory cells. The number of ciliated and secretory cells increased rapidly after birth. Glands were not found in the osseous tube, tympanic orifice, or other portions of the middle ear cavity in fetal, newborn, or suckling rats, while they are abundant in the cartilaginous portion of the tube. The findings of this study indicate that both secretory and ciliated cells are normal components of middle ear mucosa although these cells are restricted to the tympanic orifice and transitional zone, and that the mucociliary defense system starts to develop during the fetal stage.