Ex vivo modeling of oral HIV transmission in human palatine tonsil.

The majority of newly acquired HIV infections are believed to occur following transmission of virus infectivity across mucosal surfaces, although many mechanistic details still remain unresolved. We have used human ex vivo organ cultures and primary cell populations to analyze the cellular and molecular basis for mucosal HIV transmission. By using human palatine tonsil from routine tonsillectomies and semen from HIV-positive donors, we have created an experimental equivalent to oral HIV transmission. HIV infection was readily transferred into tonsillar lymphocytes, but this transmission into lymphocytes was dramatically reduced when the exposed lymphocyte populations were protected by intact mucosal surfaces. In this study, we consider the impact that leukocyte activation and morphological aberrations in surface structure may have on susceptibility to primary HIV infection and introduce novel time-lapse confocal microscopy procedures that begin to reveal the dynamic complexity associated with cell-mediated HIV transmission.     

Postnatal growth of the rat palatine gland

To elucidate how the palatine glands grow postnatally, the palatine glands of rats from 0 to 8 weeks of age were investigated histologically and immunohistochemically. Under light microscope, three dimensions of the right part of the palatine glands were measured and the total number of excretory ducts of the glands was counted from the parasagittal serial sections. Immunohistochemistry with anti-5-bromo-2'-deoxyuridine (BrdU) monoclonal antibody was also employed to detect the cellular proliferative activity. At birth (0 weeks), the palatine glands consisted of ducts and immature acini. The ducts in the glands were connected with excretory ducts. After 2 weeks, there was no duct in the glands. Most acinar cells became mature as mucous cells and took the form of tubulo-acini connected directly with excretory ducts. In the posterior region of the glands, serous acinar cells forming demilunes were occasionally seen. All three dimensions of the palatine glands became longer, and the number of excretory ducts tended to increase. Immunohistochemistry showed acinar and duct cells were highly proliferative in early stage of postnatal life and their proliferative activity decreased thereafter. This study demonstrated that immature rat palatine glands of newborn rats grow three-dimensionally during maturation, and that the parenchymal cell proliferation contributes to the growth of the rat palatine glands. In addition, it is suggested that the glandular tissue arises from the excretory ducts formed postnatally.     

Characteristic distribution of immunoglobulin-containing cells in palatine tonsils

Using fluorescein-labelled antibodies against γ, μ and α chains, Ig-containing cells* in palatine tonsils were studied in 120 patients. The aim of this study was to determine the most frequently repeated typical findings as regards the numbers and localisation of these cells in tonsils and to confront the data obtained with the concept that tonsils are a component of the local immunity system. The preponderance of IgG over IgA cells was confirmed, both cell types being preferentially localized in extrafollicular tissue whereas IgM was mostly found in germinal centres. Together with progressing tonsillar atrophia, the frequency of positive findings of IgM decreased, whereas the numbers of IgG and IgA cells were proportional to the amount of remaining lymphoid tissue. IgA cells were not preponderant in tonsils and their localization in the surface layer of epithelium was rather exceptional, SC antigen could not be demonstrated unequivocally and the morphological picture in germinal centres was characteristic for IgM production rather for IgA. Thus the palatine tonsils according to the content and distribution of immunocytes, correspond to the lymph node rather than to an organ involved significantly in the local antibody formation.     

Prenatal development of the palatine gland of rats

The present study aimed to elucidate the prenatal development of the rat palatine gland. Parasagittal 5 microm thick serial sections made from Wistar rats at embryonic days (E) 17 to 22 were stained with haematoxylin-eosin (HE), Alcian blue-Kernechtrot or immunohistochemistry for 5-bromo-2'-deoxyuridine (BrdU) as a marker of proliferating cells. Additionally, three-dimensional images of developing glandular parenchyma were reconstructed from serial HE sections with a personal computer. At E 17, several thickenings of the palatal epithelium had appeared which thereafter became the epithelial cords. Branching and lumenization commenced at E 20, and immature acini were observed at E 21. Three-dimensional reconstruction showed that the proximal part of the epithelial cord differentiated into the duct, and the distal part of the epithelial cord differentiated into the acinus. In immunohistochemical staining, there were many BrdU-positive cells in the epithelial cords including thickenings of the palatal epithelium, ducts, and acini. The BrdU labeling index of the cells of the epithelial cord was the highest (statistically significant) of the three in the primitive palatine gland. In conclusion, during the development of the rat palatine gland, epithelial cords with very high proliferative activity arise from the palatal epithelium, and then the proximal part of the epithelial cord differentiates into the duct, and the distal part of the epithelial cord differentiates into the acinus. Proliferation of these glandular parenchyma contributes to the growth of the developing palatine gland.     

The palatine bone and its associations in gadoid fishes

The articulation of the palatine bone in gadoid fishes has been thought of as a specialization of that group. It is shown that there are, in fact, three principal types of articulation, two of which are shared with other gadiform groups. The type of palatine articulation in other paracanthopterygians is briefly described and compared with that of various acanthopterygians. The supposed relationships of some gadoids are commented upon in the light of the specialized nature of some types of palatine articulation.     

Expression and function of tight junctions in the crypt epithelium of human palatine tonsils.

The human palatine tonsils have surface and crypt stratified epithelium and may be initiated via the epithelium to mount immune responses to various presenting antigens. Here we investigated the expression and function of tight junctions in the epithelium of human palatine tonsils from patients with tonsillar hypertrophy or recurrent tonsillitis. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, -7, -8, and -14 mRNAs were detected in tonsillar hypertrophy. Occludin and claudin-14 were expressed in the uppermost layer of the tonsil surface epithelium, whereas ZO-1, JAM-1, and claudin-1, -4, and -7 were found throughout the epithelium. In the crypt epithelium, claudin-4 was preferentially expressed in the upper layers. In freeze-fracture replicas, short fragments of continuous tight junction strands were observed but never formed networks. In the crypt epithelium of recurrent tonsillitis, the tracer was leaked from the surface regions where occludin and claudin-4 disappeared. Occludin, ZO-1, JAM-1, and claudin-1, -3, -4, and -14, but not claudin-7, mRNAs were decreased in recurrent tonsillitis compared with those of tonsillar hypertrophy. These studies suggest unique expression of tight junctions in human palatine tonsillar epithelium, and the crypt epithelium may possess an epithelial barrier different from that of the surface epithelium.     

Focal palatine erosion associated with dental malocclusion in captive cheetahs

A severe palatine disorder caused by maloccluded molars was discovered in captive adult cheetahs at the San Diego Wild Animal Park. This defect has been labeled focal palatine erosion (FPE). Subsequently, a total of 59 cheetahs from several institutions have been examined to evaluate the occurrence and etiology of this disorder. Maloccluded lower molars contacting the palatal mucosa appear to be the primary source of irritation. Infection develops when decaying food and grass particles become lodged in the resulting defect. Eventually, complete palatine perforation results which can extend into the nasal passages and eventually lead to systemic disorders. Of 59 cheetahs studied, 15 displayed various stages of FPE. Examination of 26 museum skull specimens revealed four cases of palatine perforation. These four were from a group of eight animals that were zoo raised. Focal palatine erosion appears to be a result of dietary factors. All cheetahs with FPE received a commercially prepared soft diet while in captivity. The lack of normal biting, tearing, and pulling action associated with natural prey capture and consumption could result in malocclusion caused by atrophy from disuse of the masticatory apparatus. Improper occlusion could also stem from insufficient wear or unsynchronized development of the opposing dental arches. All but two cases of FPE were found in cheetahs imported from a limited area in southwest Africa in 1970, or their offspring. Since molar size and jaw structure can be inherited, there may be genetic factors involved but more data are needed to support this idea. Treatment includes changing diet, reducing the height of the offending molar, controlling infection, eliminating irritants, and in some cases, surgical reconstruction.