Environment Affects Function and Lymphocyte Activity in Lacrimal Glands of Female Rabbits
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In a previous article we reported that mastication played an important role in the development of submandibular glands in male mice. Submandibular glands contain epidermal growth factor (EGF) which stimulates the proliferation of various cells in developing animals. In this study, the effects of the hypotrophy of submandibular glands caused by reduction of mastication and the removal of the glands on the growth ability of isoproterenol (IPR)-stimulated parotid glands and other tissues were investigated. The animals in the experiment were male mice and they divided into three groups, a control group fed a solid diet, a group fed a paste diet and a group with removed submandibular glands fed a solid diet. In comparison with the group fed a solid diet, in the group fed a paste diet a small decrease was found, and in the group with the ectomized submandibular gland a significant decrease in the rise of ornithine decarboxylase (ODC) activity, S-adenosylmethionine decarboxylase (SAMDC) activity and DNA synthesis of parotid glands caused by IPR stimulation were found. The DNA synthesis of the heart tissue of mice with ectomized submandibular glands was lower than that of the control group, but in liver, lung, stomach and testis tissue no decrease of DNA synthesis was found. These results suggest that mastication and the submandibular glands have an effect of the growth of the tissues in male mice.
Mastication
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The current investigators have shown that androgen treatment suppresses inflammation and stimulates the function of lacrimal glands in mouse models of Sjögren's syndrome. Recently, others have hypothesized that androgen insufficiency induces an autoimmune process in lacrimal tissue, leading to inflammation, a Sjögren's syndrome-like pathology, and aqueous tear deficiency. The purpose of the present study was to test this hypothesis.Lacrimal glands were obtained from adult testicular feminized (Tfm) and control mice; castrated rats, guinea pigs, and rabbits; and castrated rats without anterior or whole pituitary glands and were processed for histology and image analysis. Tear volumes were measured in mice, in patients taking antiandrogen medications, and in age-matched human control subjects.Tfm mice, which are completely resistant to classical androgen action, did not have increased lymphocyte infiltration in their lacrimal glands or decreased tear volumes. No inflammation was evident in lacrimal tissues of male or female rats, guinea pigs, or rabbits 12 to 31 days after castration, no inflammation existed in rat lacrimal glands 15 to 31 days after orchiectomy and pituitary removal, and no aqueous tear deficiency was apparent in patients receiving antiandrogen therapy.Androgen deficiency may promote the progression of Sjögren's syndrome and its associated lacrimal gland inflammation, meibomian gland dysfunction, and severe dry eye. However, androgen insufficiency alone does not cause lacrimal gland inflammation, a Sjögren's syndrome-like pathology in lacrimal tissue, or aqueous tear deficiency in nonautoimmune animals and humans.
Androgen Deficiency
Lacrimal apparatus
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Circulation (fluid dynamics)
Blood circulation
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Submaxillary gland
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Testosterone propionate
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Androgens are known to regulate the level of secretory component (SC) in tears of male rats. The purpose of the present study was to explore the underlying mechanism of this hormone action by (i) identifying the ocular tissue(s) involved in SC production; and (ii) determining whether androgens increase SC production by this tissue. We also examined whether androgen administration influenced the concentration of SC in tears of female rats. Ocular tissues from adult Sprague-Dawley rats were cultured in the presence or absence of cycloheximide in the incubation medium. Secretory component in the culture media was measured by an RIA which detects primarily free SC. Analysis of media obtained after incubation of exorbital (lacrimal) glands, 'lid' tissues, globes, and Harderian glands revealed that only exorbital glands released substantial amounts of SC. This exorbital gland production of SC, which was significantly greater in tissues from male rats, as compared to those of female rats, was reduced by approximately 50% when cycloheximide was present in the culture medium. To determine whether SC production by exorbital glands was influenced by androgens, orchiectomized glands was influenced by androgens, orchiectomized rats were administered either saline or testosterone (2.0 mg/day for 4 days), and exorbital glands were cultured 24 hr after the last injection. Testosterone treatment in vivo induced a significant, cycloheximide-sensitive increase in SC production in vitro, compared to the glandular SC output of saline-injected controls. It is interesting that similar androgen treatment of ovariectomized females also resulted in elevated tear SC concentrations and enhanced output of SC by their exorbital glands in vitro. These findings indicate that the exorbital gland is primarily responsible for SC production in the rat eye and that androgens may modulate the synthesis of SC in this gland.
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Purpose. The fluid secretory impairment of lacrimal and salivary glands in Sjögren's syndrome (SS) is thought to be related to the extent of lymphocytic infiltration (LI) and subsequent loss of glandular tissue. In this study, we examine the correlation between the extent of tear flow reduction and the extent of LI of lacrimal glands in the NZB/W mouse, a model of SS. Methods. We stimulated tear production by topical application of carbachol onto the gland while fluid was collected from the lacrimal duct. The lacrimal glands were removed after fluid collection for histology. Results. Fluid secretion in response to carbachol was less in the majority of young NZB/W females compared to C57 control animals and none of the glands showed LI. Fluid secretion was also impaired in the majority of old NZB/W females, and the extent of LI was highly variable. Some of the old SW females also showed blunted fluid secretory responses and some degree of focal LI. Young SW females showed no LI and most animals exhibited normal flow responses. Analysis of paired flow and LI measurements showed no correlation between LI and flow impairment in any of the groups or in the pooled data. Carbachol-stimulated protein secretion from lacrimal gland slices in vitro were similar in young and old SW and NZB/W mice. Conclusions. These results suggest that LI alone is not sufficient to explain the secretory dysfunction in the NZB/W mouse model of Sjögren's syndrome.
Infiltration (HVAC)
Lymphocytic infiltration
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Abstract A series of experiments were designed to determine the origin of a nerve growth promoting protein found in high concentration in the tubular portions of the submandibular glands of adult male mice. This protein is necessary for the growth and development of immature sympathetic nerve cells. The quantities of this protein can be increased in the glands of female mice to levels found in the submandibular glands of adult male mice by injecting testosterone into preadolescent or adult female mice. When testosterone was given to young mice or to adult female mice together with an antiserum prepared against the nerve growth factor (NGF), the NGF content of the testosterone‐treated mice increased in the same manner as in testosterone‐ and normal serum‐treated mice. Although antiserum against the nerve growth protein could be demonstrated in the sera of mice during the course of the entire experiment, the antiserum had no effect on the content of NGF in the submandibular glands. After the intravenous injection of NGF in large quantities, it could not be localized in liver, spleen or submandibular gland cells of the mouse as determined by fluorescent antibody techniques. The results suggested that the nerve growth promoting protein found in high concentration in the submandibular glands of adult male mice and in testosterone‐treated female mice is synthesized and stored in cells of the tubular portion of these glands.
Adult male
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It is generally known that glucocorticoids exert an essential influence on digestive tract physiology (2). Many investigations carried out refer to the changes observed in the pancreas under different experimental conditions (4, 5, 6, 7, 8). The investigations of the influence of glucocorticoids on salivary glands and mainly on a parotid gland are very general. Salivary glands play an important role in the initial stages of taking up and assimilating food. Moreover, the produced growth factors and parotin play an important role in tissue development and maturation in young animals (12).
White (mutation)
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