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PubMed1997

Shared TCR Vbeta gene expression by the pancreas and salivary gland in immunodeficient alymphoplasic mice.

Mice with the homozygous mutation alymphoplasia (aly) lack lymph nodes and Peyer's patches and show defects in both humoral and cellular immunity. In these mice, spontaneous infiltration of mononuclear cells was observed in multiple exocrine organs, including the pancreas, salivary glands, and lacrimal glands from the age of 15 wk, progressing to a marked tissue destruction at the age of 25 wk. Using this strain, we examined the phenotypes and TCR Vbeta gene expression of infiltrating T cells to identify the pathologic role of T cell immunity in idiopathic pancreatitis. Most of the infiltrating cells were CD4+ and Thy-1+ cells. Analysis of the TCR gene expression on T cells infiltrating the pancreas and salivary glands showed a high expression of Vbeta1 and Vbeta5 in both organs at the age of 15 wk. In contrast, a diverse expression of TCR Vbeta genes was noted at 25 wk. Sequence analysis of complementarity-determining region 3 (CDR3) of the most prominent TCR Vbeta gene family expressed in these cells, Vbeta1, showed oligoclonal expansion of infiltrating T cells in both organs. Frequent use of glutamine and proline at position 97 was observed in paired tissues. Our data suggest that oligoclonal expansion of organ specific T cells might be one of the etiologic mechanisms of chronic pancreatitis and that common autoantigens could trigger autoimmunity in multiple organs.

Animals↗
PubMed2004

Spontaneous development of multiple glandular and extraglandular lesions in aged IQI/Jic mice: a model for primary Sjogren's syndrome.

OBJECTIVE: In primary Sjögren's syndrome (SS), systemic exocrine and non-exocrine organs are frequently affected, in addition to the major target tissues of the lacrimal and salivary glands. This study aimed to examine whether the IQI/Jic mouse, an animal model of SS whose autoimmune dacryoadenitis and sialoadenitis have been documented, develops inflammatory lesions in multiple organs as in primary SS. METHODS: Systemic histopathological analysis was performed on IQI/Jic mice at various ages. Phenotypes of infiltrated lymphocytes were determined using immunohistochemical techniques. RESULTS: Inflammatory lesions were observed not only in the lacrimal and salivary glands, but also in multiple organs, including the lung, pancreas and kidney at advanced ages, and were mainly composed of CD4(+) T cells and B cells. The incidence and severity of the inflammatory lesions increased with age in all these organs. The histological appearance and spreading of lesions were similar to those in human primary SS. CONCLUSIONS: IQI/Jic mice spontaneously develop inflammatory cellular infiltrates in multiple exocrine and non-exocrine organs. This characteristic distinguishes IQI/Jic mice from other murine models, making them favourable for studies on the pathogenesis of systemic involvement in primary SS.

Aging↗
PubMed1996

Cyclosporine therapy suppresses ocular and lacrimal gland disease in MRL/Mp-lpr/lpr mice.

PURPOSE: MRL/Mp-lpr/lpr (MRL/lpr) mice spontaneously develop an autoimmune disease characterized by lymphoproliferation, vasculitis, glomerulonephritis, autoantibody production, and ocular and lacrimal gland inflammation. Lacrimal gland lesions in MRL/lpr mice are a model for the human disorder Sjögren's syndrome. The target organ lesions in MRL/lpr mice, including those in the eye and lacrimal gland, are composed largely of CD4+ T cells, with lesser numbers of CD8+ T cells and B cells. Cyclosporine therapy was evaluated for its effect on the autoimmune disease, particularly in the eye and lacrimal gland. METHODS: MRL/lpr mice were administered cyclosporine intraperitoneally at a dosage of 2 mg daily from age 1 to 5 months. Animals were killed at 5 months and evaluated for the presence of autoimmune disease. Control groups consisted of animals given daily injections with either saline or the cyclosporine diluent. RESULTS: Cyclosporine therapy was effective in reducing the ocular and lacrimal gland disease. Intraocular inflammation was present in 73% of control animals but in only 15% of cyclosporine-treated animals (P < 0.003). Multifocal lacrimal gland inflammatory infiltrates were present in 100% of controls but in only 23% of cyclosporine-treated animals (P < 0.0001). Mean percent area involved by lacrimal gland inflammation was reduced from 19.7% to 4.7% by cyclosporine therapy (P = 0.0003). Systemic autoimmune disease manifestations, including lymphoproliferation, vasculitis, glomerulonephritis, and serologic abnormalities, also were improved. CONCLUSIONS: Chronic cyclosporine therapy, started at an early age, is effective in controlling the autoimmune disease in MRL/lpr mice, including the ocular and lacrimal gland lesions.

Animals↗
PubMed1994

Transfer of Sjögren's syndrome-like autoimmune lesions into SCID mice and prevention of lesions by anti-CD4 and anti-T cell receptor antibody treatment.

We describe the successful transfer of murine Sjögren's syndrome-like autoimmune lesions from MRL/lpr mice (H-2k) to severe combined immunodeficiency (SCID) mice (H-2d) and prevention of lesions by anti-CD4 and -T cell receptor V beta 8 antibody treatment. Mononuclear cells (1 x 10(6)) isolated from the inflamed submandibular salivary gland tissues of MRL/lpr mice were transferred intraperitoneally into SCID mice. Autoimmune lesions resembling those seen in Sjögren's syndrome developed in the salivary and lacrimal glands of SCID mice 8 weeks after the injection, whereas other organs did not show any lesion. This pathology resembles Sjögren's syndrome in humans involving both the salivary and lacrimal glands. Immunohistochemically, a major proportion of these infiltrating cells in transferred SCID mice were CD4+ and V beta 8+. When the spleen cells from MRL/lpr mice were injected, severe inflammatory lesions, probably resulting from a graft-versus host reaction, were observed in multiple organs of SCID mice. The disease could not be induced by intraperitoneal administration of the sera from MRL/lpr mice, or of the spleen cells from C3H/He (H-2k) and BALB/c (H-2d) mice. We detected autoantibody production specific for the salivary gland tissue in sera from transferred SCID mice. Moreover, we found that the lesions were prevented by administration of the isolated cells treated in vitro with anti-CD4 and anti-V beta 8 monoclonal antibodies. These results suggest that CD4- and V beta 8-bearing T cells are involved in recognizing an autopeptide and triggering autoimmunity in the salivary and lacrimal glands, and therapies designed with anti-CD4 and anti-V beta 8 antibodies may prove effective in treating the murine autoimmune disease.

Animals↗
PubMed1991

Gastrointestinal motor dysfunction in acquired selective cholinergic dysautonomia associated with infectious mononucleosis.

This report documents the disturbance in gastrointestinal motor function in a patient with selective cholinergic dysautonomia that occurred following acute infectious mononucleosis. Apart from the gut, other organs affected included the pupils, sweat glands, lacrimal and salivary glands, and urinary bladder. Autonomic function tests showed the preservation of sympathetic adrenergic functions in contrast to the generalized involvement of postganglionic parasympathetic and sympathetic cholinergic nerves, including denervation hypersensitivity of the pupil and urinary bladder to exogenous cholinergic agonists. Cardiac and abdominal vagal responses were abnormal. Colon myenteric plexus ganglion cells were normal by morphological and immunohistochemical studies, suggesting that the selective cholinergic dysautonomia was the most likely pathophysiologic process responsible for the observed motility disorder. This study documents the occurrence of selective cholinergic dysautonomia following a viral illness, the importance of the extrinsic neural control on the motor function of the gastrointestinal tract, and the usefulness of combined motility and autonomic function testing in the evaluation of patients with symptoms suggestive of gut dysmotility.

Adult↗
PubMed2006

Mechanisms of autoantibody production and the relationship between autoantibodies and the clinical manifestations in Sjögren's syndrome.

The major target organs of Sjögren's syndrome (SS) are lacrimal glands and salivary glands where prominent lymphocytic infiltration occurs, which may induce varying levels of autoantibody production. Multiple factors, including environmental stress, viral infection, hormonal imbalance, and apoptosis, are thought to be involved in the pathogenesis of SS. Production of anti-SS-A/Ro and anti-SS-B/La antibodies is thought to be regulated by the presentation of autoantigens in context with an aberrant expression pattern of human leukocyte antigen (HLA) in situ. Molecular mimicry with some viral sequences is also hypothesized. The apoptosis-resistance phenotype of B cells in labial salivary glands (LSGs) of SS is important in autoantibody production. CD40/CD40L (CD40 ligand) and Bcl-2 family proteins, in tandem with B cell-activating factor (BAFF), are supposed to protect infiltrating lymphocytes from apoptosis. Anti-muscarinic3 receptor antibody plays an important role in cholinergic hyperresponsiveness in SS. Fragmentation of autoantigens such as SS-B/La or alfa-fodrin during the process of apoptosis causes the redistribution of these autoantigens, leading to the production of autoantibodies in SS. In this review, the role of autoantibodies found in SS, corresponding to clinical aspects of each antibody as well as the mechanisms of production, is discussed.

Antigen-Antibody Reactions↗
PubMed2005

Wound healing in the cornea: a review of refractive surgery complications and new prospects for therapy.

PURPOSE: The corneal wound healing response is of particular relevance for refractive surgical procedures since it is a major determinant of efficacy and safety. The purpose of this review is to provide an overview of the healing response in refractive surgery procedures. METHODS: Literature review. RESULTS: LASIK and PRK are the most common refractive procedures; however, alternative techniques, including LASEK, PRK with mitomycin C, and Epi-LASIK, have been developed in an attempt to overcome common complications. Clinical outcomes and a number of common complications are directly related to the healing process and the unpredictable nature of the associated corneal cellular response. These complications include overcorrection, undercorrection, regression, corneal stroma opacification, and many other side effects that have their roots in the biologic response to surgery. The corneal epithelium, stroma, nerves, inflammatory cells, and lacrimal glands are the main tissues and organs involved in the wound healing response to corneal surgical procedures. Complex cellular interactions mediated by cytokines and growth factors occur among the cells of the cornea, resulting in a highly variable biologic response. Among the best characterized processes are keratocyte apoptosis, keratocyte necrosis, keratocyte proliferation, migration of inflammatory cells, and myofibroblast generation. These cellular interactions are involved in extracellular matrix reorganization, stromal remodeling, wound contraction, and several other responses to surgical injury. CONCLUSIONS: A better understanding of the complete cascade of events involved in the corneal wound healing process and anomalies that lead to complications is critical to improve the efficacy and safety of refractive surgical procedures. Recent advances in understanding the biologic and molecular processes that contribute to the healing response bring hope that safe and effective pharmacologic modulators of the corneal wound healing response may soon be developed.

Animals↗
PubMed1994

Pathogenesis of Sjögren's syndrome-like autoimmune lesions in MRL/lpr mice.

Sjögren's syndrome in humans is a chronic inflammatory disease with a presumed autoimmune etiology of the exocrine organs, involving in particular the salivary and lacrimal glands. The pathogenesis of this syndrome remains unclear, but the majority of infiltrating cells in the salivary glands are CD4+ T cells both in humans and rodents. Since many cytokines are involved in the development of T cell-mediated autoimmunity, local cytokine gene expression was analyzed in vivo using an animal model for Sjögren's syndrome in MRL/lpr mice. Overexpression of interleukin-1 (IL-1)beta and tumour necrosis factor (TNF) was detected before the onset of inflammatory lesions in the salivary gland, and the upregulation of IL-6 mRNA was also found in accordance with autoimmune sialadenitis in MRL/lpr mice. The inflammatory cytokines such as IL-1 beta, TNF, and IL-6 have proved to play important roles as regulatory proteins inducing autoimmune phenomena. In addition, the expression of T cell antigen receptor beta (TCR) beta transcripts in the salivary gland tissues was analyzed. Transcript for V beta 8 was predominantly detected in the T cells infiltrating sialadenitis from the onset of the disease, suggesting that CD4+ T cells bearing TCR V beta 8 play an essential role in recognizing unknown autopeptide in the autoimmune sialadenitis of MRL/lpr mice. Furthermore, Sjögren's syndrome-like autoimmune lesions were successfully transferred into severe combined immunodeficiency (SCID) mice, and these lesions were prevented by administration of anti-CD4, and anti-V beta 8 monoclonal antibodies. This article will review recent observations of these pathogenetic analyses of autoimmune sialadenitis as it occurs in MRL/lpr mice.

Animals↗
PubMed1986

[Structuro-functional units of the salivary and lacrimal glands].

By means of the multilayer graphic and plastic reconstruction methods using series of semithin sections, spatial tridimensional organization of the epithelial complexes and blood microcirculatory bed in the rat palatal salivary glands and the lacrimal gland of the human newborn have been studied. Since their ducts serve not only for discharging their secrete into the external medium, but also for accumulation (as collectors), the sublobular unit--adenomere should be referred to as a part of elementary level of organization of the epithelial complexes. The adenomere has in its composition a collecting centrally situating duct. However, while studying structure of the blood microcirculatory bed, it is found out that there is not any strict territorial correspondence between its functional units and structural units of the glandular epithelium. Nevertheless, giving a great importance to a tight syntopic connection of the collecting ducts of the adenomeres with the postcapillary venules (that belong to filtrating microvessels), these are sublobular units--adenomeres that are distinguished as structural-functional units in the glands.

Animals↗
PubMed1984

Prevention by pinealectomy of short-photoperiod-induced ultrastructural changes in the hamster Harderian gland.

Harderian gland ultrastructure was examined at biweeky intervals for 16 weeks after either pinealectomy or sham-operation of male and female hamsters kept in 1L:23D and 14L:10D photoperiods. Female characteristics such as membrane formations and extensive smooth endoplasmic reticulum appeared in the males kept under short photoperiod conditions. Similarly, male characteristics such as the tubular clusters appeared in the glands of females kept in the short photoperiod. When male and female hamsters were pinealectomized and exposed to the short photoperiod, the glands in each sex retained the characteristics typical of that sex. Atrophy of the testes and uteri was also observed in the sham-operated hamsters maintained under short photoperiods, but not in the pinealectomized animals. The changes observed in the Harderian glands and reproductive organs of hamsters kept in the short photoperiod were not observed in the hamsters maintained in the long photoperiod. The photoperiod-induced ultrastructural changes in the hamster Harderian glands are most likely due to changes in hormonal levels brought about by the regression of reproductive organs and can be prevented by pinealectomy.

Animals↗
PubMed2006

Polyethersulfone dead-end tube as a scaffold for artificial lacrimal glands in vitro.

Polyethersulfone (PES) dead-end tubes were fabricated by means of a phase inversion technique, and then were used as scaffolds for artificial lacrimal glands. The wall of the dead-end tubes could allow nutrients such as ascorbic acid, L-tryptophan, and glucose to pass through, but prevents rat IgG from passing through. Lacrimal acinar epithelial cells of Sprague-Dawley rats were cultured in vitro, and cell-associated secretory component was detected with an immunofluorescence technique to identify the acinar cells. The second passage of the cells showed high degree of cellular differentiation, and was used to seed on the PES tubes. The results showed that the PES tube could support the attachment, the growth, and the proliferation of the rat lacrimal acinar cells. Thus, PES is a substrate for the growth of lacrimal acinar cells and may be a useful scaffolding biomaterial for tissue engineering, such as a scaffold for artificial lacrimal glands.

Animals↗
PubMedDate not supplied

A day/night rhythm of vasopressin and oxytocin in rat retina, pineal and harderian gland.

Arginine vasopressin (AVP), oxytocin (OT) and neurophysins (Np) have been found in the pineal gland and the retina of the rat. Because the retina, pineal gland and Harderian gland (HG) serve analogous functions, we undertook a study to determine the presence of these peptides in these three organs of rats. They were detected by two specific methods: HPLC and specific radioimmunoassays. For Np, total neurophysins (NpT) were measured. To determine a 24 hr rhythm, the animals were maintained under a light/dark cycle of 12 hr/12 hr for 3 weeks. The pineal glands, retinae and HG were collected. Day/night rhythms of AVP, OT and NpT were demonstrated in the retina and HG; but the pineal gland had only AVP rhythm. A significant decrease in the rhythms at 4 a.m. was demonstrated in the retina and HG. The 24 hr variation of AVP in the retina seemed parallel to that of the HG.

Animals↗
PubMed1982

Microtubules and protein secretion in rat lacrimal glands: localization of short-term effects of colchicine on the secretory process.

The pathway and kinetics of the secretory protein transport in rat lacrimal exorbital gland have been established by an in vitro time-course radioautographic study of pulse-labeled protein secretion. The colchicine-sensitive steps have been localized by using the drug at various times with respect to the pulse labeling of proteins. Colchicine (10 microM) does not block any step of the secretory protein transport, but when introduced before the pulse it decreases the transfer of labeled proteins from the rough endoplasmic reticulum to the Golgi area, suppressing their temporary accumulation in the Golgi area before any alteration of this organelle is detectable. Moreover, colchicine inhibits protein release only from the secretory granules formed in its presence because the peroxidase discharge is diminished 1 h after colchicine addition, and the secretion of newly synthesized proteins is strongly inhibited only when colchicine is introduced before secretory granule formation. Morphometric studies show that there is a great increase of secondary lysosomes, related to crinophagy, as early as 40-50 min after colchicine is added. However, changes in lysosomal enzymatic activities remained biochemically undetectable. We conclude that: (a) the labile microtubular system does not seem indispensable for protein transport in the rough endoplasmic reticulum-Golgi area but may facilitate this step, perhaps by maintaining the spatial organization of this area; and (b) in the lacrimal gland, colchicine inhibits protein release not by acting on the steps of secretion following the secretory granule formation, but by acting chiefly on the steps preceding secretory granule formation, perhaps by making the secretory granules formed in its presence incapable of discharging their content.

Animals↗
PubMed1980

[Light and electron microscopy studies of actinomycosis of the lacrimal duct].

For the first time we present electron-microscopic results of an actinomycosis of the lacrimal canaliculus. The interior of the actinomycotic conglomerate showed no evidence of a cellular defence reaction but in the loosly woven outer network of hyphae we observed a massive granulocytic reaction. Also, after phagocytosis the structure of the actinomycotic micro-organisms within the granulocytes is not significantly damaged. Within the tissue of the lacrimal canaliculus adjacent to the actinomycotic conglomerate we observed an increased number of plasmacells but no pathogenic organisms.

Actinomycosis↗
PubMed1997

Squamate Harderian gland: an overview.

BACKGROUND: The Harderian gland is an orbital feature found in most terrestrial vertebrates. Although there have been several reports on the structure of the squamate Harderian gland, there has been little recent discussion as to its potential function. This article reviews both the recent morphological observations and their implications on the potential functions of the squamate Harderian gland. METHODS: Literature on the gross structure, histochemistry, and ultrastructure of the squamate Harderian gland and associated structures was reviewed. These observations were then used to assess morphologically the likelihood of the proposed functions. RESULTS: A high level of morphological variation was found in the squamate Harderian gland. Three functional hypotheses, including roles in orbital lubrication, digestion, and vomerolfaction, were considered. Both morphology of the squamate Harderian gland and the presence of alternate secretory sources suggest that it is unlikely to function in orbital lubrication. There is little evidence to suggest a function in digestion. Both the presence of the connecting lacrimal apparatus and the reduced intrinsic secretory capacity of the vomeronasal organ suggest that the Harderian gland may function in vomerolfaction. CONCLUSIONS: The most likely role of the squamate Harderian gland seems to be in vomerolfaction. Morphological variations observed in the Harderian gland may mirror the different degrees and mechanisms of vomerolfaction. Further studies, including comparative morphological, experimental, and microchemical analyses, are required to test this hypothesis.

Animals↗
PubMed1976

Plasma cell content of main and accessory lacrimal glands and conjunctiva.

The size, weight, and plasma cell content of main and accessory lacrimal glands were examined and compared to the number of plasma cells in the conjunctiva. There were from four to 35 accessory lacrimal glands in the upper conjunctiva and a rare accessory gland in the lower conjunctiva. The total accessory gland mass was approximately one tenth of the lacrimal gland mass although the number of plasma cells was approximately 1/20 of the mass. The number of plasma-cells in the lacrimal gland was estimated to be 3,200,000; in the conjunctiva, 2,100,000; and for the accessory glands, 180,000. Because of the many plasma cells in the relatively inaccessible lacrimal gland, cells of the lymphatic series may home to the lacrimal gland by non-antigenic mechanisms.

Adult↗
PubMed2004

Lymphoproliferative disorders in Sjögren's syndrome.

Sjögren's syndrome (SS) is a chronic organ-specific autoimmune disease characterized by lymphocytic infiltration into the salivary and lacrimal glands. About half of primary SS patients develop systemic disorders. Primary SS can be divided into three stages according to the extent of organ damage and the course of the disease. In stage I, (approx. 45% of cases), patients have only sicca syndrome and do not experience any systemic involvement, even after 10 years. In stage II (approx. 50% of cases), patients experience lymphocytic organ damage, which may involve the pulmonary, renal, hepatic, hematologic, and/or dermatologic systems, among others. Finally, in stage III (approx. 5% of cases), patients develop malignant lymphomas. Lymphomas in salivary glands are thought to arise from lymphoepithelial lesions in which there are close interactions among epithelial cells, T cells, and B cells. The B cells in the lesions become activated through the interaction between CD40L and CD40. The progression from polyclonal lymphoproliferation to monoclonal lymphoproliferation, to mucosa-associated lymphoid tissue (MALT) lymphoma, and finally to high-grade malignant lymphoma is regarded as a multi-step process. Antigenic activation of B cells, together with oncogenic events, including p53 inactivation and bcl-2 activation, may play important roles in B cell monoclonal proliferation and malignant transformation. The rheumatoid factor clone is regarded as a candidate B cell clone that undergoes transformation.

B-Lymphocytes↗