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At least 649 records · Page 36Linked to original sources
PubMed1993

Adoptive transfer of experimental autoimmune dacryoadenitis in susceptible and resistant mice.

Strains of mice with diverse genetic backgrounds were compared for their ability to develop experimental autoimmune dacryoadenitis (EAD) after immunization with a purified lacrimal gland antigen (LG-Ag) in complete Freund's adjuvant. Susceptibility to the induction of EAD was linked to the murine H-2 histocompatibility background. SJL/J mice with the H-2s haplotype were the most susceptible to EAD, developing extensive cellular infiltration of the lacrimal gland, but those with the H-2d haplotype (BALB/c mice) or H-2q haplotype (DBA/J mice) were resistant to EAD, having little or no infiltration of the lacrimal gland. There was no correlation between the development of EAD and either the antibody response or the in vitro lymphocyte proliferative response to LG-Ag. The differences in the induction of EAD observed between susceptible and resistant strains resided in the different capacity of their lymphocytes to transfer disease. Splenocytes from susceptible SJL/J mice sensitized with LG-Ag in CFA could be activated in vitro with LG-Ag to transfer disease to normal syngeneic recipients. The capacity for adoptive transfer was abrogated by treatment with anti-Thy 1.2 antibody plus complement, an indication that T cells are responsible for the transfer of EAD. However, EAD cannot be transferred with the donor cells from resistant mice even after they have been cultured in vitro with LG-Ag. These results suggest that T cells play a major role in the induction of EAD and that variations in susceptibility are under the control of distinct genetically inherited mechanisms that may include active suppression.

Animals↗
PubMed1996

Mechanism of the development of autoimmune dacryodenitis in the mouse model for primary Sjögren's syndrome.

To elucidate the mechanism of development in autoimmune lacrimal gland disease, we analyzed different aspects of autoimmune dacryoadenitis in a newly established mouse model for primary Sjögren's syndrome, focusing on the local expressions of cytokine genes, and the repertoire of T cell receptor (TCR) V beta genes transcribed within the inflammatory infiltration in the lacrimal glands. We found that the vast majority of inflammatory infiltration into the lacrimal glands were CD4+ V beta 8+ T cells. We detected the up-regulation of local cytokine genes (IL-1 beta, TNF-alpha, IL-2, IFN-gamma, IL-10, IL-12p40) in the lacrimal glands with very early inflammatory lesions by reverse transcriptase (RT)-PCR analysis. The predominant expression of the V beta 8 gene segment was detected from a very early stage, while extensive age-related diversity of TCR V beta gene usage was observed. Single-strand conformation polymorphism (SSCP) analysis demonstrated a distinct and a common binding pattern in the PCR product of the V beta 8 gene on the infiltrating cells during the course of the disease. These data suggest that in autoimmune dacryoadenitis of the mouse model for primary Sjögren's syndrome there may be a restricted usage of TCR V beta elements on a very early stage of the autoimmune lesion to recognize unknown self-antigen, and the autoreactive CD4+ T cells constitute a unique cytokine profile in the autoimmune lacrimal gland disease.

Animals↗
PubMed1993

Treatment of experimental autoimmune dacryoadenitis with cyclosporin A.

Experimental autoimmune dacryoadenitis (EAD) was induced in SJL/J mice by a single injection of purified lacrimal gland antigen (LG-Ag) in complete Freund's adjuvant. The disease is characterized by lymphocytic infiltration of the lacrimal gland and production of lacrimal gland-specific antibodies. We examined the effects of cyclosporin A (CsA) on the development and progression of this inflammatory disease. CsA (100 mg/kg/day), given from the time of immunization for 14 days, completely blocked the development of EAD in all treated mice. Both cellular and humoral immune responses to LG-Ag were markedly reduced by the administration of CsA as evidenced by the near absence of lymphocyte proliferative response and the reduced production of circulating anti-LG-Ag antibodies. Delayed CsA treatment beginning on Day 7 after immunization totally abrogated the development of lacrimal histological lesions and lymphocyte proliferative response to LG-Ag. However, serum anti-LG-Ag titers were only marginally decreased in CsA-treated animals. Treatment with CsA was found effective even when daily injections were started 14 days after immunization with LG-Ag. CsA prevented the inflammatory cell response in 5 of 10 mice when the disease was established. The lymphocyte proliferative response to LG-Ag was moderately depressed in CsA-treated animals, but antibody titers were the same as those in the oil-treated control. These studies demonstrate that CsA has a therapeutic effect in this murine model of dacryoadenitis and suggest a critical role for T lymphocytes in the pathogenesis of EAD.

Animals↗
PubMed1993

HgCl2-induced glandular pathosis in the brown Norway rat.

Low doses of HgCl2 induce a genetically restricted autoimmune syndrome in Brown Norway (BN) rats (BN(Hg)). Part of the syndrome includes spontaneously developing mononuclear cell foci in salivary and lacrimal glands, morphologically similar to focal sialoadenitis in Sjögren's syndrome in man. In this study, we have shown that Hg-induced focal adenitis in BN rat is not female predominant and not solely dependent on Hg uptake in the glands. In BN(Hg), focal adenitis was found to develop in several different glands (parotid, submandibular, lacrimal, thyroid) as a specific manifestation of immunopathosis induced by Hg in the RT1n-haplotype-carrying BN. Such manifestations were absent in another strain, the Hg-resistant Lewis (RT1l). Also a potent contact sensitizer, DNFB, induced focal adenitis in isolated glands, provided that strong sensitization had occurred. Immunohistochemical characterization of focal adenitis in BN(Hg) with monoclonal antibodies showed that T cells and dendritic cells dominate the early infiltrates, whereas B cells were absent.

Animals↗
PubMed1998

Lacrimal gland innervation is not altered with the onset and progression of disease in a murine model of Sjögren's syndrome.

The lacrimal glands of patients with Sjögren's syndrome develop extensive lymphocytic infiltration, but also contain a large number of seemingly healthy looking acinar and ductal cells. Despite this, the secretory function of this tissue is impaired, leading to aqueous tear-deficient dry eye. This raises the possibility that there is a defect in the neural innervation of the remaining portion of the lacrimal gland. To test for this possibility, we used antibodies specific to various markers of the parasympathetic, sympathetic, and sensory nerves and performed immunohistochemical analyses of lacrimal glands from a murine model of Sjögren's syndrome, the MRL/Mp-Fas-lpr/lpr (MRL/lpr) and the control mice MRL/Mp-+/+ (MRL/+). Our results show that the MRL/lpr, but not the MRL/+, lacrimal glands become infiltrated with lymphocytes starting at 8 weeks of age which worsens by 12 and 18 weeks. The density and the pattern of parasympathetic, sympathetic, and sensory innervation of the noninflamed acinar tissue of MRL/lpr lacrimal glands, at 4, 8, 12, and 18 weeks, is indistinguishable from that of age-matched control MRL/+ lacrimal glands. We conclude that the loss of the secretory function in Sjögren's syndrome lacrimal glands is not due to a loss or decrease of its innervation.

Aging↗
PubMed1998

Ca2+ signaling by cholinergic and alpha1-adrenergic agonists is up-regulated in lacrimal and submandibular glands in a murine model of Sjögren's syndrome.

Innervation of the lacrimal gland of MRL/Mp-Fas-lpr/lpr (MRL/lpr), a murine model for Sjögren's syndrome, is unaltered with the onset or progression of the lymphocytic infiltration. To determine whether lacrimal and submandibular gland cells are able to respond to external stimuli, acini were prepared from MRL/lpr (diseased) and MRL/Mp-+/+ (MRL/+, control) mice at 4, 8, and 12 weeks of age and loaded with the fluorescent dye fura-2 to monitor changes in the intracellular Ca2+ concentration ([Ca2+]i) in response to cholinergic and alpha1-adrenergic stimulation, two major stimuli of lacrimal gland protein secretion. Cholinergic-induced [Ca2+]i increase was up-regulated 3- and 4-fold in lacrimal gland acini isolated from 8- and 12-week-old MRL/lpr mice, respectively, compared to 4-week-old animals, but was not up-regulated in age-matched MRL/+ control mice. Similarly, alpha1-adrenergic-induced [Ca2+]i increase was up-regulated 7- and 12-fold in acini isolated from 8- and 12-week-old MRL/lpr mice, respectively, compared to 4-week-old animals, but was not up-regulated in MRL/+ mice. Cholinergic-induced [Ca2+]i increase in submandibular gland acini of MRL/lpr and MRL/+ mice was the same at all ages. In contrast, alpha1-adrenergic-induced [Ca2+]i increase was up-regulated 3-fold in acini from 12-week-old MRL/lpr mice, compared to 4-week-old mice, but was not up-regulated in age-matched MRL/+ mice. We conclude that the Ca2+ signaling portion of cholinergic and alpha1-adrenergic pathway in the lacrimal gland and the Ca2+ signaling portion of alpha1-adrenergic pathway in the submandibular gland is up-regulated with the onset and progression of the lymphocytic infiltration in the MRL/lpr murine model of Sjögren's syndrome.

Adrenergic alpha-Agonists↗
PubMed1999

Impact of gender on exocrine gland inflammation in mouse models of Sjögren's syndrome.

Sjögren's syndrome is a complex autoimmune disorder, that occurs almost exclusively in females, induces extensive lymphocyte accumulation in lacrimal and salivary glands, and represents one of the leading causes of dry eye and mouth in the world. The purpose of this study was to determine whether the profound, gender-related differences observed in the magnitude of exocrine gland inflammation in Sjögren's syndrome may also be found in tissues of mouse models of this disorder. Lacrimal and submandibular glands were obtained from adult MRL/lpr, MRL+/+ (MRL+), NZB/NZW F1 (F1), C3H/lpr, C3H/gld (gld), C57BL/6-lpr/lpr [B6/lpr; with (bcl-2(+)/lpr) or without (bcl-2(-)/lpr) bcl-2 transgene insertion] and nonobese diabetic (NOD) mice after the onset of autoimmune disease, and processed for microscopy and image analysis. Our results showed that: (1) the extent of inflammation was significantly greater in lacrimal glands of female MRL/lpr, MRL+, F1, C3H/lpr and gld mice, and salivary glands of female MRL+, F1 and gld mice, relative to those of males; (2) the severity of inflammation in NOD mice showed a tissue-specific pattern: inflammation was far worse in lacrimal glands of males, whereas immune pathology was far greater in salivary tissues in females; and (3) no gender-related variations were present in the degree of inflammation in lacrimal glands of bcl-2(+)/lpr and bcl-2(-)/lpr mice or in submandibular tissues of MRL/lpr, C3H/lpr, bcl-2(+)/lpr and bcl-2(-)/lpr mice. Our findings demonstrate that gender-, strain- and tissue-related differences exist in the extent of inflammation in several mouse models of Sjögren's syndrome.

Animals↗
PubMed2000

Autologous lacrimal-lymphoid mixed-cell reactions induce dacryoadenitis in rabbits.

Autoimmune dacryoadenitis, such as occurs in Sjögren's syndrome, is a frequent cause of lacrimal insufficiency, which in turn can cause dry eye. Rabbits are used frequently to test ocular therapies. Our goal is to develop a rabbit model of autoimmune dacryoadenitis to identify and test candidate therapies. Our approach arises from the observations that lacrimal gland epithelial cells stimulate proliferation in cultured autologous lymphocyte preparations and that an anti-MHC II antibody blocks this proliferation. The purpose of this study was to determine if injecting this proliferating autologous mixed cell reaction could induce dacryoadenitis in rabbits. After establishing that irradiated lacrimal gland epithelial cells stimulate proliferation in autologous peripheral blood lymphocytes, irradiated cells from a single lacrimal gland were co-cultured with autologous lymphocytes and after 5 days the mixed cell reaction, or components of the reaction, were injected into the contralateral lacrimal gland of the donor rabbit. After 2 weeks, the injected glands were removed and lymphocytic infiltration quantitated using digital image analysis of immunostained histological sections. Injecting an autologous mixed cell reaction of co-cultured irradiated lacrimal gland epithelial cells and lymphocytes reliably induced abundant periductal foci of >200 lymphocytes expressing CD18 and/or a rabbit thymic lymphocyte antigen (RTLA). Injection of medium or autologous lymphocytes alone elicited little response; injections of lymphocytes cultured with lysates of lacrimal gland epithelial cells elicited variable, modest responses. These lysates did not stimulate proliferation in the mixed cell reaction and proliferation was not observed if a porous membrane separated co-cultured lacrimal gland cells and lymphocytes. The results demonstrate that injecting an autologous mixed cell reaction of lacrimal gland epithelial cells and lymphocytes reliably creates a model of autoimmune dacryoadenitis. The relative ineffectiveness of components of the reaction to do the same supports the hypothesis that lacrimal gland epithelial cells trigger or exacerbate lacrimal autoimmune disease by presentation of autoantigens via MHC II. This experimental system can aid efforts to further understand mechanisms of diseases, and to identify and test candidate therapies.

Animals↗
PubMed1978

Anatomy of the naso-lacrimal duct in new-borns: therapeutic considerations.

The topography and morphology of the lacrimal ducts in newborn infants was demonstrated by means of post mortem dacryocystograms and microphotograms of histologic slides. Because of bends in the course of the lower tear duct, a percentage of probings will fail to effect satisfactory perforation of the Hasner membrane. In most cases, the soft texture of this membrane requires no more than syringing under pressure, using a hollow probe as described by Bangerter (1953).

Autopsy↗
PubMed1996

Indirect immunofluorescence study of the cornea and the conjunctiva in a xenogeneic system: analysis of humoral reactivity in patients with Wegener's granulomatosis.

BACKGROUND: Ocular involvement in patients with Wegener's granulomatosis (WG) can cause progressive loss of vision. The pathophysiological events leading to the WG-specific ocular inflammation are unknown. METHODS: A method involving indirect immunofluorescence on bovine and porcine corneoconjunctival frozen sections was used to detect antibodies to corneal and conjunctival epithelium in serum samples from patients suffering from WG with ophthalmic involvement (orbital granuloma or ocular vasculitis, both active and inactive phase). Normal persons and WG patients without ophthalmic involvement served as control groups. Anti-human IgG, IgA and IgM were tested. RESULTS: Five different immunofluorescence patterns could be distinguished in each species. There were differences in the reactivity with bovine and porcine tissue. Every pattern was caused mainly by human IgG. The antibodies were directed to the cell nuclei or to extranuclear structures. All patterns also occurred frequently in normal sera. No pattern was found that occurred specifically in the serum of patients with WG and ocular inflammation. CONCLUSIONS: The results indicate that this immunofluorescence system does not detect a characteristic antibody profile that could be attributed to the serum of WG patients. Hence the approach lacks clinical usefulness as a diagnostic procedure.

Animals↗
PubMed1991

Chronic bilateral dacryo-adenitis in identical twins: a possible incomplete form of Sjögren syndrome.

We report an unusual case of chronic bilateral dacryo-adenitis in 10-year-old identical twin sisters. Both girls presented with bilateral lacrimal gland enlargement and developed moderate xerophthalmia and keratitis. Both the lacrimal and minor salivary gland biopsies showed a non-granulomatous inflammatory infiltration of mono-nuclear cells. All granulomatous diseases and neoplasms could therefore be ruled out and only Sjögren syndrome and very few other forms of chronic dacryo-adenitis remained as possible diagnoses. Both patients and their parents were evaluated for auto-antibodies. Very low titres of smooth muscle antibodies were found in one, antinuclear antibodies in two and anti-dsDNA antibodies in all four members of the family. Even though the titres of antinuclear and anti-dsDNA antibodies increased in one of the sisters, both patients did not develop any sign or symptom of a systemic connective tissue disease. During the 6 years' follow up, both patients showed persistent tarsal gland enlargement but no other symptoms apart from a moderate xerophthalmia and occasional mild keratitis.

Biopsy↗
PubMed1983

Clinical and histocytopathological study of chronic dacryoadenitis.

Chronic dacryoadenitis occurs mainly in males over 40 years of age and is characterized by mild inflammatory signs, such as swelling and redness of the eyelid without tenderness, bulbar conjunctival stasis and chemosis. The patient has slight exophthalmos, good visual acuity and almost normal fundi. The clinical findings of chronic dacryoadenitis differ from those of benign mixed tumor. CT scan showed tumor shadows in the orbit of all our patients with chronic dacryoadenitis, but failed to differentiate this disease from benign mixed tumor. Antibiotics and steroid hormone did not improve chronic dacryoadenitis, but extirpation was effective, and there was no recurrence. When examined by light microscopy, chronic dacryoadenitis showed prominent proliferation of connective tissues and local infiltration of monocytes, lymphocytes and eosinophils. On electron microscopy, the basal lamina of myoepithelial cells of some acini was thickened. In some acini, intercellular spaces between epithelial cells or epithelial and myoepithelial cells were wide, but the intercellular junction looked intact.

Adult↗
PubMed1990

Immunohistochemical characterization of epithelial cells in human lacrimal glands. II. Inflammatory and neoplastic lesions of lacrimal glands.

The distribution of cytokeratins (CK), actin, lactoferrin (Lf), lysozyme (Ly), vimentin and S-100 protein was immunohistochemically investigated in paraffin-embedded specimens of five inflammatory and five neoplastic lesions of lacrimal glands (LGs). Atrophic acini in dacryoadenitis reacted with antibodies (ABs) KL1 and Pkk1 (CK 7, 8, 17, 18) in a manner similar to ducts. Apart from myoepithelial cells and some luminal-duct cells, the remaining epithelia in dacryoadenitis were negative with AB 34 beta E12 (CK 5). The number of AB HHF35 (actin)-positive myoepithelial cells was not altered in dacryoadenitis. Epithelia in dacryoadenitis reacted weakly but consistently with Lf while revealing weak and inconsistent staining for Ly. Vimentin was negative in epithelial cells in dacryoadenitis except in one case. S-100 protein was detected only in epithelia of inflammatory major LGs. Epimyoepithelial islands in lymphoepithelial proliferation reacted variably for CKs, Lf, Ly and vimentin and remained negative for actin and S-100. In pleomorphic adenomas, neoplastic cells showing duct-like differentiation (luminal) reacted consistently with CK 7, 8, 17, 18 and S-100 protein and inconsistently with CK 5, Lf and Ly but remained negative for actin and vimentin. Other neoplastic cells (ovoid/peripheral cells) stained consistently for CK 5, vimentin and S-100 protein and focally for CK 7, 8, 17, 18, actin, Lf and Ly. Spindle-form neoplastic cells found in the stroma exhibited vimentin and S-100 protein and, less frequently, actin. Determination of these antigens in pleomorphic LG adenomas may help to evaluate their prognosis.

Actins↗