ABSTRACT
The vomeronasal organ (VNO) is a tubular pheromone-sensing organ in which the lumen is covered with sensory and non-sensory epithelia. This study used immunohistochemistry and lectin histochemistry techniques to evaluate developmental changes, specifically of the glycoconjugate profile, in the horse VNO epithelium. Immunostaining analysis revealed PGP9.5 expression in some vomeronasal non-sensory epithelium (VNSE) cells and in the vomeronasal receptor cells of the vomeronasal sensory epithelium (VSE) in fetuses, young foals, and adult horses. Olfactory marker protein expression was exclusively localized in receptor cells of the VSE in fetuses, young foals, and adult horses and absent in VNSE. To identify the glycoconjugate type, lectin histochemistry was performed using 21 lectins. Semi-quantitative analysis revealed that the intensities of glycoconjugates labeled with WGA, DSL, LEL, and RCA120 were significantly higher in adult horse VSE than those in foal VSE, whereas the intensities of glycoconjugates labeled with LCA and PSA were significantly lower in adult horse VSE. The intensities of glycoconjugates labeled with s-WGA, WGA, BSL-II, DSL, LEL, STL, ConA, LCA, PSA, DBA, SBA, SJA, RCA120, jacalin, and ECL were significantly higher in adult horse VNSE than those in foal VNSE, whereas the intensity of glycoconjugates labeled with UEA-I was lower in adult horse VNSE. Histochemical analysis of each lectin revealed that various glycoconjugates in the VSE were present in the receptor, supporting, and basal cells of foals and adult horses. A similar pattern of lectin histochemistry was also observed in the VNSE of foals and adult horses. In conclusion, these results suggest that there is an increase in the level of N-acetylglucosamine (labeled by WGA, DSL, LEL) and galactose (labeled by RCA120) in horse VSE during postnatal development, implying that they may influence the function of VNO in adult horses.
Subject(s)
Vomeronasal Organ , Male , Humans , Horses , Animals , Vomeronasal Organ/metabolism , Prostate-Specific Antigen/metabolism , Epithelium/metabolism , Lectins/metabolism , Glycoconjugates/analysis , Glycoconjugates/metabolismABSTRACT
Experimental autoimmune uveitis (EAU), an animal model of human uveitis, is characterized by infiltration of autoimmune T cells in the uvea as well as in the retina of susceptible animals. EAU is induced by the immunization of uveitogenic antigens, including either retinal soluble-antigen or interphotoreceptor retinoid-binding proteins, in Lewis rats. The pathogenesis of EAU in rats involves the proliferation of autoimmune T cells in peripheral lymphoid tissues and breakdown of the blood-retinal barrier, primarily in the uvea and retina, finally inducing visual dysfunction. In this review, we describe recent EAU studies to facilitate the design of a therapeutic strategy through the interruption of uveitogenic factors during the course of EAU, which will be helpful for controlling human uveitis.
ABSTRACT
Osteopontin (OPN) is an extracellular matrix protein with a diverse range of functions, including roles in cell adhesion, migration, and immunomodulation, which are associated with the modulation of neuroinflammation in the central nervous system. The present study was performed to evaluate the involvement of OPN in the eyes of an experimental autoimmune uveoretinitis (EAU) model. The EAU model was developed by immunization of Lewis rats with interphotoreceptor retinoid-binding protein. The results showed the OPN level was remarkably upregulated in the eye of EAU rats on day 9 post-immunization. The level of CD44, a ligand of OPN, was increased in the ciliary body of EAU rats. Furthermore, OPN was also detected in the ciliary body and activated microglia/macrophages in the EAU retina. The results suggest that OPN was significantly upregulated in the eyes of EAU rats, and that it may be useful as an early biomarker of ocular autoimmune diseases. All animal experiments were approved by the Institutional Animal Care and Use Committee of Jeju National University (approval No. 2020-0012) on March 11, 2020.
ABSTRACT
Experimental autoimmune uveitis (EAU) is an animal model of human autoimmune uveitis that is characterized by the infiltration of autoimmune T cells with concurrent increases in pro-inflammatory cytokines and reactive oxygen species. This study aimed to assess whether betaine regulates the progression of EAU in Lewis rats. EAU was induced via immunization with the interphotoreceptor retinoid-binding protein (IRBP) and oral administration of either a vehicle or betaine (100 mg/kg) for 9 consecutive days. Spleens, blood, and retinas were sampled from the experimental rats at the time of sacrifice and used for the T cell proliferation assay, serological analysis, real-time polymerase chain reaction, and immunohistochemistry. The T cell proliferation assay revealed that betaine had little effect on the proliferation of splenic T cells against the IRBP antigen in an in vitro assay on day 9 post-immunization. The serological analysis showed that the level of serum superoxide dismutase increased in the betainetreated group compared with that in the vehicle-treated group. The anti-inflammatory effect of betaine was confirmed by the downregulation of pro-inflammation-related molecules, including vascular cell adhesion molecule 1 and interleukin-1ß in the retinas of rats with EAU. The histopathological findings agreed with those of ionized calcium-binding adaptor molecule 1 immunohistochemistry, further verifying that inflammation in the retina and ciliary bodies was significantly suppressed in the betaine-treated group compared with the vehicle-treated group. Results of the present study suggest that betaine is involved in mitigating EAU through anti-oxidation and anti-inflammatory activities.
ABSTRACT
Periostin plays a critical role in tissue regeneration and homeostasis. The aim of this study was to evaluate the changes in periostin levels in the hearts of rats with experimental autoimmune myocarditis (EAM). Western blot analysis revealed that the expression levels of periostin and alpha-smooth muscle actin were significantly increased at day 14 post-immunization. Immunohistochemical analysis indicated that periostin was expressed in macrophages and fibroblasts in the hearts of EAM-induced rats. In conclusion, these results suggest that increased periostin expression in macrophages and fibroblasts promotes cardiac fibrosis in EAM-induced rats, potentially by enhancing immune cell infiltration. Therefore, periostin should be further investigated as a candidate therapeutic target for myocarditis.
