Abnormal Histones Acetylation In Patients With Primary Sjögren’s Syndrome

2020 ◽  
Author(s):  
Yan Li ◽  
Xiuying Lv ◽  
Mi Zhou ◽  
Yan He ◽  
Ying Wang ◽  
...  

Abstract Background pSS is an autoimmune disease characterized by an exocrine gland epithelium injury with dense lymphocytic infiltration, involvement of the peripheral nervous, pulmonary, blood, kidney, skin, and joint. Aberrant histone acetylation is increasingly thought to plays important role in the pathogenesis of AIDs. However, there is very little data on histone acetylation in pSS. Methods We investigated the expressions of HAT genes (p300, CREEBP and PCAF) by real time PCR in PBMCs from pSS patients. HAT activity and histone H3/ H4 acetylation activity measured by activity kit and histone H3/H4 acetylation verified by WB. Spearman test was utilized to analyze the association between levels of HAT activity and clinical parameters of patients with pSS. Results The expressions of p300, CREEBP and PCAF in PBMCs from pSS patients were decreased in mRNA comparison with HCs. HAT activity and histone H3/H4 acetylation were reduced in PBMCs from pSS patients. We found negatively correlations between the HAT activity and CRP and TNF-α, and positively correlations between the HAT activity and C4. Conclusions Histone hypoacetylation is observed in patients with pSS and involved in the disease duration of Sjogren's syndrome.

Diagnostics ◽  
2021 ◽  
Vol 11 (7) ◽  
pp. 1260
Author(s):  
Sneha Centala ◽  
Joyce H. Park ◽  
Diana Girnita

Sjogren’s syndrome is classically characterized by symptoms of keratoconjunctivitis sicca and xerostomia, secondary to lymphocytic infiltration of the salivary and lacrimal glands. Cutaneous findings of this disease are infrequently discussed and thus rarely considered among patients without the typical symptomatology. However, these patients can develop xerosis, alopecia, vitiligo, papular or nodular lesions, or cutaneous vasculitis. A 56-year-old Asian female presented with intermittent cutaneous erythematous lesions of her bilateral pinna and preauricular areas. Despite initial symptom presentation causing concern for tumid lupus versus cutaneous T cell lymphoma versus relapsing polychondritis, extensive serologic and histopathologic workup eventually indicated a likely diagnosis of Sjogren’s syndrome. This case brings to light that Sjogren’s syndrome is truly a multi-systemic disease and can present with primarily extra glandular cutaneous symptoms. When approaching the workup of a new patient, it is absolutely vital to maintain a broad differential and keep in mind that overlap syndromes among multiple autoimmune diseases do exist as well.


2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
M. Reale ◽  
C. D’Angelo ◽  
E. Costantini ◽  
M. Laus ◽  
A. Moretti ◽  
...  

Sjögren’s syndrome (SS) or sicca syndrome was described by Swedish ophthalmologist Sjögren in the year 1933 for the first time. The etiology of the SS is multifunctional and includes a combination of genetic predisposition and environmental as well as epigenetic factors. It is an autoimmune disease characterized by features of systemic autoimmunity, dysfunction, and inflammation in the exocrine glands (mainly salivary and lacrimal glands) and lymphocytic infiltration of exocrine glands. In fact, the involvement of lacrimal and salivary glands results in the typical features of dry eye and salivary dysfunction (xerostomia). Only in one-third of the patients also present systemic extraglandular manifestations. T cells were originally considered to play the initiating role in the autoimmune process, while B cells were restricted to autoantibody production. In recent years, it is understood that the roles of B cells are multiple. Moreover, autoantibodies and blood B cell analysis are major contributors to a clinical diagnosis of Sjögren’s syndrome. Recently, there has been rising interest in microRNA implication in autoimmunity. Unfortunately, to date, there are only a few studies that have investigated their participation in SS etiopathogenesis. The purpose of this work is to gather the data present in the literature to clarify this complex topic.


1975 ◽  
Vol 293 (24) ◽  
pp. 1228-1231 ◽  
Author(s):  
Joseph P. Michalski ◽  
Troy E. Daniels ◽  
Norman Talal ◽  
Howard M. Grey

2001 ◽  
Vol 23 (3) ◽  
pp. 199-205 ◽  
Author(s):  
Yelena Paranyuk ◽  
Nidia Claros ◽  
Aija Birzgalis ◽  
Leon C. Moore ◽  
Peter R. Brink ◽  
...  

Author(s):  
Dr Raja Singla ◽  
Dr Harish Kumar

Sjögren's syndrome is a chronic, slowly progressing autoimmune disorder characterised by lymphocytic infiltration of exocrine glands resulting in xerostomia and dry eyes (conjunctivitis). 1) The disease can present as an entity alone or in association with other auto-immune diseases like Scleroderma, RA, SLE & auto-immune thyroid disease. 2) In this article, attempt is made to understand the Sjögren's syndrome & its treatment in ayurveda by considering the concept of udakvaha srotodushti, vyadhikshamatva and vatadhikya vatrakta. Keywords:Auto-immune, Vatadhikya Vatrakta, Sjögren's syndrome, Udakvaha srotodushti


2018 ◽  
Vol 19 (11) ◽  
pp. 3628 ◽  
Author(s):  
Feeling Chen ◽  
Eliza Gaylord ◽  
Nancy McNamara ◽  
Sarah Knox

Sjögren’s syndrome (SS) is characterized by extensive lymphocytic infiltration of the salivary and lacrimal gland (LG), resulting in acinar cell destruction and organ dysfunction. The underlying pathogenesis of SS remains largely unknown, and studies historically focus on defining late-stage disease. Here, we identify tissue programs associated with disease onset using transcriptomic and immunohistological analysis of LGs from 5- and 7-week-old mice deficient in autoimmune response element (Aire). At 5 weeks of age (wk), Aire-/- mice show minimal tissue dysfunction and destruction compared to 7 wk Aire-/-, which exhibit severe dry eye, poor tear secretion, extensive lymphocytic infiltration, reduced functional innervation, and increased vascularization. Despite this mild phenotype, 5 wk Aire-/- LGs were highly enriched for signaling pathways previously associated with SS, including interferon gamma (IFNγ), interleukin 1 beta (IL1β), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), toll-like receptor (TLR) signaling, and interleukin-6/signal transducer and activator of transcription 3 (IL6/STAT3) signaling. Novel signaling pathways such as the semaphorin–plexin pathway were also noted. Intriguingly, we found an expansion of the ductal network with increasing disease. Activated STAT3, a blocker of apoptosis, was restricted to the ductal system and also increased with damage, highlighting its potential as a promoter of ductal cell survival. These data demonstrate the early activation of signaling pathways regulating inflammation, innervation, and cell survival before the onset of clinical disease indicators, suggesting their potential value as diagnostic biomarkers.


1979 ◽  
Vol 93 (9) ◽  
pp. 933-936 ◽  
Author(s):  
David M. Barrs ◽  
Thomas J. McDonald ◽  
Joseph Duffy

Synopsis-AbstractSJÖGREN's syndrome is a presumably autoimmune disease with parthologic findings of lymphocytic infiltration of the involved structures. Although the salivary and lacrimal gl ands are the most commonly involved sites, extragl andular lymphoproliferation also occurs. Upper and lower respiratory tract lymphoproliferation is known, but only one case of Sjögren's disease of the larynx has been previously reported. We present a case of laryngeal involvement in which the gross pathologic appearance is different from that in the earlier case report. The otolaryngologist should consider Sjögren's disease in the differential diagnosis of diffuse laryngeal lesions.


2012 ◽  
Vol 302 (9) ◽  
pp. C1331-C1345 ◽  
Author(s):  
Olutayo Odusanwo ◽  
Sreedevi Chinthamani ◽  
Andrew McCall ◽  
Michael E. Duffey ◽  
Olga J. Baker

Sjögren's syndrome is a chronic autoimmune disorder characterized by inflammation of salivary glands resulting in impaired secretory function. Our present studies indicate that chronic exposure of salivary epithelium to TNF-α and/or IFN-γ alters tight junction integrity, leading to secretory dysfunction. Resolvins of the D-series (RvDs) are endogenous lipid mediators derived from DHA that regulate excessive inflammatory responses leading to resolution and tissue homeostasis. In this study, we addressed the hypothesis that activation of the RvD1 receptor ALX/FPR2 in salivary epithelium prevents and/or resolves the TNF-α-mediated disruption of acinar organization and enhances monolayer formation. Our results indicate that 1) the RvD1 receptor ALX/FPR2 is present in fresh, isolated cells from mouse salivary glands and in cell lines of salivary origin; and 2) the agonist RvD1 (100 ng/ml) abolished tight junction and cytoskeletal disruption caused by TNF-α and enhanced cell migration and polarity in salivary epithelium. These effects were blocked by the ALX/FPR2 antagonist butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe. The ALX/FPR2 receptor signals via modulation of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathways since, in our study, blocking PI3K activation with LY294002, a potent and selective PI3K inhibitor, prevented RvD1-induced cell migration. Furthermore, Akt gene silencing with the corresponding siRNA almost completely blocked the ability of Par-C10 cells to migrate. Our findings suggest that RvD1 receptor activation promotes resolution of inflammation and tissue repair in salivary epithelium, which may have relevance in the restoration of salivary gland dysfunction associated with Sjögren's syndrome.


Sign in / Sign up

Export Citation Format

Share Document