Role In Triggering Research Articles

A case of late-onset and long term of anti-NMDA-receptor encephalitis in a 50-year-old patient with culturally acceptable psychosis and cognitive decline

IntroductionAnti-NMDA-receptor encephalitis is a severe rare acute form of encephalitis caused by an autoimmune process with the synthesis of autoantibodies to the glutamate receptors. The average age of onser is estimated to be 23-25 years. A typical clinical picture consist of prodromal, psychotic, areactive, hyperkinetic phases, and a phase of gradual regression of symptoms. The disease usually lasts for a several weeks with spontaneous recovery or fatal outcome and caused by neoplastic process. Our case demonstrates that the course of anti-NMDAR encephalitis is possible at more mature age in the form of a long process with cultural features, without significant catadrome, inflammation and associated neoplastic process.Objectives50-year-old Buddhist Buryat woman with complaints about hypomnesia, anosmia and dissomnia. The disease began with impaired consciousness, disorientation, seizures and memory loss 4 years ago. Then after a visit of Lama, the symtoms described above spontaneously reduced and schizophrenia-like psychosis developed (voice of Lama in the head, a belief in the existence of super-powers, disorganized behavior), mild neurological and severe neurocognitive symptoms, weight loss, intolerance to antipsychotics in minimal daily doses.MethodsExamination included: CBC, metabolic panel, coagulogram, tumor markers, CSF, MRI, PET, specialists.ResultsCBC, metabolic blood analysis, tumor markers - within the reference values. CSF: cytosis 9/3, glucose 5.5 mmol/l, Pandi++, Nonnet-Apeltau+, antibodies to the NMDA receptor - 8. MRI: signs of the consequences of encephalitis. PET: no signs of metabolic activity of the malignant process.ConclusionsThe diagnosis of anti-NMDA-receptor-encephalitis was confirmed by the laboratory and clinical criteria despite unususal course and age. The trigger role of herpes is possible, but not verified.DisclosureNo significant relationships.

Immune-Mediated Intraocular Inflammation. Review

Immune mediated inflammatory diseases are categorized into autoimmune and autoinflammatory. Autoimmune etiology is represented by autoreactive lymphocytes or autoantibodies, e.g. primary Sjögren‘s syndrome or rheumatoid arthritis. Ocular specific diseases with presumed autoimmune origin are sympathetic ophthalmia or birdshot chorioretinopathy. Autoinflammatory diseases are caused by mutations in regulatory genes for specific immunity. Hereditary periodic fevers represent monogenic autoinflammatory diseases; eye specific is Blau syndrome also named sarcoidosis with early onset. This article reviews the actual knowledge about immune mediated uveitides, their immunological mechanisms and the possible trigger role of infection in autoimmune inflammation. Immune privilege provides a protection of the eye against any strong immune reaction to foreign antigen, based on physical, immune, humoral and molecular mechanisms. Antigens hidden within the eye are revealed in case of damage of hematoretinal barrier caused by infection or mechanical insult. These ocular antigens have not been set as tolerable during the development and immune reaction is initiated subsequently. Current studies demonstrate that uveogenic trigger might be generated by own microbiome, particularly when dysregulated, so called dysbiosis. There is a known association between idiopathic inflammatory bowel disease with ankylosing spondylitis and anterior uveitis in humans. Intensive research is focused on microbiome and immune mediated inflammatory disease to influence therapeutically the intestinal microbiome. The animal models are used to study the immunopathological mechanisms of uveitis and the new therapeutic strategies, because of relatively low incidence of immune mediated uveitis in humans.

Evaluation of shear slip stress transfer mechanism for induced microseismicity at In Salah CO2 storage site

Stress transfer caused by injection-induced fault reactivation plays a significant role in triggering induced seismicity. This work aims to investigate to which extent the shear slip stress transfer mechanism might have contributed to a 4-month period of heightened microseismicity around one of the horizontal injection wells (KB-502) at the In Salah CO2 storage site. Building upon previous reservoir modelling and history matching work by the authors, coupled geomechanical and reservoir modelling of CO2 injection at KB-502 was carried out, featuring the explicit simulation of injection-induced fault reactivation and stress transfer, and the implementation of a strain-dependent permeability model to represent the fault hydrological behaviour. This approach allows a much-improved overall match to the field bottomhole pressures at KB-502 over the previous results, where fault zone reactivation and associated dynamic permeability behaviour were not considered, especially over the 4-month period of interest. Based upon the coupled modelling results, Coulomb stress changes were used to evaluate the potential for enhanced microseismicity related to CO2 injection-induced fault reactivation at KB-502. Analyses on the potential for microseismicity have shown that seismic events are likely to take place in both hydraulically connected regions and stress transfer influenced regions. The variation of computed Coulomb stress changes in near-fault areas compares favourably with the heightened field recorded seismicity during the period modelled. The integrated interpretation of microseismic monitoring and coupled geomechanics and reservoir modelling have suggested that the shear slip stress transfer mechanism was active and contributed to the occurrence of induced seismicity at In Salah.

Takotsubo Syndrome: Clinical Manifestations, Etiology and Pathogenesis.

The purpose of the review is the analysis of clinical and experimental data on the etiology and pathogenesis of takotsubo syndrome (TS). TS is characterized by contractile dysfunction, which usually affects the apical region of the heart without obstruction of coronary artery, moderate increase in myocardial necrosis markers, prolonged QTc interval (in 50% of patients), sometimes elevation of ST segment (in 19% of patients), increase N-Terminal Pro-B-Type Natriuretic Peptide level, microvascular dysfunction, sometimes spasm of the epicardial coronary arteries (in 10% of patients), myocardial edema, and life-threatening ventricular arrhythmias (in 11% of patients). Stress cardiomyopathy is a rare disease, it is observed in 0.6 - 2.5% of patients with acute coronary syndrome. The occurrence of takotsubo syndrome is 9 times higher in women, who are aged 60-70 years old, than in men. The hospital mortality among patients with TS corresponds to 3.5% - 12%. Physical or emotional stress do not precede disease in all patients with TS. Most of patients with TS have neurological or mental illnesses. The level of catecholamines is increased in patients with TS, therefore, the occurrence of TS is associated with excessive activation of the adrenergic system. The negative inotropic effect of catecholamines is associated with the activation of β2 adrenergic receptors. An important role of the adrenergic system in the pathogenesis of TS is confirmed by studies which were performed using 125I-metaiodobenzylguanidine (125I -MIBG). TS causes edema and inflammation of the myocardium. The inflammatory response in TS is systemic. TS causes impaired coronary microcirculation and reduces coronary reserve. There is a reason to believe that an increase in blood viscosity may play an important role in the pathogenesis of microcirculatory dysfunction in patients with TS. Epicardial coronary artery spasm is not obligatory for the occurrence of TS. Cortisol, endothelin-1 and microRNAs are challengers for the role of TS triggers. A decrease in estrogen levels is a factor contributing to the onset of TS. The central nervous system appears to play an important role in the pathogenesis of TS.

Role of protons in calcium signaling.

Thirty-six years after the publication of the important article by Busa and Nuccitelli on the variability of intracellular pH (pHi) and the interdependence of pHi and intracellular Ca2+ concentration ([Ca2+]i), little research has been carried out on pHi and calcium signaling. Moreover, the results appear to be contradictory. Some authors claim that the increase in [Ca2+]i is due to a reduction in pHi, others that it is caused by an increase in pHi. The reasons for these conflicting results have not yet been discussed and clarified in an exhaustive manner. The idea that variations in pHi are insignificant, because cellular buffers quickly stabilize the pHi, may be a limiting and fundamentally wrong concept. In fact, it has been shown that protons can move and react in the cell before they are neutralized. Variations in pHi have a remarkable impact on [Ca2+]i and hence on some of the basic biochemical mechanisms of calcium signaling. This paper focuses on the possible triggering role of protons during their short cellular cycle and it suggests a new hypothesis for an IP3 proton dependent mechanism of action.

Near-surface softening and healing in eastern Honshu associated with the 2011 magnitude-9 Tohoku-Oki Earthquake

The near-surface part of the crust, also called the skin of the earth, is the arena of human activity of which the stiffness is of great concern to engineers in infrastructure construction. The stiffness reduction of near-surface geomaterials also plays a vital role in geohazards triggering. However, the physical mechanism behind the material softening is still not fully understood. Here, we report a coseismic shear-wave velocity reduction in the near surface by up to a few tens of percent during the strongest shaking from the 11 March 2011 Tohoku-Oki Earthquake and a subsequent two-stage healing process including a rapid recovery within a few minutes and a slow recovery over many years. We also present a theoretical contact model between mineral grains in geomaterials containing multiple metastable contacts at small separations due to the oscillatory hydration interaction, which can explain the emergence of different stages in the healing process.

Medication-Related Osteonecrosis of the Jaw (MRONJ): Are Antiresorptive Drugs the Main Culprits or Only Accomplices? The Triggering Role of Vitamin D Deficiency.

Osteonecrosis of the jaw (ONJ) is a severe clinical condition characterized mostly but not exclusively by an area of exposed bone in the mandible and/or maxilla that typically does not heal over a period of 6–8 weeks. The diagnosis is first of all clinical, but an imaging feedback such as Magnetic Resonance is essential to confirm clinical suspicions. In the last few decades, medication-related osteonecrosis of the jaw (MRONJ) has been widely discussed. From the first case reported in 2003, many case series and reviews have appeared in the scientific literature. Almost all papers concerning this topic conclude that bisphosphonates (BPs) can induce this severe clinical condition, particularly in cancer patients. Nevertheless, the exact mechanism by which amino-BPs would be responsible for ONJ is still debatable. Recent findings suggest a possible alternative explanation for BPs role in this pattern. In the present work we discuss how a condition of osteomalacia and low vitamin D levels might be determinant factors.

Expression Level of Mature miR172 in Wild Type and StSUT4-Silenced Plants of Solanum tuberosum Is Sucrose-Dependent.

In potato plants, the phloem-mobile miR172 is involved in the sugar-dependent transmission of flower and tuber inducing signal transduction pathways and a clear link between solute transport and the induction of flowering and tuberization was demonstrated. The sucrose transporter StSUT4 seems to play an important role in the photoperiod-dependent triggering of both developmental processes, flowering and tuberization, and the phenotype of StSUT4-inhibited potato plants is reminiscent to miR172 overexpressing plants. The first aim of this study was the determination of the level of miR172 in sink and source leaves of StSUT4-silenced as well as StSUT4-overexpressing plants in comparison to Solanum tuberosum ssp. Andigena wild type plants. The second aim was to investigate the effect of sugars on the level of miRNA172 in whole cut leaves, as well as in whole in vitro plantlets that were supplemented with exogenous sugars. Experiments clearly show a sucrose-dependent induction of the level of mature miR172 in short time as well as long time experiments. A sucrose-dependent accumulation of miR172 was also measured in mature leaves of StSUT4-silenced plants where sucrose export is delayed and sucrose accumulates at the end of the light period.

Characterizing the building blocks of Problematic Use of the Internet (PUI): The role of obsessional impulses and impulsivity traits among Italian young adults

BackgroundProblematic Use of the Internet (PUI) is a considerable issue of the modern era, but its risk factors are still poorly understood. Impulsivity and obsessive-compulsive symptoms have been associated with PUI, but this relationship is still debated. In this article we focus on the relationships of PUI with obsessive-compulsive and impulsive symptoms in a cohort of Italian young adults, in order to identify possible vulnerability factors for PUI. MethodsA sample of 772 Italian individuals aged 18–30 (mean age 23.3 ± 3.3 years old; 38% males and 62% females) was assessed via online survey using the Internet Addiction Test (IAT), the Mini International Neuropsychiatric Interview (MINI) Screen, the Padua Inventory-Washington State University Revision (PI-WSUR) and the Barratt Impulsiveness Scale (BIS-11). ResultsNinety-seven subjects (12.6% of the sample) reported IAT scores at risk for PUI. PUI participants reported higher levels of impulsivity, obsessive-compulsive symptoms and a higher burden of co-occurrent psychiatric symptoms. In a logistic regression model, obsessional impulses to harm (OR = 1.108, p < 0.001), attentional impulsivity (OR = 1.155, p < 0.001) and depressive symptomatology (OR = 1.246, p = 0.012) had significant association with PUI. Finally, higher severity of PUI has been associated with manic/psychotic symptoms and with attentional impulsivity. ConclusionsOur findings confirmed the role of impulsivity in PUI, while also underling the association of obsessional impulses with this pathological behavior. We could hypothesize a trigger role of obsessive impulses for the engagement in PUI, together with factors as negative affective states. Further research is needed with respect to more severe forms of PUI, also for establishing tailored interventions.

Exogenous factors in the pathogenesis of atopic dermatitis: Irritants and cutaneous infections.

Atopic dermatitis (AD) is a chronic relapsing inflammatory cutaneous disease that is often associated with other atopic symptoms, such as food allergy, allergic rhinitis and asthma, leading to significant morbidity and healthcare costs. The pathogenesis of AD is complicated and multifactorial. Although the aetiology of AD remains incompletely understood, recent studies have provided further insight into AD pathophysiology, demonstrating that the interaction among genetic predisposition, immune dysfunction and environmental provocation factors contributes to its development. However, the increasing prevalence of AD suggests that environmental factors such as irritation and cutaneous infection play a crucial role in triggering and/or aggravating the disease. Of note, AD skin is susceptible to bacterial, fungal and viral infections, and microorganisms may colonize the skin and aggravate AD symptoms. Overall, understanding the mechanisms by which these risk factors affect the cutaneous immunity of patients with AD is of great importance for developing a precision medicine approach for treatment. This review summarizes recent developments in exogenous factors involved in the pathogenesis of AD, with special emphasis on irritants and microbial infections.

Are employees' emotional labor strategies triggering or reducing customer incivility: a sociometer theory perspective

PurposePrior studies have mainly attributed customer incivility to dispositional characteristics, whereas little attention has been paid to exploring service employees' role in triggering or reducing customer incivility. The purpose of the present study is to propose and test a model in which service employees' emotional labor strategies affect customer incivility via influencing customers' self-esteem threat, as well as examine the moderating role of customer's perception of service climate.Design/methodology/approachBased on a matched sample consisting of 317 employee-customer dyads in China, multiple regression analysis and indirect effect tests were employed to test our model.FindingsThe study shows that employee surface acting is positively related to customer incivility, whereas deep acting is negatively associated with customer incivility. Moreover, customer self-esteem threat mediates the relationship between both types of emotional labor and customer incivility. Customer perception of service climate moderates the relationship between deep acting and customer self-esteem threat.Originality/valueThe current research broadens the antecedents of customer incivility from the employee perspective and sheds more light on the role of customer self-esteem in the interactions between employees and customers. It also demonstrates a complementary relationship between service climate and individual employees' emotional labor strategies, thereby expanding the existing understanding of the management of employees' emotional labor.

Nutritional Factors in the Prevention of Atopic Dermatitis in Children.

Atopic dermatitis is one of the most frequent chronic skin diseases worldwide and often develops within the first few years of life. Recent advancements in our knowledge of its pathophysiology have brought to light the role of genetic predisposition and environmental triggers. With the increasing prevalence of allergic diseases, there is a strong need for a better understanding of the various modifiable eliciting factors of such conditions. The concomitant rise in food allergy and insights into the skin barrier function has highlighted the role of nutrition and diet in the prevention and modification of allergic disorders. Furthermore, the identification of the skin as an important route of sensitization, and the risk of progression to asthma later in life, stress the significance of optimizing our management of skin inflammation in the prevention of allergies. Many nutritional factors, including the type of maternal diet during pregnancy, the duration of breastfeeding, the epicutaneous exposure of allergenic food proteins in the first few years of life, the timing of the introduction of complementary foods, the supplementation of vitamins and probiotics/prebiotics during prenatal and early life, have been assessed as potential targets for the prevention of atopy and eczema. Here, we review the latest data addressing prenatal and perinatal nutritional and dietary interventions in the primary prevention of atopic dermatitis. Also, we define knowledge gaps and targets for future research in the prevention of atopic dermatitis.

Early Diagenesis in Sediments of the Venice Lagoon (Italy) and Its Relationship to Hypoxia

This work focuses on sediments of a shallow water lagoon, located in a densely populated area undergoing multiple stressors, with the goal of increasing the understanding of the links between diagenetic processes occurring in sediments, the dynamics of dissolved oxygen (DO) in the water column, and potential consequences of hypoxia. Sediment data were collected over three consecutive years, from 2015 to 2017, during spring–summer, at five stations. Measured variables included: sediment porosity, grain size and organic carbon content, porewater microprofiles of O2, pH and H2S, porewater profiles of dissolved inorganic carbon (DIC), total alkalinity (TA), NH4+, NO3–, dissolved Fe, and SO42–. In addition, long-term time series of oxygen saturations in the water column (years 2005–2017) were utilized in order to identify the occurrence and duration of hypoxic periods. The results show that the median DO saturation value in summer months was below 50% (around 110 μmol L–1), and that saturation values below 25% (below the hypoxic threshold) can persist for more than 1 week. Sediment stations can be divided in two groups based on their diagenetic intensity: intense and moderate. At these two groups of stations, the average DIC net production rates, estimated trough a steady-state model (Profile) were, respectively, of 2.8 and 1.0 mmol m–2 d–1, SO42– consumption rates were respectively 1.6 and 0.4 mmol m–2 d–1, while diffusive oxygen uptake fluxes, calculated from the sediment microprofile data, were of 28.5 and 17.5 mmol m–2 d–1. At the stations characterized by intense diagenesis, total dissolved sulfide accumulated in porewaters close to the sediment-water interface, reaching values of 0.7 mM at 10 cm. Considering the typical physico-chemical summer conditions, the theoretical time required to consume oxygen down to the hypoxic level by sediment oxygen demand ranges between 5 and 18 days, in absence of mixing and re-oxygenation. This estimation highlights that sediment diagenesis may play a crucial role in triggering and maintaining hypoxia of lagoon waters during the summer season in specific high intensity diagenesis zones. This role of the sediment could be enhanced by changes in regional climate conditions, such as the increase in frequency of summer heat waves.

Macrophage Polarization and Liver Ischemia-Reperfusion Injury

Ischemia-reperfusion injury refers to organ damage caused by the previous insufficient supply of oxygen and nutrients and the involvement of metabolic by-products after blood flow is restored. Liver ischemia-reperfusion injury (IRI) has become a hot research in recent years, because it occurs in many clinical scenarios. After the introduction of liver transplantation and vascular control techniques in liver surgery, liver ischemia-reperfusion injury is considered to be an important factor affecting postoperative mortality and morbidity. As the largest immune organ in the human body, liver contain a lot of immune cells such as resident macrophages (Kupffer cells), dendritic cells, natural killer cells, and natural killer T cells which play a key role in ischemia-reperfusion injury. Among those, macrophage-mediated excessive inflammatory response is considered to be an important factor in liver ischemia-reperfusion injury. The prominent feature of liver injury is an increase in the number of macrophages in liver due to the infiltration of blood monocytes and differentiation into monocyte-derived macrophages. Liver macrophages can be divided into M1 macrophages which can promote inflammation progress and M2 macrophages that inhibit inflammation progress according to their different phenotypes and functions. Both of them can regulate liver aseptic inflammation, and play an important role in triggering, maintaining, and improving liver ischemia-reperfusion injury. This review summarizes studies of macrophage polarization on liver ischemia-reperfusion injury in recent years, to provide potential ideas for translation application in future clinical management.

Free-running data acquisition system for the AMBER experiment

Triggered data acquisition systems provide only limited possibilities of triggering methods. In our paper, we propose a novel approach that completely removes the hardware trigger and its logic. It introduces an innovative free-running mode instead, which provides unprecedented possibilities to physics experiments. We would like to present such system, which is being developed for the AMBER experiment at CERN. It is based on an intelligent data acquisition framework including FPGA modules and advanced software processing. The system provides a triggerless mode that allows more time for data filtering and implementation of more complex algorithms. Moreover, it utilises a custom data protocol optimized for needs of the free-running system. The filtering procedure takes place in a server farm playing the role of the highlevel trigger. For this purpose, we introduce a high-performance filtering framework providing optimized algorithms and load balancing to cope with excessive data rates. Furthermore, this paper also describes the filter pipeline as well as the simulation chain that is being used for production of artificial data, for testing, and validation.

Progesterone surge as the trigger of ovulation

A large number of studies have addressed the issue of ovulation, with specific hormones having well-determined roles. Despite the fact that estrogens are known to play a critical role when mature oocytes are set for the process of ovulation, recent studies have disputed the role of the true physiological ovulation trigger, indicating progesterone as the genuine one. The current discussion raises an interesting debate, as progesterone surge may be the real trigger of ovulation. The current mentioned subject needs further investigation in order to ascertain unambiguous conclusions.

Inflammatory bowel disease: An Indian perspective.

Inflammatory bowel disease (IBD) in recent times is causing a significant healthcare burden as both ulcerative colitis and Crohn's disease (CD) require lifelong therapy and constant monitoring. The current review highlights the concerns in a country like India with special reference to the changing trends of IBD, risk attribution and the financial issues. Indian immigrants behave like residential Indians, whereas their children show IBD prevalence similar to the West, highlighting the role of environmental triggers. However, the environmental and genetic factors in Indians with IBD are not well understood. Men appear to be more frequently affected than women in India. The disease severity is milder in the patients, both males and females, but the risk for colorectal cancer (CRC) is similar to the West. The incidence of paediatric IBD is on the rise. The major burden of IBD in the Indian subcontinent at present is in children, adolescents and teens. Cost towards the management of complications, non-adherence to treatment, differentiating tuberculosis from CD and finally screening for CRC in patients with IBD are the points to ponder in the Indian scenario.

Genuine Empty Follicle Syndrome: Role of Double Trigger and Delayed Oocyte Retrieval (DTDO).

Background:Empty follicle syndrome (EFS) is a condition of undetermined etiology where no oocytes are retrieved in an ART cycle despite adequate response to ovarian stimulation and diligent follicular aspiration. Because of the rarity of this condition, no much published strategies are available to tackle this.Aim:The aim of this study was to evaluate whether sequential administration of gonadotropin-releasing hormone agonist (GnRHa) and human chorionic gonadotropin (hCG) as a trigger at 40 h and 36 h, respectively, before oocyte retrieval (OCR) could correct genuine empty follicle syndrome (GEFS).Study Setting and Design:This retrospective observational cohort study was conducted in a tertiary fertility center over a period of 6 years from January 2014 to December 2019. Patients with a history of GEFS were administered GnRHa and recombinant hCG subcutaneously at 40 h and 36 h, respectively, before OCR, i.e., double trigger and delayed oocyte retrieval (DTDO) (n = 13). The primary outcome measures studied were number of mature oocytes retrieved, oocyte maturation index (OMI), number of fertilized oocytes, and number of embryos available for embryo transfer. The secondary outcome measures were clinical pregnancy rate (CPR), miscarriage rate (MR) and live birth rate (LBR) per first frozen embryo transfer (FET) cycle, incidence of inadvertent premature ovulation, and ovarian hyperstimulation syndrome.Statistical Analysis:Comparison between the groups was analysed by Fisher's exact test and paired t-test.Results:Patients in the DTDO group showed a significant improvement (P < 0.01) in the number of mature oocytes retrieved, OMI, number of fertilized oocytes, and number of embryos available for embryo transfer. In the first FET cycle, CPR (44.44%), LBR (44.44%), and MR (11.11%) were observed in the DTDO group.Conclusion:Our findings implicate that double trigger and delayed OCR (DTDO) is a safe and efficacious treatment strategy for GEFS.

The role of infective trigger for macrophage activation syndrome in rheumatic diseases. A retrospective analysis in a tertiary pediatric care centre and review of the literature

Background: The role of infection in Macrophage Activation Syndrome (MAS) is controversial. In order to evaluate the prevalence of infections preceding the onset of MAS, we retrospectively analysed the cases of MAS complicating rheumatic diseases recorded in our tertiary hospital between 2005 and 2015. Methods: The clinical records of patients diagnosed with MAS and hospitalised between January 2005 and December 2015 were reviewed in order to identify their demographic characteristics, underlying rheumatological diseases, clinical and laboratory data, treatments, and complications. There was considered if an infection was documented during the 15 days preceding the onset of MAS. The presence of specific immunoglobulin M was considered separately as a possible indirect sign of recent infection Findings: Twelve children (eight females and four males) with underlying rheumatic disorders developed MAS during the study period: six were affected by systemic-onset juvenile idiopathic arthritis, three by systemic lupus erythematosus, two by dermatomyositis, and one by undifferentiated arthritis. There were 14 MAS-related events (one patient experienced three episodes). MAS occurred within 30 days of the onset of rheumatic disease in five cases, and during disease relapses in nine. In two cases, it followed the start of treatment with a new drug. Twelve of the 14 MAS episodes were suspected to be preceded by infections due to various pathogens, including Clostridium difficile, group A Streptococcus, Staphylococcus hominis, Escherichia coli, Entamoeba histolytica, Endolimax nana, Pseudomonas aeruginosa, Borrelia burgdorferi, Adenovirus, Coxsackie virus, Epstein-Barr virus, and Cytomegalovirus. Conclusions: The prevalence of infections in patients developing MAS may be underestimated, and their pathogenetic role should be considered also in patients with underlining rheumatic diseases.

IMMUNE-MEDIATED INTRAOCULAR INFLAMMATION. AREVIEW.

Immune mediated inflammatory diseases are categorized into autoimmune and autoinflammatory. Autoimmune etiology is represented by autoreactive lymphocytes or autoantibodies, e.g. primary Sjögrenssyndrome or rheumatoid arthritis. Ocular specific diseases with presumed autoimmune origin are sympathetic ophthalmia or birdshot chorioretinopathy. Autoinflammatory diseases are caused by mutations in regulatory genes for specific immunity. Hereditary periodic fevers represent monogenic autoinflammatory diseases; eye specific is Blau syndrome also named sarcoidosis with early onset. This article reviews the actual knowledge about immune mediated uveitides, their immunological mechanisms and the possible trigger role of infection in autoimmune inflammation. Immune privilege provides aprotection of the eye against any strong immune reaction to foreign antigen, based on physical, immune, humoral and molecular mechanisms. Antigens hidden within the eye are revealed in case of damage of hematoretinal barrier caused by infection or mechanical insult. These ocular antigens have not been set as tolerable during the development and immune reaction is initiated subsequently. Current studies demonstrate that uveogenic trigger might be generated by own microbiome, particularly when dysregulated, so called dysbiosis. There is aknown association between idiopathic inflammatory bowel disease with ankylosing spondylitis and anterior uveitis in humans. Intensive research is focused on microbiome and immune mediated inflammatory disease to influence therapeutically the intestinal microbiome. The animal models are used to study the immunopathological mechanisms of uveitis and the new therapeutic strategies, because of relatively low incidence of immune mediated uveitis in humans.