Exacerbation Of Chronic Inflammation Research Articles

Indoxyl Sulfate-Induced Macrophage Toxicity and Therapeutic Strategies in Uremic Atherosclerosis.

Cardiovascular disease (CVD) frequently occurs in patients with chronic kidney disease (CKD), particularly those undergoing dialysis. The mechanisms behind this may be related to traditional risk factors and CKD-specific factors that accelerate atherosclerosis and vascular calcification in CKD patients. The accumulation of uremic toxins is a significant factor in CKD-related systemic disorders. Basic research suggests that indoxyl sulfate (IS), a small protein-bound uremic toxin, is associated with macrophage dysfunctions, including increased oxidative stress, exacerbation of chronic inflammation, and abnormalities in lipid metabolism. Strategies to mitigate the toxicity of IS include optimizing gut microbiota, intervening against the abnormality of intracellular signal transduction, and using blood purification therapy with higher efficiency. Further research is needed to examine whether lowering protein-bound uremic toxins through intervention leads to a reduction in CVD in patients with CKD.

Altered gut microbiome plays an important role in AKI to CKD transition in aged mice.

This study investigated the role of renal-intestinal crosstalk in the transition from acute kidney injury (AKI) to chronic kidney disease (CKD) in elderly individuals. Using young and aged mice, we induced bilateral ischemia-reperfusion injury (IRI) and compared intestinal and kidney inflammation over 28 days. To determine the role of the microbiome in gut-kidney crosstalk, we analyzed the microbiome of fecal samples of the young vs. aged mice and examined the effects of probiotic supplementation. In the post-IRI recovery phase, prolonged intestinal and renal inflammation along with dysbiosis were evident in aged vs. younger mice that was associated with severe renal dysfunction and fibrosis progression in aged mice. Probiotic supplementation with Bifidobacterium bifidum BGN4 and Bifidobacterium longum BORI alleviated intestinal inflammation but not intestinal leakage, characterized by decreased inflammatory cytokine levels and decreased infiltration of macrophages, neutrophils, and Th17 cells. This was associated with improved M1-dominant renal inflammation and ultimately improved renal function and fibrosis, suggesting that renal-intestinal crosstalk in aged mice contributes to the transition from AKI to CKD. Our study findings suggest that exacerbation of chronic inflammation through the gut-kidney axis might be an important mechanism in the transition from AKI to CKD in the elderly.

Prevention of Complications of Removal of the mandibular Third molars

Aim: Study of the causes that may contribute to complications during and after tooth extraction to justify treatment and prevention measures. materials and methods: A retrospective analysis of the content of ambulatory cards and protocols of operations of 168 patients for the period from 2016 to 2018 and evaluation of the results of personal work for 2018-2020 related to surgical interventions in 134 patients which removed the third lower molars. Results: According to the retrospective material, damage to the inferior alveolar nerve was found in 5.9% of cases, lingual nerve – in 3.3% of cases, the prevalence of alveolitis with simple removal was 16.3% of cases, at difficult and surgical removal – 3.9% of cases. The application of our proposed treatment and prevention complex allowed to reduce their rates to 3.1%, 2.3%, 8.0% and 3.8% of cases, respectively. Risk factors for complications have been identified. Conclusions: when planning the method of surgical removal of third lower molars it is necessary to take into account the probability of its intimate location in relation to inferior alveolar nerve and lingual nerve. The presence of focus of destruction with signs of acute or exacerbation of chronic inflammation in the periodontal bone tissue of the causative tooth is a risk factor for alveolitis and an indication for the appointment of treatment and prevention in the preoperative period, even with simple removal.

The cardiac lymphatic system stimulates resolution of inflammation following myocardial infarction.

Myocardial infarction (MI) arising from obstruction of the coronary circulation engenders massive cardiomyocyte loss and replacement by non-contractile scar tissue, leading to pathological remodeling, dysfunction, and ultimately heart failure. This is presently a global health problem for which there is no effective cure. Following MI, the innate immune system directs the phagocytosis of dead cell debris in an effort to stimulate cell repopulation and tissue renewal. In the mammalian adult heart, however, the persistent influx of immune cells, coupled with the lack of an inherent regenerative capacity, results in cardiac fibrosis. Here, we reveal that stimulation of cardiac lymphangiogenesis with VEGF-C improves clearance of the acute inflammatory response after MI by trafficking immune cells to draining mediastinal lymph nodes (MLNs) in a process dependent on lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1). Deletion of Lyve1 in mice, preventing docking and transit of leukocytes through the lymphatic endothelium, results in exacerbation of chronic inflammation and long-term deterioration of cardiac function. Our findings support targeting of the lymphatic/immune cell axis as a therapeutic paradigm to promote immune modulation and heart repair.

Air pollution, oxidative stress, and exacerbation of autoimmune diseases.

A number of epidemiological studies have shown a strong association between exposure to ambient airborne particulate matter (PM 2.5, PM < 1.0) and lung or cardiovascular diseases characterised by high mortality and morbidity. However, much less is known about the role of air pollution in the pathogenesis of autoimmune diseases, which constitutes a significant problem in modern society.This paper summarises the state of current research regarding the influence of PM on the development and/or progression of autoimmune diseases. A brief review of the great body of research concerning pathogenesis of autoimmune disorders is presented. Then, the scope of our review is narrowed to the research related to the impact of particulate matter on oxidative and nitrosative stress, as well as exacerbation of chronic inflammation, because they can contribute to the development of autoimmune diseases. Moreover, we discuss the impact of various components of PM (metal, organic compounds) on PM toxicity and the ability to generate oxidants.

Immunoexpression of Interleukin 17 in Apical Periodontitis Lesions

IntroductionInterleukin (IL)-17 expression has been detected in apical periodontitis lesions, but its role in the disease process remains unclear. The present study compared the expression of IL-17 in periradicular cysts and granulomas and evaluated the association of this cytokine with clinical and radiographic findings. MethodsApical periodontitis lesions (18 cysts and 20 granulomas) were obtained from 38 patients subjected to periradicular surgery. Some clinical, radiographic, and cone-beam computed tomographic features were recorded. Silanized slides containing paraffin sections were used for the immunohistochemical reactions using anti–IL-17 antibody. Image analysis was performed using an optical microscope, and each sample was divided into 5 high-power fields, which were evaluated for the expression of IL-17 in the epithelium and connective tissues. Results were evaluated for correlations with the lesion size and the occurrence of symptoms and sinus tract. ResultsExpression of IL-17 was significantly higher in cysts than in granulomas (P = .02). Among the periradicular cysts, a thin epithelium showed significantly increased labeling for IL-17 when compared with a hyperplastic epithelium (P = .003). IL-17 expression was usually associated with focal accumulations of polymorphonuclear leukocytes. No association of IL-17 expression with symptoms, sinus tract, or lesion size was observed (P > .05). ConclusionsThe present study reinforces the notion that IL-17 may take part in the pathogenesis of apical periodontitis lesions. A role in the exacerbation of chronic inflammation and cyst formation is suspected. Further studies are required to shed light on the specific functions of IL-17 in periradicular inflammatory processes.

Treatment of Chronic Cystitis in Children

Chronic inflammatory processes of the urinary bladder’s wall dominate in the structure of urologic diseases in children, but the issue of their treatment still remains very acute. Despite the use of modern methods of treatment, children with chronic recurrent cystitis constitute a significant part of the total number of hospitalized patients (19 to 21%). In recent years quite many morphological studies of the bladder’s mucosa during inflammatory diseases were held. However, the mechanism that leads to the damage of the urothelium in chronic cystitis and factor that determines the type of metaplasia during inflammation of the bladder are unclear. Endoscopic examination, in some cases, does not allow differentiating inflammatory from tumor-like lesions of the mucosa. Destructive lesions of the bladder’s mucosa occur during exacerbation of chronic inflammation or severe, far gone acute inflammation. Therefore, conducting endovesical biopsy is necessary for clarifying forms of chronic cystitis and identifying urothelial hyperplasia or dysplasia and is critical in the diagnosis of diseases of the urinary bladder. It is still unclear under what endoscopic and morphological forms of recurrent cystitis in children neurogenic bladder disorders are more frequent and for what form of recurrent cystitis most pronounced neurogenic bladder dysfunctions are more likely to occur. The nature and extent of neurogenic disorders in children with various forms of recurrent cystitis in the late periods after antireflux surgeries remain unexplored.

Identification of a Chemokine Network That Recruits FoxP3+ Regulatory T Cells Into Chronically Inflamed Intestine

It has been unclear which chemokine network is involved in migration of T-cell subsets to chronically inflamed lesions of the intestine. SAMP1/YP mice develop a spontaneous chronic transmural intestinal lesion specifically in the ileum. Using these mice, we investigated the gut chemokine network involved in specific migration of T-cell subsets to the inflamed lesion of the intestine. We performed expression analyses of chemokines and their receptors, chemokine receptor blocking studies, and migration studies in vitro and in vivo to identify the gut chemokine network induced in intestinal inflammation and to determine its role in migration of conventional and FoxP3(+) suppressor T cells to the inflamed intestine. The expression of homeostatic chemokines was largely unchanged in the inflamed lesion of SAMP1/YP mice compared with control mice. However, an additional chemokine axis (CCL5-CCR5) was up-regulated in the inflamed intestine of SAMP1/YP mice compared with control mice. Activated T cells of SAMP1/YP mice compared with control mice were hyperresponsive to CCL5 in chemotaxis. CCR5(+) T cells preferentially migrated to the inflamed lesion, which can be blocked by a CCR5 antagonist. Importantly, the FoxP3(+) regulatory T cells of the inflamed lesion of SAMP1/YP mice highly expressed CCR5. CCR5 blockade suppressed the migration of FoxP3(+) T cells into the inflamed intestine and significantly exacerbated the intestinal inflammation. The CCL5-CCR5 chemokine axis is involved in preferential recruitment of FoxP3(+) regulatory T cells, which prevents further exacerbation of chronic inflammation in the intestine.