Abstract: Introduction. Acne vulgaris is a multifactorial disease. Recent study showed that inflammation does have a central role in the formation of both inflammatory and noninflammatory lesions in acne vulgaris. There are various findings of proinflammatory cytokines related to acne vulgaris, but no previous study correlate interleukin- (IL-) 19 to acne vulgaris. This pilot study aims to look at difference in IL-19 serum concentration on degrees of severity of acne vulgaris. Methods. This is an analytical observational cross-sectional study. Sample subjects were patients with acne vulgaris who met the inclusion criteria. Enzyme-linked immunosorbent assay (ELISA) study was applied to measure IL-19 serum. Result. Analysis test found statistically significant difference between IL-19 serum concentration of group of patients with mild acne vulgaris and that of group of patients with severe acne vulgaris. Moreover, analysis revealed significant difference between IL-19 serum concentration of group of patients with moderate acne vulgaris and that of group of patients with severe acne vulgaris. Conclusions. There are differences in serum levels of IL-19 on the severity of acne vulgaris. The significant difference might show that inflammation has a core role in severity of acne vulgaris, and IL-19 might potentially be related to acne vulgaris. PubDate: Sun, 01 Apr 2018 06:25:51 +000
Abstract: Cumulative evidence indicates that estrogen receptor (ER) agonists attenuate neuroinflammation. Equol, a major isoflavone from soybean, exhibits estrogen-like biological activity, but their effect on inflammatory response has not been well established. Here, we investigated the effect of S-equol on nitric oxide (NO) production, well-known inflammatory change in astrocytes stimulated by LPS. S-Equol attenuated LPS-induced NO production with a concomitant decrease in expression of inducible NO synthase (iNOS). S-Equol did not affect LPS-induced increase in intracellular ROS production. Intracellular ER blocker ICI 182.780 had no effect on S-equol-induced decrease in NO production. Addition of G-15, antagonist of G protein-coupled receptor 30 which is nongenomic ER and located on cell surface, partially recovered S-equol-induced attenuation of NO production. These findings suggest that attenuation of NO production by S-equol may mitigate LPS-induced neuroinflammation in astrocytes. S-Equol may exert a glioprotective effect, at least in part, via a nongenomic effect. PubDate: Mon, 05 Mar 2018 00:00:00 +000
Abstract: Toll-Like Receptors (TLRs) are the innate immunity receptors that play an activating role when interacting with molecules released by bacteria and viruses (PAMPs, pathogen-associated molecular patterns) or with molecules released by injured cells and tissues (DAMPs, danger-associated molecular patterns). TLR triggering leads to the induction of proinflammatory cytokines and chemokines, driving the activation of both innate and adaptive immunity. In particular, Toll-Like Receptor 4 (TLR4) has been described to be involved in the inflammatory processes observed in several pathologies (such as ischemia/reperfusion injury, neuropathic pain, neurodegenerative diseases, and cancer). Molecules obtained by natural sources have been discovered to exert an anti-inflammatory action by targeting TLR4 activation pathways. This review focuses on TLR4 antagonists obtained from bacteria, cyanobacteria, and plants. PubDate: Thu, 01 Mar 2018 00:00:00 +000
Abstract: Various parts of the turmeric plant have been used as medicinal treatment for various conditions from ulcers and arthritis to cardiovascular disease and neuroinflammation. The rhizome’s curcumin extract is the most studied active constituent, which exhibits an expansive polypharmacology with influence on many key inflammatory markers. Despite the expansive reports of curcucmin’s therapeutic value, clinical reliability and research repeatability with curcumin treatment are still poor. The pharmacology must be better understood and reliably mapped if curcumin is to be accepted and used in modern medical applications. Although the polypharmacology of this extract has been considered, in mainstream medicine, to be a drawback, a perspective change reveals a comprehensive and even synergistic shaping of the NF-kB pathway, including transactivation. Much of the inconsistent research data and unreliable clinical outcomes may be due to a lack of standardization which also pervades research standard samples. The possibility of other well-known curcumin by-products contributing in the polypharmacology is also discussed. A new flowchart of crosstalk in transduction pathways that lead to shaping of nuclear NF-kB transactivation is generated and a new calibration or standardization protocol for the extract is proposed which could lead to more consistent data extraction and improved reliability in therapy. PubDate: Mon, 15 Jan 2018 00:00:00 +000
Abstract: Type 2 diabetes mellitus (T2DM) is a severe health problem worldwide, reaching epidemic levels. High susceptibility to infections of T2DM patients indicates dysregulated immune responses to pathogens. However, innate immune responses, including monocyte functions, in T2DM are poorly investigated. Therefore, in this study we aimed to assess lipopolysaccharide- (LPS-) induced immune responses of circulating monocytes from T2DM patients. The results showed that monocytes from T2DM were hyporesponsive to LPS challenge as reflected by significantly suppressed secretion of TNFα () and expression of CD11b () and TLR4 () compared to those in monocytes from healthy subjects. Furthermore, LPS-induced IL-10 levels were similar in diabetic and healthy supernatants, while expression levels of CD163 were found to be downregulated on monocytes from T2DM () suggesting impaired ability of monocytes to switch their phenotype to anti-inflammatory. Taken together, our results suggest compromised function of monocytes in T2DM, which may explain, at least partly, high incidence of infection in these patients. PubDate: Sun, 14 Jan 2018 00:00:00 +000
Abstract: Background. Interactions between alcohol, infection, and surgery and their effect on differentiation and functionality of T helper cells are not yet completely understood. We hypothesized that alcohol and surgery disturb differentiation of T helper cells and contribute to an impaired immune response. Methods. Mice were treated with alcohol for two weeks. Saline treatment served as control. Clinical performance and weight were assessed. On day 14, a median laparotomy was performed and animals were challenged with Klebsiella pneumoniae intranasally. Bacterial load was determined in lungs and blood. T helper cell subpopulations and the released cytokines were assessed in lungs, spleens, and plasma. Key transcription factors of T cell differentiation were evaluated. Results. Alcohol significantly impaired clinical appearance and body weight of animals with postsurgical infection . Bacterial load was significantly higher after alcohol treatment . T helper cell subsets and released cytokine levels were significantly altered in lung, but not in spleen. Expression of transcription factors of T helper cell lineage commitment did not translate into different counts of T helper cells. Conclusions. Alcohol and surgery lead to significant cellular and functional modulations of T helper cells during postsurgical infection. These effects may contribute to an impaired immune response after surgery. PubDate: Mon, 20 Nov 2017 00:00:00 +000
Abstract: Inflammatory bowel diseases (IBD) are chronic inflammatory diseases involving all or part of the gastrointestinal tract. The stress-activated serine-threonine protein kinase D1 (PKD1) protein has previously been implicated in intestinal immune regulation. The objective of this study was to evaluate the effects of human PKD1 in relation to intestinal inflammation, using a co-culture model of intestinal epithelial Caco-2 cells and RAW264.7 macrophages. An inflammatory response was induced in the macrophages by lipopolysaccharide (LPS), upregulating the expression of tumour necrosis factor alpha (TNF-α), interleukin- (IL-) 1β, and IL-6 besides increasing the secretion of TNF-α protein. The effect of administering PKD1 to Caco-2 was evaluated in relation to both amelioration of inflammation and the ability to suppress inflammation initiation. Administration of PKD1 (10–100 ng/ml) following induction of inflammation induced downregulation of TNF-α expression in RAW264.7 cells. In addition, PKD1 administered for 3 h prior to LPS stimulation reduced the subsequent inflammatory response through downregulation of TNF-α, IL-1β, and IL-6 in RAW264.7 cells. These results demonstrate a potential role of PKD1 in the intercellular communication between intestinal epithelial and immune cells, proposing a protective effect of PKD1 on the induction of an inflammatory response in macrophages, an important aspect during the pathogenesis of IBD. PubDate: Thu, 26 Oct 2017 00:00:00 +000
Abstract: Purpose. Neutrophil Extracellular Traps (NETs) are extracellular neutrophil derived DNA webs which have been implicated in cancer progression and in the development of metastases. NETs production in patients with colorectal cancer was investigated to elucidate their role and prognostic significance. Methods. Systemic neutrophils were isolated from consecutive patients with colorectal cancer and from age-matched healthy volunteers. Neutrophils were stimulated to produce NETs which were quantified by a measure of the fluorescence of the extracellular DNA. The impact of cancer location, tumour stage, and patient outcomes (complications, length of stay, and mortality) on NET production was investigated. Results. Quantification of NET formation was performed in patients with colorectal cancer () and in well-matched healthy individuals (). Significant increases in NETs production in response to no stimulant (9,735 AFU versus 11347 AFU, ), IL-8 (8,644 AFU versus 11,915 AFU, ), and LPS (10,576 AFU versus 12,473 AFU, ) were identified in patients with colorectal cancer. A significant increase in NETs production in response to fMLP was detected in patients who developed significant postoperative complications (11,760 AFU versus 18,340 AFU, ) and who had a prolonged hospital recovery (9,008 AFU versus 12,530 AFU, ). An increase in NETs production was also observed in patients who died, but this did not reach statistical significance. Cancer location and tumour stage did not appear to affect preoperative NETs production. Conclusions. Patients with colorectal cancer have significantly increased NETs production in vitro when compared to healthy volunteers, possibly implicating them in cancer development. Adverse patient outcomes were associated with increased preoperative NETs production, which highlights them as potential therapeutic targets. PubDate: Sun, 30 Jul 2017 08:19:54 +000
Abstract: Wound healing is a complex event that develops in three overlapping phases: inflammatory, proliferative, and remodeling. These phases are distinct in function and histological characteristics. However, they depend on the interaction of cytokines, growth factors, chemokines, and chemical mediators from cells to perform regulatory events. In this article, we will review the pathway in the skin healing cascade, relating the major chemical inflammatory mediators, cellular and molecular, as well as demonstrating the local and systemic factors that interfere in healing and disorders associated with tissue repair deficiency. Finally, we will discuss the current therapeutic interventions in the wounds treatment, and the alternative therapies used as promising results in the development of new products with healing potential. PubDate: Tue, 25 Jul 2017 00:00:00 +000
Abstract: Introduction. The current study was designed to evaluate the association of neutrophil-to-lymphocyte ratio (NLR) with coronary artery disease (CAD) presence. We also aimed to propose a suitable cut-off of NLR for diagnosis of CAD in Western Indians. Methods. Total 324 patients undergoing coronary angiography were enrolled and were subdivided into two groups: group 1 (; population without CAD) and group 2 (; population with CAD). Results. The results indicated significant () positive association between elevated levels of WBC, neutrophil, monocyte, NLR, hs-CRP, CPK-MB, and troponin I and disease presence. According to subgroup analysis, the association was more profound in male and older population. Among all the markers NLR showed the strongest predictive potential for CAD with highest odds ratio (1.495; 95% CI: 0.942–2.371; ). Optimum cut-off of NLR for diagnosis of CAD was 2.13 (AUC-0.823; ; sensitivity: 83.64%; specificity: 63.46%). Association of NLR with other biochemical markers such as hs-CRP, CPK-MB, and troponin I was also observed in quartile analysis. Conclusion. NLR is a simple indicator that could be effectively used for the diagnosis of CAD with a cut-off of 2.13 in Western Indian population. PubDate: Mon, 24 Jul 2017 06:58:17 +000
Abstract: Defective tissue repair and remodeling are main aspects of Chronic Obstructive Pulmonary Disease (COPD) pathophysiology. Bone marrow mesenchymal stem cells (BM-MSCs) have been implicated in this direction, as their functional impairment and recruitment could possibly contribute to disease development and progression. The present study characterizes for the first time the expression of migration related chemokine receptors and their ligands in BM-MSCs from COPD patients. CXCR4/SDF1a and CCR7/CCL19-CCL21 mRNA levels were evaluated in BM-MSCs obtained from twelve COPD patients and seven healthy donors. SDF1a protein levels in sera and BM-MSCs’ conditioned media were also evaluated. CXCR4, SDF1a, CCL19, and CCL21 mRNA levels were significantly reduced in COPD BM-MSCs while CCR7 levels were undetectable. Notably, SDF1a protein levels were marginally elevated in both patient sera and BM-MSCs’ conditioned media while the increase in SDF1a serum levels significantly correlated with disease severity in COPD. Our findings show posttranscriptional regulation of SDF1a levels in BM-MSCs of COPD patients and significant downregulation of SDF1a and CXCR4 mRNA indicating an involvement of the SDF1a signaling pathway in the disease pathophysiology. PubDate: Wed, 19 Jul 2017 07:48:25 +000
Abstract: Pernicious anaemia (PA) is an autoimmune condition where antibodies target intrinsic factor and parietal cells, reducing the patient’s ability to absorb cobalamin promoting atrophic gastritis. Treatment guidelines are based on excretion data of hydroxocobalamin from healthy individuals obtained 50 years ago. This manuscript describes the use of phorbol 12-myristate 13-acetate (PMA) to stimulate low grade inflammation in an epithelial colorectal cell line to assess the efficacy of methylcobalamin and hydroxocobalamin. Nitric oxide increased significantly in cells exposed to higher doses of PMA (100 ng/ml, 150 ng/ml, and 200 ng/ml) accompanied by a loss of the characteristic cobblestone morphology with no negative effect on cell activity or viability. A significant reduction in nitric oxide production was associated with the addition of 200 pg/ml hydroxocobalamin, alongside a return to the characteristic cobblestone morphology. This study highlights the use of PMA to promote low grade inflammation in human cell lines to model gastric inflammation associated with autoimmunity; furthermore it raises questions regarding the concentration of cobalamin administered clinically to restore cell functionality, feasibly allowing the patient to receive reduced quantity of the vitamin more regularly, providing the patient with levels which are akin to dietary intake. PubDate: Tue, 06 Jun 2017 00:00:00 +000
Abstract: Many studies have been done to evaluate the effect of various natural products in controlling asthma symptoms. Virgin coconut oil (VCO) is known to contain active compounds that have beneficial effects on human health and diseases. The objective of this study was to evaluate the effect of VCO inhalation on airway remodelling in a rabbit model of allergic asthma. The effects of VCO inhalation on infiltration of airway inflammatory cells, airway structures, goblet cell hyperplasia, and cell proliferation following ovalbumin induction were evaluated. Allergic asthma was induced by a combination of ovalbumin and alum injection and/or followed by ovalbumin inhalation. The effect of VCO inhalation was then evaluated via the rescue or the preventive route. Percentage of inflammatory cells infiltration, thickness of epithelium and mucosa regions, and the numbers of goblet and proliferative cells were reduced in the rescue group but not in preventive group. Analysis using a gas chromatography-mass spectrometry found that lauric acid and capric acid were among the most abundant fatty acids present in the sample. Significant improvement was observed in rescue route in alleviating the asthma symptoms, which indicates the VCO was able to relieve asthma-related symptoms more than preventing the onset of asthma. PubDate: Sun, 04 Jun 2017 08:15:55 +000
Abstract: Vitamin D plays a significant role in the immune system modulation and may confer a protective role in autoimmune diseases. We conducted a case-control study to compare 25(OH)D levels in patients with BD who were managed at a regional rheumatology programme in the midwest region of Ireland compared to matched controls. Healthy controls were selected from the Irish health system and matched in 1 : 5 ratio for age, sex, and the month of the year. 25(OH)D levels PubDate: Sun, 04 Jun 2017 07:02:36 +000
Abstract: Clinical Relevance. Nonsteroidal Anti-Inflammatory Drugs (NSAIDs) including aspirin are of intensive use nowadays. These drugs exert their activity via the metabolism of arachidonic acid (AA) by cyclooxygenase inhibition. Though beneficial for health in some instances, both unspecific and specific cyclooxygenase inhibitor activity interfere with AA metabolism producing also proinflammatory lipids that may promote cancer. Materials and Methods. This review is based on available literature on clinical uses, biochemical investigations, molecular medicine, pharmacology, toxicity, and epidemiology-clinical studies on NSAIDs and other drugs that may be used accordingly, which was collected from electronic (SciFinder, Medline, Science Direct, and ACS among others) and library searches of books and journals. Results. Relevant literature supports the notion that NDSAID use may also promote proinflammatory biochemical events that are also related to precancerous predisposition. Several agents are proposed that may be employed in immediate future to supplement and optimize treatment with NSAIDs. In this way serious side effects arising from promotion of inflammation and cancer, especially in chronic NSAID users and high risk groups of patients, could be avoided. PubDate: Wed, 10 May 2017 06:31:39 +000
Abstract: Toll-like receptors (TLRs), part of the innate immune system that recognises molecular signatures, are important in the recognition of pathogenic components. However, when specific cellular contexts develop in which TLRs are inappropriately activated by self-components, this may lead to sterile inflammation and result in the occurrence of autoimmunity. This review analyses the available data regarding TLR biochemistry, the specific mechanisms which are brought about by TLR activation, and the importance of these mechanisms in the light of any existing and potential therapies in the field of autoimmunity. PubDate: Wed, 03 May 2017 08:39:44 +000
Abstract: Activation of naive CD4+ T cells results in the development of several distinct subsets of effector Th cells, including Th2 cells that play a pivotal role in allergic inflammation and helminthic infections. SWAP-70-like adapter of T cells (SLAT), also known as Def6 or IBP, is a guanine nucleotide exchange factor for small GTPases, which regulates CD4+ T cell inflammatory responses by controlling Ca2+/NFAT signaling. In this study, we have identified a novel alternatively spliced isoform of SLAT, named SLAT2, which lacks the region encoded by exons 2–7 of the Def6 gene. SLAT2 was selectively expressed in differentiated Th2 cells after the second round of in vitro stimulation, but not in differentiated Th1, Th17, or regulatory T (Treg) cells. Functional assays revealed that SLAT2 shared with SLAT the ability to enhance T cell receptor- (TCR-) mediated activation of NFAT and production of IL-4 but was unable to enhance TCR-induced adhesion to ICAM-1. Ectopic expression of SLAT2 or SLAT in Jurkat T cells resulted in the expression of distinct forms of filopodia, namely, short versus long ones, respectively. These results demonstrate that modulating either SLAT2 or SLAT protein expression could play critical roles in cytokine production and actin reorganization during inflammatory immune responses. PubDate: Mon, 24 Apr 2017 00:00:00 +000
Abstract: Background. The prevalence of allergies is steadily increasing worldwide; however, the pathogenesis is still unclear. We hypothesized that Mycobacterium avium subsp. paratuberculosis (MAP) may contribute to allergy development. This organism can be present in dairy foods, it can elicit an immunomodulatory switch from a Th1 to a Th2 response, and it has been speculated that it is linked to several human autoimmune diseases. To determine the contribution, sera from 99 individuals with various atopic disorders and 45 healthy nonallergic controls were assessed for total IgE levels and successively for MAP-specific IgE by ELISA. Results. The mean total serum IgE level in allergic patients was IU/mL, and in the healthy controls it was IU/mL (AUC = 0.88; ). Among the patient groups, 50 of the 99 subjects had increased IgE total level ≥ 150 IU/mL, while 49 subjects had IgE ≤ 150 IU/mL (mean level: IU/mL versus IU/mL; ). Additionally, 6 out of 50 subjects (12%) with IgE ≥ 150 IU/mL and none (0%) with IgE ≤ 150 IU/mL were positive for specific MAP IgE (AUC = 0.63; ). Conclusion. The present study revealed that MAP has the ability to induce specific IgE and might contribute to the induction of allergic inflammation in genetically predisposed individuals. PubDate: Mon, 24 Apr 2017 00:00:00 +000
Abstract: Background. To analyse the clinical informativity of the neutrophil oxidative response level (“Response”) during an Endotoxin Activity Assay (EAA) as a new biomarker defining the indications and effectiveness of intensive care in cardiac surgical patients with septic complications. Methods. Blood samples were taken from 198 adult patients who were admitted to the ICU after cardiac surgery (SIRS: 34, MODS: 36, and sepsis: 128). The composite of laboratory studies included CRP, PCT, EAA with “Response” level, and presepsin. Results. 83% of patients had a “normal” neutrophil response, 12% of patients had a low neutrophil response, and 5% of patients had a critically low neutrophil response. Patients with critically low responses had the lowest values of the EAA and the highest concentrations of PSP and D-dimer (). Conclusions. EAA results should be interpreted with the level of neutrophil response. “Response” > 0.5 has a negative predictive value; the EAA < 0.6 at “Response” < 0.5 may indicate a high level of endotoxaemia. PubDate: Wed, 12 Apr 2017 09:56:55 +000
Abstract: Otitis media (OM), characterized by the presence of mucus overproduction and excess inflammation in the middle ear, is the most common childhood infection. Nontypeable Haemophilus influenzae (NTHi) pathogen is responsible for approximately one-third of episodes of bacteria-caused OM. Current treatments for bacterial OM rely on the systemic use of antibiotics, which often leads to the emergence of multidrug resistant bacterial strains. Therefore there is an urgent need for developing alternative therapies strategies for controlling mucus overproduction in OM. MUC5AC mucin has been shown to play a critical role in the pathogenesis of OM. Here we show that curcumin derived from Curcuma longa plant is a potent inhibitor of NTHi-induced MUC5AC mucin expression in middle ear epithelial cells. Curcumin inhibited MUC5AC expression by suppressing activation of p38 MAPK by upregulating MAPK phosphatase MKP-1. Thus, our study identified curcumin as a potential therapeutic for inhibiting mucin overproduction in OM by upregulating MKP-1, a known negative regulator of inflammation. PubDate: Wed, 12 Apr 2017 07:35:01 +000
Abstract: In Syria, health risk data on young males are limited. Hence, the aim of the present study was to evaluate cardiovascular disease (CVD) risk factors along with C-reactive protein levels measured by high-sensitive method (hsCRP) in a group of healthy males of university students (, 18–25 years old). Participants’ anthropometric characteristics; alcohol drinking, smoking, and physical activity habits; parents medical history; and some inflammatory biomarkers were inspected for their associations with hsCRP. Results. Regarding hsCRP level, 19 participants were at average (1–3 mg/L) and 13 were at high (>3 mg/L) risk of CVD. Nonparametric statistical tests ( value < 0.05) revealed that hsCRP level was higher in participants who had high body mass index (BMI), had high BMI with high waist-to-hip ratio (WHR), or did not practice sport frequently. Unexpectedly, it did not vary between smokers and nonsmokers. In general, it correlated positively with anthropometric and erythrocyte sedimentation rate (ESR) measurements. Nevertheless, it negatively correlated with sports practicing in overall and nonsmoker groups and in participants whose parents were without medical history. Finally, when participants with high BMI were smokers, did not practice sport frequently, or had a parent with medical history, their hsCRP levels were higher than others who had the same circumstances but with low BMI. PubDate: Mon, 10 Apr 2017 07:39:38 +000
Abstract: Crohn’s disease (CD) is a chronic inflammatory disorder, characterized by cytokine imbalance and transcription signaling pathways activation. In addition, the increase of mesenteric adipose tissue (MAT) near the affected intestinal area is a hallmark of CD. Therefore, we evaluated the transcription signaling pathways and cytokines expression in intestinal mucosa and MAT of active CD patients. Ten patients with ileocecal CD and eight with noninflammatory diseases were studied. The biopsies of intestinal mucosa and MAT were snap-frozen and protein expression was determined by immunoblotting. RNA levels were measured by qPCR. The pIkB/IkB ratio and TNFα level were significantly higher in intestinal mucosa of CD when compared to controls. However, STAT1 expression was similar between intestinal mucosa of CD and controls. Considering the MAT, the pIkB/IkB ratio was significantly lower and the anti-inflammatory cytokine IL10 was significantly higher in CD when compared to controls. Finally, the protein content of pSTAT1 was higher in MAT of CD compared to controls. These findings reinforce the predominance of the proinflammatory NF-kB pathway in CD intestinal mucosa. For the first time, we showed the activation of STAT1 pathway in MAT of CD patients, which may help to understand the physiopathology of this immune mediated disease. PubDate: Sun, 09 Apr 2017 00:00:00 +000
Abstract: Cytokines, including interleukins, interferons, tumor necrosis factors, and chemokines, have a variety of pro- and anti-inflammatory effects in the body through a number of biochemical pathways and interactions. Stimuli, actions, interactions, and downstream effects of cytokines have been investigated in more depth in recent years, and clinical research has also been conducted to implicate cytokines in causal patterns in certain diseases. However, particular cutoffs of cytokines as biomarkers for disease processes have not been well studied, and this warrants future work to potentially improve diagnoses for diseases with inflammatory markers. A limited number of studies in this area are reviewed, considering diseases correlated with abnormal cytokine profiles, as well as specific cutoffs at which cytokines have been deemed clinically useful for diagnosing those diseases through Receiver Operator Characteristics modeling. In light of studies such as those discussed in this review, cytokine testing has the potential to support diagnosis due to its lack of invasiveness and low cost, compared to other common types of testing for infections and inflammatory diseases. PubDate: Sun, 09 Apr 2017 00:00:00 +000
Abstract: Background. Psoriasis affects joints in around 30% of the patients. Recent studies have demonstrated an increased risk of essential hypertension, ischemic heart disease, and stroke in psoriatic patients. However, the prevalence of renal disease in patients with psoriasis has not been evaluated properly. Objectives. Objectives were to evaluate renal functions in patients with psoriasis and to assess any possible relationship of renal failure with psoriasis and psoriatic arthritis. Methods. In this cross-sectional study, 30 participants were recruited into the following three groups: group-A, psoriatic arthritis; group-B, psoriasis without arthritis; and group-C, healthy subjects. Renal function tests were performed for every participant of each group. The data was analyzed by using SPSS version 16. Chi-squared and one-way ANOVA tests were applied, considering a value of less than 0.05 as a standard criterion. Results. Serum creatinine, urea, and phosphate were the highest in group-A, higher in group-B, and normal in group-C, . Similarly, GFR was the lowest in group-A, lower in group-B, and normal in group-C. The difference in mean GFR values was statistically significant, , . Moreover, proteinuria (gm/day) was seen in 96.7% of the patients with psoriatic arthritis, (, ) against 10% of the psoriatic patients without arthritis (, ). Conclusion. Derangement of renal function is more prevalent in psoriatic patients, especially in those with concomitant psoriatic arthritis. Therefore, each psoriatic patient must be routinely screened for an underlying renal failure. PubDate: Wed, 22 Mar 2017 07:07:39 +000
Abstract: Severe acute pancreatitis (SAP) starts as a local inflammation of pancreatic tissue that induces the development of multiple extrapancreatic organs dysfunction; however, the underlying mechanisms are still not clear. Ischemia-reperfusion, circulating inflammatory cytokines, and possible bile cytokines significantly contribute to gut mucosal injury and intestinal bacterial translocation (BT) during SAP. Circulating HMGB1 level is significantly increased in SAP patients and HMGB1 is an important factor that mediates (at least partly) gut BT during SAP. Gut BT plays a critical role in triggering/inducing systemic inflammation/sepsis in critical illness, and profound systemic inflammatory response syndrome (SIRS) can lead to multiple organ dysfunction syndrome (MODS) during SAP, and systemic inflammation with multiorgan dysfunction is the cause of death in experimental SAP. Therefore, HMGB1 is an important factor that links gut BT and systemic inflammation. Furthermore, HMGB1 significantly contributes to multiple organ injuries. The SAP patients also have significantly increased circulating histones and cell-free DNAs levels, which can reflect the disease severity and contribute to multiple organ injuries in SAP. Hepatic Kupffer cells (KCs) are the predominant source of circulating inflammatory cytokines in SAP, and new evidence indicates that hepatocyte is another important source of circulating HMGB1 in SAP; therefore, treating the liver injury is important in SAP. PubDate: Tue, 21 Feb 2017 08:44:52 +000
Abstract: Sterile neuroinflammation is essential for the proper brain development and tissue repair. However, uncontrolled neuroinflammation plays a major role in the pathogenesis of various disease processes. The endogenous intracellular molecules so called damage-associated molecular patterns or alarmins or damage signals that are released by activated or necrotic cells are thought to play a crucial role in initiating an immune response. Sterile inflammatory response that occurs in Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke, hemorrhage, epilepsy, or traumatic brain injury (TBI) creates a vicious cycle of unrestrained inflammation, driving progressive neurodegeneration. Neuroinflammation is a key mechanism in the progression (e.g., AD and PD) or secondary injury development (e.g., stroke, hemorrhage, stress, and TBI) of multiple brain conditions. Hence, it provides an opportunity for the therapeutic intervention to prevent progressive tissue damage and loss of function. The key for developing anti-neuroinflammatory treatment is to minimize the detrimental and neurotoxic effects of inflammation while promoting the beneficial and neurotropic effects, thereby creating ideal conditions for regeneration and repair. This review outlines how inflammation is involved in the pathogenesis of major nonpathogenic neuroinflammatory conditions and discusses the complex response of glial cells to damage signals. In addition, emerging experimental anti-neuroinflammatory drug treatment strategies are discussed. PubDate: Tue, 03 Jan 2017 11:44:29 +000
Abstract: Beyond its role in calcium and phosphorus metabolism for healthy bone mineralization, there is increasing awareness for vitamin D contribution in modulation of immune reactions. Given that ankylosing spondylitis (AS) is a chronic inflammatory disease involving excess immune/inflammatory activity and posing great therapeutic challenges, it is conceivable to claim that vitamin D treatment may be a safe and effective treatment to influence or modify the primary disease and its related comorbidities. Nevertheless, consistent body of research supporting this hypothesis is still lacking. In this paper, we examine whether systematic screening and treatment for vitamin D deficiency are feasible at present. We will review the immunomodulatory role of vitamin D and its contribution in initiation and progression of AS, as well as how they would determine the occurrence of comorbid conditions. Our conclusion is that despite the overwhelmed interest about vitamin D treatment in AS patients, systematic screening and treatment for vitamin D deficiency of all AS patients are not feasible as yet. This stresses the need for further extensive well-designed research to prove vitamin D efficacy in AS beyond bone protection. And if utility is proven, personalized treatment regimes, duration of treatment, and threshold values for vitamin D should be provided. PubDate: Mon, 02 Jan 2017 06:54:36 +000
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