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The relationship between clinical outcomes and serum anti-TNF levels is controversial. TheConsecutive IBD patients who received maintenance anti-TNF-α therapy were enrolled. The number of TNF-α positive cells in the mucosa was detected using immunofluorescent labeling on biopsy samples. Serum, mucosal and fecal anti-TNF-α, serum anti-drug antibody, and fecal calprotectin levels were determined using ELISA. Each patient underwent body composition analysis as well.Data of 50 patients were analyzed. The number TNF-α positive cells was significantly higher in the inflamed part of the colon than in the un-inflamed part of the colon. Tissue and fecal drug levels did not show any association with serum drug levels; moreover, serum anti-TNF concentration did not correlate with endoscopic activity. Mucosal anti-TNF levels were higher only in IFX-treated patients in remission and IFX-treated patients with detectable fecal anti-TNF had lower tissue drug levels. Presence of the drug in the feces was significantly different according to disease activity.Fecal drug concentration is suggested to be a better predictor of endoscopic activity and loss of response, and fecal drug monitoring may improve the estimation accuracy of tissue drug levels.

The negative membrane potential of bacterial cells influences crucial cellular processes. Inspired by the molecular scaffold of the antimicrobial peptide PGLa, we have developed antimicrobial foldamers with a computer-guided design strategy. The novel PGLa analogues induce sustained membrane hyperpolarization. When co-administered as an adjuvant, the resulting compounds – PGLb1 and PGLb2 – have substantially reduced the level of antibiotic resistance of multi-drug resistant Escherichia coli, Klebsiella pneumoniae and Shigella flexneri clinical isolates. The observed antibiotic potentiation was mediated by hyperpolarization of the bacterial membrane caused by the alteration of cellular ion transport. Specifically, PGLb1 and PGLb2 are selective ionophores that enhance the Goldman–Hodgkin–Katz potential across the bacterial membrane. These findings indicate that manipulating bacterial membrane electrophysiology could be a valuable tool to overcome antimicrobial resistance., Antimicrobial foldamers reduce the antibiotic resistance in multi-drug resistant Gram-negative bacteria. They hyperpolarize the membrane at low concentrations by acting as selective ionophores, enhancing the GHK-potential across the membrane.

Antimicrobial peptides (AMPs) are promising antimicrobials, however, the potential of bacterial resistance is a major concern. Here we systematically study the evolution of resistance to 14 chemically diverse AMPs and 12 antibiotics in Escherichia coli. Our work indicates that evolution of resistance against certain AMPs, such as tachyplesin II and cecropin P1, is limited. Resistance level provided by point mutations and gene amplification is very low and antibiotic-resistant bacteria display no cross-resistance to these AMPs. Moreover, genomic fragments derived from a wide range of soil bacteria confer no detectable resistance against these AMPs when introduced into native host bacteria on plasmids. We have found that simple physicochemical features dictate bacterial propensity to evolve resistance against AMPs. Our work could serve as a promising source for the development of new AMP-based therapeutics less prone to resistance, a feature necessary to avoid any possible interference with our innate immune system., Antimicrobial peptides (AMPs) are emerging as drug candidates, but the risk of pathogen resistance is not well understood. Here, the authors investigate AMP resistance evolution in E. coli, finding physicochemical features that make AMPs less prone to resistance and no cross- or horizontally-acquired resistance.

Both multi-walled carbon nanotubes (MWCNTs) and metal or metal oxides have demonstrated virus removal efficacy in drinking water applications. In this study, MWCNTs were coated with copper(I) oxide (Cu

Antibiotics that inhibit multiple bacterial targets offer a promising therapeutic strategy against resistance evolution, but developing such antibiotics is challenging. Here we demonstrate that a rational design of balanced multitargeting antibiotics is feasible by using a medicinal chemistry workflow. The resultant lead compounds, ULD1 and ULD2, belonging to a novel chemical class, almost equipotently inhibit bacterial DNA gyrase and topoisomerase IV complexes and interact with multiple evolutionary conserved amino acids in the ATP-binding pockets of their target proteins. ULD1 and ULD2 are excellently potent against a broad range of gram-positive bacteria. Notably, the efficacy of these compounds was tested against a broad panel of multidrug-resistant Staphylococcus aureus clinical strains. Antibiotics with clinical relevance against staphylococcal infections fail to inhibit a significant fraction of these isolates, whereas both ULD1 and ULD2 inhibit all of them (minimum inhibitory concentration [MIC] ≤1 μg/mL). Resistance mutations against these compounds are rare, have limited impact on compound susceptibility, and substantially reduce bacterial growth. Based on their efficacy and lack of toxicity demonstrated in murine infection models, these compounds could translate into new therapies against multidrug-resistant bacterial infections., This study designs novel antimicrobial compounds that inhibit multiple bacterial targets, making the spontaneous evolution of resistance extremely rare. These compounds inhibited the growth of all multidrug resistant Staphylococcus aureus (MRSA) isolates tested, while existing antibiotics remained largely ineffective.

Background Inflammatory bowel disease (IBD) is characterized by an unregulated immune response generating unbalance cytokine homeostasis. Analysis of patient-specific cytokine profiles may open new therapeutic targets or identify biomarkers that distinguish responders from non-responders before initiating therapy. Therefore, the aim of the present study was to determine cytokine profile of IBD patients and identify cytokines with predictive potential. Methods Blood and biopsy samples were obtained from 79 clinically active IBD patients and 28 controls without IBD. Inclusion criteria included change of therapy or initiation of new treatment for IBD patients. Organoid culture (OC) was generated from 5 clinically active IBD patients and 5 controls. Cytokine Array was used to analyse cytokine expression patterns. Total protein and mRNA were isolated from biopsies and from OCs. Protein levels were measured by ELISA and gene expression by qRT-PCR in serum, mucosa and in OCs. Results Pro-inflammatory cytokines were not detected in control samples, whereas in IBD biopsies the cytokine profiles enabled the discrimination between inflamed or non-inflamed areas. The mucosal expression of Serpin E1 was detected in all inflamed biopsy samples, whereas it was below the detection limit in healthy subjects. In responders Serpin E1 gene expressions were significantly (p Conclusion Our results suggest that serum and mucosal Serpin E1 expression reflects endoscopic activity in IBD, which could be used to follow-up disease activity and possibly therapeutic response. Organoids mimicked the expression of Serpin E1 in the original biopsies suggesting that OCs can be used to study the effect of Serpin E1 inhibition.

Background Inflammatory bowel diseases (IBD) are characterized by chronic inflammation of the gastrointestinal tract which is associated with imbalanced pro- and anti-inflammatory cytokines. Anti-TNF-α therapy is widely used, but 10–30% of the patients are primarily not responding to the treatment or lose response over time. In vitro organoid cultures (OCs) generated from tissue specific adult stem cells can mimic cellular diversity and function of the organ of origin and might be used as a predictive tool for patient specific therapeutic response. However, the reductionist nature of the OCs and lack of knowledge about the proper representation of the disease features currently limit the utilization of the OCs as ex vivo IBD models. Methods Therefore our aims were to determine and compare cytokine profiles of colonic biopsies collected from IBD patients and OCs generated from the same biopsies, and to follow the changes of cytokine expression over time. In this study samples from 20 IBD and 8 non-IBD patients were used. Biopsies were taken during colonoscopy from inflamed part of the colon of IBD patients. Crypts were isolated from biopsy samples to establish colon OCs. Total protein and RNA were isolated from biopsies and OCs. Cytokine Array was used to determine cytokine patterns in our samples. Gene expressions of control and IBD OCs after first passage was compared by qPCR. TNF-α concentrations and cellular expression was determined by EILSA and immunostainings, respectively in control and IBD OCs. To determine therapeutic response OCs were treated with anti-TNF-α therapy. Results Cytokine patterns of colon biopsies and OCs were remarkably similar until first passage. The major pro-inflammatory cytokines, IL-1β, IL-6, IL-8, were detected both in biopsies and OCs. After second passage the cytokine expression decreased or disappeared in OCs. TNF-α was also measurable in the OCs, however a similar decrease was observed, which was also confirmed by immunostaining. Gene expression analysis in IBD OCs showed an increased TNF-α, IL-1β and IL-6 levels compared to healthy control OCs after first passage. ELISA also showed higher TNF-α concentration in organoids from inflamed origin compared to controls. After anti-TNF-α treatment we detected a decrease in the IL-6 gene expression in treated OCs. Conclusion Our results suggest that colon OCs maintain the cytokine expression ex vivo until the 2nd passage and show inflammatory characteristics. Moreover, in vitro treatment induces changes in the cytokine expression. Based on these results the utility of patient-derived organoids to predict the therapeutic response can be investigated.

Background Inflammatory bowel disease potentially elevates the risk of infections, furthermore, disease activity and medical treatment(s) can increase the risk as well. However, both international data and recent studies do not confirm these preliminary conceptions regarding the SARS-CoV-2 infection. In addition, a number of studies have reported that less antibodies are produced against the virus in IBD patients. In January, 2021, the vaccination campaign has begun in Hungary as well, however, questions have been raised about the effectiveness and safety of the vaccine. Methods In this multicentre study, we assessed the prevalence and risk factors of COVID-19 infection, the willingness to receive COVID-19 vaccine and the efficacy of vaccination among IBD patients receiving biological therapy, based on a cross-sectional questionnaire-based study. To assess safety and antibody response to COVID-19 vaccines, we conducted a prospective study in the same Hungarian IBD centers. IgG antibody was quantified to SARS-CoV-2 spike protein and nucleocapsid, 1 week before and after the first vaccine and, 4 and, 8 weeks after the second vaccinane, respectively. Results 472 patients were enrolled in the first part of our study. SARS-CoV-2 infection was confirmed in, 16.9% of patients. Wearing gloves and masks were found to be effective in preventing infection (p=0.02; p=0.005), avoidance of communal areas had no effect on infection rates. Male sex increased the risk (p=0.008) of viral infection. Based on subjective complaints, UC patients had a worse disease course (p=0.002). Biological therapies did not increase the risk of infections. Patients vaccinated with mRNA vaccine had a significantly higher spike protein antibody titer one month after the second vaccination (p=0.004) compared to other vaccine types (Sinopharm©, Sputnik V©, Astra Zeneca©). Seropositivity was detected in, 98% of patients. Sinopharm© vaccination triggered the lowest number of side effect (p Conclusion Face mask was the most effective preventive tool. The risk of infection was not increased by biological therapy, therefore therapy discontinuation is not justified. Almost every vaccinated patient developed seropositivity two month after vaccination independently from the type of the vaccine, however, spike protein antibody was significantly higher following mRNA vaccinations.

Background Faecal drug concentration is not routinely measured as per therapeutic drug monitoring strategies in inflammatory bowel disease (IBD) patients receiving anti-TNF therapy. However, our previous research work suggested the importance of faecal drug monitoring of anti-TNF agents since active disease may be present in spite of normal serum anti-TNF levels. The aim of the present study was to examine the correlation between faecal calprotectin and faecal infliximab (IFX) concentration and to evaluate the cut-off value of faecal drug concentration in the respect of faecal calprotectin in patients treated with maintenance IFX therapy. Methods Consecutive patients with IBD receiving maintenance IFX therapy at 1st Department of Medicine, University of Szeged were enrolled in the present study. Faecal samples were obtained before the subsequent IFX infusion. Faecal calprotectin and IFX concentrations were determined with ELISA. The correlation between faecal calprotectin and faecal IFX concentration was statistically assessed. Results Sixty-seven IBD patients were enrolled. Female/male ratio was 49%–51%. Sixty-five point six% of the patients were diagnosed with Crohn’s disease and 34.3% with ulcerative colitis. Mean disease duration was 14.9 years (SD 9.7) at the time of analysis. Mean duration of IFX therapy was 42.3 month (SD 31.6). Twenty-eight point three% of the patients received escalated IFX therapy. Mean faecal calprotectin concentration was 545.7 µg/g (SD 379.4 µg/g). Mean faecal IFX concentration was 1 ng/ml (SD 1.3). Faecal calprotectin and faecal IFX concentration showed significant correlation (r=0.37, p = 0.002). A cut-off value of faecal IFX level of 0.6 ng/ml was determined at faecal calprotectin concentration of 500 µg/g. Conclusion According to our results IFX is detectable in the faeces at a calprotectin concentration of 500 µg/g. The cut-off value for faecal IFX concentration proved to be 0.6 ng/ml. Simultaneous determination of faecal anti-TNF and faecal calprotectin concentration is supposed to have a higher benefit in the evaluation of response to IFX therapy.

Background Inflammatory bowel diseases (IBD) are characterized by chronic inflammation of the gastrointestinal tract which is associated with the imbalanced pro- and anti-inflammatory cytokines. Anti-TNF-α is widely used as a therapeutic agent, but 10–30% of the patients are not responding to the treatment or in time it become less affective. In vitro organoid cultures generated from stem cells can mimic the cellular diversity and function of the organ of origin and might be used as a predictive tool for patient specific response. However, the in vitro cytokine expression pattern of the IBD colon organoid cultures have never been determined or compared with the cytokine expression of the colon mucosa. Methods Our aim was to determine and compare the cytokine profiles of the colon biopsy samples in IBD patients and organoid cultures generated from these biopsies. In this study samples from 5 IBD patients were used. Biopsies were taken during colonoscopy from inflamed part of the colon. Crypts were isolated from the biopsy samples to start colon organoid culture. Total protein was isolated from the biopsies and the organoids. Cytokine Array was used to determine the cytokine patterns in both samples. ELISA was used to measure the TNF-α concentrations and immunofluorescence staining to localize it in the organoids. Results We determined the cytokine profile of the biopsy samples and the colon organoid cultures. The cytokine patterns were remarkably similar until the first passage. The major pro-inflammatory cytokines, IL-1β, IL-6, IL-8, were detected in the organoids after the first passage. After the second passage the cytokine expression decreased or disappeared. ELISA revealed that TNF-α was also expressed in the organoid cultures, however a similar decrease in the expression was observed, which was also confirmed by immunofluorescence staining. TNF-α positive cells were present in the organoids, but it decreased after every passage. Conclusion Our results suggest that the colon organoid cultures maintain the cytokine profile of the tissue of origin until a limited time (until the first passage). Therefore, organoids might be used to determine patient specific therapy for drug tests.

Background Inflammatory Bowel Disease (IBD) occurs as a consequence of abnormal immune response generating unbalance between pro- and anti-inflammatory signalling. Analysis of cytokine profiles in view of different cytokine targeting or immunosuppressive therapy may open up new therapeutic targets and may reveal biological profiles that distinguish responders from non-responders before initiating therapy. The aim of present study was to determine cytokine profile of IBD patients and identify cytokines with predictive potential. Methods IBD patients with clinically active disease were enrolled in study. Blood and biopsy samples were obtained from 22 IBD patients and 5 healthy controls. Biopsies were taken from inflamed and non-inflamed part of colon of IBD patients. Total protein and mRNA were isolated from biopsy samples. Cytokine Array was used to analyse cytokine expression patterns. Serum and mucosal SerpinE1 levels were measured by ELISA and qRT-PCR. Results In samples from IBD patients, remarkable discrimination between inflamed, or non-inflamed areas was observed, whereas no pro-inflammatory cytokines were detected in control samples. SerpinE1 was presented in every inflamed biopsy samples, which was analyzed in more details. Mucosal expression of SerpinE1 differed significantly in healthy subjects compared to IBD patients with active disease (0 vs 24.06 pg/mg, p=0.02). After therapy induction a remarkable decrease was observed in the mucosal SerpinE1 concentration in responders (45.5 vs 9.7 pg/mg, p=0.02) versus non-responders (45 vs 61.2 pg/mg, p=0.3). Moreover, mean value of mucosal SerpinE1 did not differ significantly in healthy subjects compared to responders (5.7 vs. 0 pg/mg, p=0.12). In non-responders the fold changes of SerpinE1 gene expressions were significantly (p=0.001) higher than in responders. Lowest expression of SerpinE1 gene was measured in control samples, whereas the highest in untreated, inflamed biopsy samples. Serum and mucosal SerpinE1 concentrations were significantly higher in patients with active disease compared to inactive (tissue: 5 vs 47.4 pg/mg, p=0.00003; serum: 22.4 vs 25.94 mg/ml, p=0.022). Correlation analysis revealed that serum SerpinE1 correlates with disease activity (p0.1, sensitivity=72%, specificity=77.8%, accuracy=73.5%). Conclusion These results suggest that serum and mucosal SeprinE1 expression reflects endoscopic activity of IBD. Correlation of SerpinE1expression between the blood and the bowel mucosa would open up new possibilities in non-invasive disease monitoring of IBD.

Background Anti-tumour necrosis factor (TNF) therapy has dramatically changed the treatment of inflammatory bowel disease (IBD). The relationship between clinical outcomes and serum anti-TNF levels is controversial. This study aimed to perform simultaneous analyses of the serum, mucosal and faecal infliximab and adalimumab levels to determine the mucosal expression of TNF-α and assess the relationship of the anti-TNF-α levels in these biological samples with the endoscopic and clinical activities and body composition in IBD patients. Methods Consecutive IBD patients who received maintenance anti-TNF-α therapy and underwent colonoscopy were enrolled. We assessed the clinical disease activity, collected the blood, faecal and biopsy samples. The number of TNF-α positive cells in the mucosa was detected using immunofluorescent labelling. Serum, mucosal and faecal anti-TNF-α levels, anti-drug antibody level in the serum and faecal calprotectin were determined using ELISA. Each patient underwent body composition analysis. Results Fifty consecutive patients have been analysed in the study. The number TNF-α positive cells was significantly higher in the inflamed than in the un-inflamed part of the colon (p = 0.01); however, such a difference was not detected in case of tissue drug levels. Tissue drug level did not correlate with the serum drug level. Nevertheless, tissue drug levels of the samples obtained from the un-inflamed part of the colon were significantly higher in patients who were in remission (p = 0.03467). The presence of the drug in the faeces was significantly different according to disease activity (p = 0.0022). Drug levels in the biological samples did not show any association with the presence of anti-drug antibodies. Body composition parameters had no significant impact on the serum and tissue drug levels. Faecal calprotectin showed significant correlation with faecal drug concentration (p = 0.0162) and clinical and endoscopic activity (p < 0.001). Conclusion To the best our knowledge, this is the first study to measure drug concentrations in all the relevant biological samples. Our findings highlight the importance of faecal drug monitoring because active disease may be present in spite of normal serum anti-TNF levels. Simultaneous determination of faecal drug concentration and faecal calprotectin may be more accurate for evaluating therapeutic responses in the future.

Aspirin, one of the most widely used non-steroidal anti-inflammatory drugs, has extensively studied effects on the cardiovascular system. To reveal further pleiotropic, beneficial effects of aspirin on a number of pro- and anti-inflammatory microglial mechanisms, we performed morphometric and functional studies relating to phagocytosis, pro- and anti-inflammatory cytokine production (IL-1β, tumor necrosis factor-α (TNF-α) and IL-10, respectively) and analyzed the expression of a number of inflammation-related genes, including those related to the above functions, in pure microglial cells. We examined the effects of aspirin (0.1mM and 1mM) in unchallenged (control) and bacterial lipopolysaccharide (LPS)-challenged secondary microglial cultures. Aspirin affected microglial morphology and functions in a dose-dependent manner as it inhibited LPS-elicited microglial activation by promoting ramification and the inhibition of phagocytosis in both concentrations. Remarkably, aspirin strongly reduced the pro-inflammatory IL-1β and TNF-α production, while it increased the anti-inflammatory IL-10 level in LPS-challenged cells. Moreover, aspirin differentially regulated the expression of a number of inflammation-related genes as it downregulated such pro-inflammatory genes as Nos2, Kng1, IL1β, Ptgs2 or Ccr1, while it upregulated some anti-inflammatory genes such as IL10, Csf2, Cxcl1, Ccl5 or Tgfb1. Thus, the use of aspirin could be beneficial for the prophylaxis of certain neurodegenerative disorders as it effectively ameliorates inflammation in the brain.

In this work we present the results of the check test of the properties of casts, made by the method of smelted models in the precise foun- dry THE ARMATURA in Lodz. Casts were made according to the new technological solution, worked out during the realization of the purposeful project. The determination of the technological parameters of the productive process, enabling making precise casts from the alloys of aluminum, made in ceramic forms about the ambient temperature was the effect of led works.The ultrasonic method was applied to the tests of proprieties received casts. The inhomogeneity of metal material and the influence of the temperature of form on the elastic proprieties of casts were investigated. Characteristic for casts values of the velocity of longitudinal and transversal ultrasonic waves were used also to calculate the materials constants: the Young modulus E, the shear modulus G and Poisson’s coefficient μ. The obtained values of the Young modulus for tested casts carried out from 70,5 GPa to 79,9 GPa.It was shown that ultrasonic tests in quick and nondestructive way allow on the examination of density and anisotropy of casts, and also can characterize of cast using their materials constants.

Rapid decomposition of silicon nitride at high temperatures has been successfully used to manufacture ceramic nanopowders in the Si-C-N and Si-O-N systems. For powder processing, the solid combustion called self-propagating high-temperature synthesis (SHS) was realized and investigated. The well-mixed powdered reactants were placed in porous container; then, the reaction was locally ignited and combustion was propagated in a self-sustaining regime, achieving temperatures of over 2000°C. In all these experiments, combustion propagated with the formation of the transient Si3N4 phase resulted in either SiC or Si2ON2 nanosized grains. To elucidate the role of the decomposition of silicon nitride in the formation of nanosized products, thermodynamic data, temperature profiles, morphology (SEM, TEM), dispersion (BET) and phase composition (XRD) of the products were evaluated. It was found that, in both Si-C-N and Si-O-N systems, silicon nitride forms transiently at early stages of combustion because of thermodynamic and kinetic considerations. Finally, it was demonstrated that the technology of silicon carbide and silicon oxynitride nanopowders achieved by the decomposition of Si3N4 is very efficient compared to other conventional techniques. The powders obtained are well sinterable and, after further processing, can be used in a wide range of applications, such as refractory materials, ceramic armor, elements of chemical equipment, etc.

The synthesis of AlN–SiC solid solutions from Si3N4, Al, and C was investigated using the induction-field-activated/self-propagating high-temperature synthesis/static pseudo-isostatic compaction technique. Careful x-ray diffraction analyses were made on the products of combustion to determine reaction routes. Optical microscopy as well as scanning electron microscopy with an electron probe microanalysis was used for microstructural analysis. It was found that initially molten aluminum reacted with silicon nitride producing an Al–Si alloy. At higher temperatures, aluminum evaporated from the Al–Si liquid and the synthesis of AlN via a vapor phase process took place. Subsequently, dissolution of AlN into molten Si resulted in the formation of an AlN–SiC solid solution from the Al–N–Si–C liquid phase. However, below 1850 °C, the resulting solid solution of 4AlN–3SiC was not fully crystallized. Combustion temperatures above or equal to 1850 °C were required to prepare a highly crystallized solid solution with a morphology exhibiting hexagonal platelets. Based on these observations, a model for the formation of AlN–SiC solid solution is proposed.

VER 70% OF HODGKIN’S DISEASE (HD) patients can be successfully treated with conventionaldose combination chemotherapy and/or radiotherapy. The cure rate is even higher in those with the early stage of the

Microglial activation results in profound morphological, functional and gene expression changes that affect the pro- and anti-inflammatory mechanisms of these cells. Although statins have beneficial effects on inflammation, they have not been thoroughly investigated for their ability to affect microglial functions. Therefore the effects of rosuvastatin, one of the most commonly prescribed drugs in cardiovascular therapy, either alone or in combination with bacterial lipopolysaccharide (LPS), were profiled in pure microglial cultures derived from the forebrains of 18-day-old rat embryos. To reveal the effects of rosuvastatin on a number of pro- and anti-inflammatory mechanisms, we performed morphometric, functional and gene expression studies relating to cell adhesion and proliferation, phagocytosis, pro- and anti-inflammatory cytokine (IL-1β, tumor necrosis factor α (TNF-α) and IL-10, respectively) production, and the expression of various inflammation-related genes, including those related to the above morphological parameters and cellular functions. We found that microglia could be an important therapeutic target of rosuvastatin. In unchallenged (control) microglia, rosuvastatin inhibited proliferation and cell adhesion, but promoted microspike formation and elevated the expression of certain anti-inflammatory genes (Cxcl1, Ccl5, Mbl2), while phagocytosis or pro- and anti-inflammatory cytokine production were unaffected. Moreover, rosuvastatin markedly inhibited microglial activation in LPS-challenged cells by affecting both their morphology and functions as it inhibited LPS-elicited phagocytosis and inhibited pro-inflammatory cytokine (IL-1β, TNF-α) production, concomitantly increasing the level of IL-10, an anti-inflammatory cytokine. Finally, rosuvastatin beneficially and differentially affected the expression of a number of inflammation-related genes in LPS-challenged cells by inhibiting numerous pro-inflammatory and stimulating several anti-inflammatory genes. Since the microglia could elicit pro-inflammatory responses leading to neurodegeneration, it is important to attenuate such mechanisms and promote anti-inflammatory properties, and develop prophylactic therapies. By beneficially regulating both pro- and anti-inflammatory microglial functions, rosuvastatin may be considered as a prophylactic agent in the prevention of inflammation-related neurological disorders.