Dane literaturowe z ostatnich lat jednoznacznie wskazują na udział lizosomów w programowanej śmierci komórki. Dysfunkcje lizosomów upośledzają fuzję autofagosomów z lizosomami, co prowadzi do wakuolizacji cytoplazmy. Obecność wakuoli autofagalnych obładowanych uszkodzonymi organellami i nieprawidłowymi białkami jest cechą charakterystyczną wielu chorób neurodegeneracyjnych. Agregacja niezdegradowanego materiału zaburza homeostazę komórki powodując śmierć neuronu w wyniku apoptozy i/lub nekrozy. Ponadto indukowany kalpainami lub spowodowany mutacjami rozpad błony lizosomu uwalnia katepsyny, które indukują szlak śmierci komórki. W artykule przedstawiono mechanizm śmierci komórki nerwowej, łączący zaburzenie szlaku autofagalno-lizosomalnego z dysfunkcjami lizosomów, zwany lizosomalnym szlakiem śmierci neuronu.
The discovery of a new class of molecules, the 22-24 nucleotides long RNA, has initiated a new chapter in genetic information regulation studies. These molecules have a significant impact on the functioning of cells by means of negative regulation of expression of targeted mRNA. Special attention is given to exogenous, circulating miRNAs, whose levels of expression in different body fluids varies and can be deregulated by pathological, as well as physiological conditions. Extensive studies on the diagnostic potential of miRNAs are currently conducted. Attempts are made to determine specific profiles of miRNAs that will correlate with disease entity. The preliminary data gives hope that in the near future miRNAs will be applied as a diagnostic and prognostic biomarkers in many diseases. One of their most significant applications can be in the diagnosis of lung cancer - the most deadly form of cancer, due to its too late diagnosis. Abundant in miRNA molecules, blood and sputum constitute excellent diagnostic material for patients with lung cancer, especially those with non-small-cell lung cancer NSCLC. Easy procedures for obtaining this diagnostic material from patients and relatively easy analysis of miRNA expression, make these molecules promising in their use in diagnosis, predicting of therapy effects and prognosis for patients with NSCLC. This work presents information related to miRNA and their specific attributes. Moreover level of deregulated circulating miRNAs occurring in body fluids of patients with NSCLC is also discussed.
Pseudomonas aeruginosa is an opportunistic pathogen that can cause several acute and chronic infections in humans, and it has become an important cause of nosocomial infections and antibiotic resistance. Biofilm represents an important virulence factor for these bacteria, plays a role in P. aeruginosa infections and avoidance of immune defence mechanisms, and has the ability to protect the bacteria from antibiotics. Alginate, Psl and Pel, three exopolysaccharides, are the main components in biofilm matrix, with many biological functions attributed to them, especially with respect to the protection of the bacterial cell from antibiotics and the immune system. Pseudomonas infections, biofilm formation and development of resistance to antibiotics all require better understanding to achieve the best results using alternative treatment with phage therapy. This review describes the P. aeruginosa pathogenicity and virulence factors with a special focus on the biofilm and its role in infection and resistance to antibiotics and summarizes phage therapy as an alternative approach in treatment of P. aeruginosa infections.
Introduction: It is known that in the pathogenesis of tick-borne encephalitis (TBE) various molecules play a significant role. The most prominent factors include IL-10, IL-28B, CD-209 and CCR5. It is reasonable to search for genetic predispositions to the development of various clinical forms of TBE related to the genetic variation of IL-10, IL-28B, CD-209 and CCR5. In this study we aimed to search for the relationship between single nucleotide polymorphism in the promoter region of the CD209, IL-10, IL-28 and 32 base pair deletion in CCR5 coding region (Δ 32) with the human predisposition to development of various clinical presentations of TBE. We tried to assess the relation between the presence of particular alleles and genotypes with laboratory and clinical parameters. Material/Methods 59 patients with TBE and 57 people, bitten by a tick who never developed TBE (Polish cohort), were included in the study. To assess the distribution of single nucleotide polymorphisms, TaqMan SNP genotyping assays were used for IL10: rs1800872 and rs1800896, for CD 209 rs4804803 and rs2287886, rs12979860 for IL 28B SNPs according to the manufacturer’s protocol using real-time PCR technology on the StepOne thermal cycler. Results Comparison between TBE patients and CG showed that in SNP rs2287886 CD 209 AG heterozygotes were more frequent in the TBE group, while homozygotes GG were more frequent in the CG group. Conclusions SNP rs2287886 CD 209 AG heterozygotes predispose humans to develop TBE. Single nucleotide polymorphism in the promoter region of the CD209, IL-10, IL-28 and CCR5 D32 genes does not correlate with the severity of TBE.
Chronic renal failure is associated with many neurological complications. Due to accumulation of uremic neurotoxins axonal degeneration with its secondary demyelination occurs, which results in development of polineuropathy in 60‑100% of patients with chronic renal failure. One of the most severe peripheral neuropathy is optic neuropathy. It is associated with visual deterioration and reduction in quality of life. Symptoms of the optic neuropathy may appear either before or after dialysis therapy. They often worsen after renal transplant, probably due to immunosuppressive regimen. Early diagnostics of the optic neuropathy became possible by using visual evoked potentials (VEP). This reliable, sensitive and noninvasive technique provides a direct measure of subclinical impairment of visual pathways. Among hemodialysed or immunosupressed patients one can observe abnormal VEP parameters - especially prolonged latency of the P100 component, less often fluctuation of its amplitude. These alterations are pronounced even if clinical examination reveals no abnormalities. This review presents a summary of current use of visual evoked potentials in monitoring of patients with chronic renal failure.
INTRODUCTION:There are two commercially available tests for measurement of serum free light chains (sFLC) in multiple myeloma (MM) patients - Freelite and N Latex FLC. The aim of this study was to perform an assessment and direct comparison of the usefulness of the methods in routine clinical practice.METHODS:40 refractory/relapsed MM patients underwent routine disease activity assessment studies, along with sFLC analysis using both assays. Correlation and concordance between the tests and sensitivity of studied methods of sFLC assessment were established. Special attention was focused on sFLC results in patients finally evaluated after completing the treatment.RESULTS:A weak correlation for the measurement of both κ [Passing-Bablok slope (PB) = 0.7681] and λ chains [(PB) = 1.542] was found. Using Bland-Altman plots, a bias of 0.0467 (κ) and -0.2133 (λ) between the measurements was documented. The concordance coefficient equaled 0.87 for κ, 0.62 for λ and 0.52 for κ/λ ratio. Ten patients had an abnormal Freelite assay κ/λ ratio and normal N Latex FLC κ/λ ratio. Three of these patients had negative serum protein electrophoresis results and fulfilled diagnostic criteria of stringent complete remission (sCR) according to N Latex FLC (but not according to Freelite). When the κ/λ ratio obtained by both methods was compared to patients' serum/urine protein electrophoresis and immunofixation results, sensitivity of Freelite and N Latex FLC was established to be 62.5% and 41%, respectively.CONCLUSIONS:There was no strong correlation or concordance between the two assays, and the sensitivity in terms of sFLC detection was different. This may cause problems when diagnosis of sCR is considered.
Interleukin 15 is a pleiotropic cytokine of the four α helix bundle family. Binding to a heterotrimeric receptor complex, which consists of a unique, high affinity IL‑15Rα‑chain and IL-2/IL-15Rβ and IL‑2Rγ chains, IL‑15 activates signaling pathways leading to activation and proliferation of T and B cells, as well as natural killer cells. At the same time, IL‑15 protects effector cells from T regulatory cells and does not induce immune tolerance. The significant regulatory action of IL‑15 on the immune system provides new opportunities for development of anti‑cancer therapies. As documented in many experiments using different tumor models, IL‑15 enhances antitumor effects. To improve the efficiency of IL‑15, several strategies, including combination with other anti‑cancer therapies such as chemotherapy, additional use of antibodies (anti‑PD‑L1, anti‑CTLA‑4, anti‑CD40), or other cytokines, have been evaluated. Increased anti‑tumor activity can also be obtained by using IL‑15 agonists. However, acting as a growth factor for immune cells but also for tumor cells, IL‑15 may promote their proliferation, survival and dissemination. Of significance seems the role of IL‑15 in the pathogenesis of hematological malignancies, which is due to the involvement in the proliferation and differentiation of NK, T and B cells. Currently, several experimental strategies are available to block biological activity of IL‑15. Among compounds inhibiting the activity of IL‑15 are not only monoclonal antibodies interacting directly with the cytokine or with IL‑15R subunits, but also mutant forms of IL‑15 and protein constructs.
G protein-coupled receptors (GPCRs) constitute a family of transmembrane proteins that mediate many cellular processes. GPR120/FFAR4, a receptor from this family that is activated by fatty acids, has received considerable attention recently. This paper presents a literature review concerning the role of GPR120 and its mechanism of action in animal and human studies as well as the potential use of GPR120 for the treatment of chronic diseases. Two electronic databases - Medline and Google Scholar - were searched for available studies addressing the review topic that were written in English and published from 2000 to June 2017. The following key terms were used in the search: GPR120, FFA4, GPR120 agonist, PUFAs, EPA, DHA, adipocyte, obesity, hyperlipidemia, inflammation, cancer, diabetes, insulin resistance, taste, atherogenesis, hepatis, central nervous system. In humans, GPR120 expression is expressed in macrophages, eosinophils, and adipose tissue, in cells of the tongue, liver, lungs, small and large intestine, gastric mucosa, and pancreas, in the central nervous system and placental microvilli. Medium- and long-chain fatty acids act as ligands for the receptor. Through the internalization of beta-arrestin-2 complex and the inhibition of NF-κB, GPR120 mediates the activation of the cell's anti-inflammatory mechanisms. The receptor is also involved in the maturation of adipocytes, the modulation of insulin signalling pathways, the regulation of glucose metabolism, and the secretion of intestinal hormones. GPR120 is a promising target for the treatment of numerous diseases, whose pathophysiology is associated with low-grade inflammation. As a result of intensive searches, a likely group of synthetic agonists of the receptor was determined with potential therapeutic applications in conditions such as obesity, impaired carbohydrate metabolism, inflammatory bowel diseases, cancer, mental disorders.
INTRODUCTION:The aim of the study was to evaluate genetic relatedness and antimicrobial susceptibility of extended-spectrum beta-lactamase-producing E. coli strains isolated from patients hospitalized in the University Hospital in Bydgoszcz (Poland).MATERIAL AND METHODS:The study included 33 extended-spectrum beta-lactamase-producing E. coli strains isolated from 31 patients. The chromosomal DNA was extracted from the strains and separated by pulsed-field gel electrophoresis. Antimicrobial susceptibility testing was performed by the agar dilution method and carried out according to the European Committee on Antimicrobial Susceptibility Testing recommendations.RESULTS:According to the pulsed-field gel electrophoresis results, 32 distinct pulsotypes were revealed. Based on Molecular Analyst Fingerprinting software analysis, the studied isolates were divided into four subgroups: 6 (18.2%) isolates showing similarity greater than 90% (group A); 19 (57.6%) showing 80-90% similarity (group B); 7 (21.2%) showing 70-79% similarity (group C); and one isolate with less than 70% similarity (group D). Among E. coli isolates showing similarity greater than 90%, four antimicrobial patterns were noted. Among the isolates showing 80-90% similarity, 18 antimicrobial patterns were observed. E. coli isolates showing 70-79% similarity presented 6 antimicrobial patterns.CONCLUSIONS:Our results show a high degree of genetic diversity of extended-spectrum beta-lactamase-producing E. coli isolates. However, based on a similarity of ≥80%, almost 75% of E. coli isolates were clonally related. Although it is difficult to identify definitive transmission events based on the recovery of indistinguishable pulsed-field gel electrophoresis types alone, we speculate that extended-spectrum beta-lactamase-producing E. coli strains may have disseminated throughout the hospital.
Pyrethroids are biocides, which belong to the third generation of insecticides. They are used as biocides, insecticides and medicines. These agents react selectively, because they are less harmful to birds and mammals (due to poor intestinal absorption and rapid detoxification in the body of homeothermic organisms) and they are poisonous for fish and insects.The aim of the article is to present the current state of knowledge on the effects of pyrethroids on the immune system based on the latest scientific research.The mechanism of action of pyrethroids include the delaying closure of voltage- sensitive sodium and chloride channels (including GABA- dependent channels). These compounds are neurotoxic.Studies have shown that they cause numerous immune disorders contributing to lowering of immunity in humans and animals. Exposure to pyrethroids can cause inhibition of proliferation of peripheral blood leukocytes and reducing the concentration of IgG immunolgobulines. They also cause reduced macrophages and decrease in interleukin 2 (IL-2), interleukin 8 (IL-8), interleukin 12p70 (IL-12p70), and interferon γ (IFN-γ). Some of these compounds cause increase of liver weight and increase of bone marrow cellularity, and may induce apoptosis of the thymus. Pyrethroids can cause allergies and asthma. Their immunosuppressive effects can impair host resistance against infections. Exposure to these compounds can also contribute to induction of the cancer, especially in patients with impaired immune function.
Pulmonary hypertension (PH) is a rare disorder associated with abnormally elevated pulmonary pressures that, if untreated, leads to right heart failure and premature death. Special population include patents with pulmonary arterial hypertension (PAH). A greater understanding of the epidemiology, pathogenesis, and pathophysiology of PAH has led to significant advances over the past few years. Modern drug therapy provides a significant improvement in patient symptomatic status and a slower rate of clinical deterioration. Despite this, PAH remains a chronic disease without a cure. There is a need for the development of novel therapies and therapeutic strategies, as treatment options are neither universally available nor always effective, possibly due to the large number of mediator and signaling pathways with downstream effectors which are implicated in the pathobiology of PH, and which are not fully reversed during PAH therapy. In the following pages, we review novel strategies for treatment of PAH. For this purpose we summarized the role of specific drug therapies that involve: endothelin receptor antagonists (ERA), phosphodiesterase type 5 inhibitors (PDE-5i) and prostacyclin and prostanoids (PGI2). We focused on novel molecular mechanisms in PAH of recently approved: Guanylate cyclase stimulator and non-prostanoid IP receptor agonist. We discussed novel approach to combined therapy, as well as a new generation of investigational drugs and promising PAH-associated signaling pathways, such as, PDGF, RhoA/ROCK RAAS, HT-5 and others.
INTRODUCTION:Type 2 diabetes mellitus (T2DM) and obesity are metabolic disorders whose major hallmark is insulin resistance. Impaired mitochondrial activity, such as reduced ratio of energy production to respiration, has been implicated in the development of insulin resistance. Uncoupling proteins (UCPs) are proton carriers, expressed in the mitochondrial inner membrane, that uncouple oxygen consumption by the respiratory chain from ATP synthesis.AIM:The aim of the study was to determine transcriptional levels of UCP1 and UCP2 in peripheral blood mononuclear cells (PBMCs) from patients with metabolic disorders: T2DM, obesity and from healthy individuals.MATERIAL/METHODS:The mRNA levels of UCP1, UCP2 were determined by Real-Time PCR method using Applied Biosystems assays.RESULTS:The UCP1 mRNA expression level was not detectable in the majority of studied samples, while very low expression was found in PBMCs from 3 obese persons. UCP2 mRNA expression level was detectable in all samples. The median mRNA expression of UCP2 was lower in all patients with metabolic disorders as compared to the controls (0.20+0.14 vs. 0.010+0.009, p=0.05). When compared separately, the differences of medians UCP2 mRNA expression level between the obese individuals and the controls as well as between the T2DM patients and the controls did not reach statistical significance.CONCLUSIONS:Decreased UCP2 gene expression in mononuclear cells from obese and diabetic patients might contribute to the immunological abnormalities in these metabolic disorders and suggests its role as a candidate gene in future studies of obesity and diabetes.
Adipokines are molecules produced and secreted by adipose tissue and are linked to multiple malignancies. Adipokines can suppress or promote particular cell behaviors in different types of cancer. The aim of this study was to investigate the impact of chemotherapy on select adipokines in patients with colorectal cancer (CRC).Blood samples were collected from 42 patients with pathologically documented advanced CRC, who required palliative chemotherapy. Leptin, adiponectin, resistin and visfatin levels were measured by ELISA before and 3 months after the administration of chemotherapy. Among the 42 patients evaluated, 18 achieved a partial response (PR), 16 achieved stable disease (SD) and 8 patients experienced disease progression (PD).We found that 5-fluorouracil-based chemotherapy regimens significantly increased plasma levels of leptin and adiponectin and decreased plasma levels of resistin and visfatin in PR and SD patients, whereas the plasma levels of these molecules were not affected in PD patients. Furthermore, the mean plasma levels of leptin were significantly lower, and the mean plasma levels of resistin and visfatin were significantly greater in patients with PD compared with PR and SD both before and after chemotherapy treatment.We conclude that palliative chemotherapy in CRC patients, in addition to providing clinical benefits, positively affects cytokine production and secretion in PR and SD patients. Specifically, we found that palliative chemotherapy increased plasma levels of the anti-inflammatory adipokine adiponectin and decreased the plasma levels of visfatin and resistin, molecules known to promote angiogenesis and cancer cell proliferation in PR and SD patients. Moreover, the baseline values of leptin, visfatin and resistin might serve as prognostic indicators of a poor response to chemotherapy.
INTRODUCTION Epigenetic mechanisms regulate the transcription of genes, which can affect the differentiation of MSCs. The aim of the current work is to determine how the histone deacetylase inhibitors TSA and VPA affect the expression of neuronal lineage genes in a culture of rat MSCs (rMSCs). MATERIALS AND METHODS We analyzed the expression of early neuron marker gene (Tubb3), mature neuron markers genes (Vacht, Th, Htr2a) and the oligodendrocyte progenitor marker gene (GalC). Moreover, changes in the gene expression after three different periods of exposure to TSA and VPA were investigated for the first time. RESULTS After six days of exposition to TSA and VPA, the expression of Tubb3 and GalC decreased, while the expression of Th increased. The highest increase of VAChT expression was observed after three days of TSA and VPA treatment. A decrease in Htr2a gene expression was observed after TSA treatment and an increase was observed after VPA treatment. We also observed that TSA and VPA inhibited cell proliferation and the formation of neurospheres in the rMSCs culture. DISCUSSION The central findings of our study are that TSA and VPA affect the expression of neuronal lineage genes in an rMSCs culture. After exposure to TSA or VPA, the expression of early neuronal gene decreases but equally the expression of mature neuron genes increases. After TSA and VPA treatment ER of the oligodendrocyte progenitor marker decreased. TSA and VPA inhibit cell proliferation and the formation of neurospheres in rMSCs culture.
BACKGROUND:Human vascular endothelial function and integrity may be regulated by many non-specific factors. However, the potential influence of specific antigens via an IgE-mediated mechanism remains unknown. The aim of the study was to determine the expression of the IgE receptors FcεRI and FcεRII in the human vascular endothelium and to assess their relevance in the IgE-mediated regulation of endothelial integrity.MATERIAL/METHODS:FcεRI and FcεRII expression in human umbilical vein endothelial cells (HUVEC) was genetically assessed by PCR with respective primers and sequencing. HUVEC were cultured with IL-4, and changes in FcεRI and FcεRII mRNA expression were analyzed by real-time PCR. Changes in the integrity of endothelium pre-treated with anti-BSA-DNP IgE following exposure to the specific BSA-DNP antigen was assessed using the Real-time Cell Electric Impedance Sensing system (RTCA-DP).RESULTS:PCR and sequencing revealed the expression of FcεRI and FcεRII receptors in the human vascular endothelium. IL-4 caused respective 2- and 3-fold increases in FcεRI and FcεRII mRNA expression. Exposure of endothelium pre-treated with anti-BSA-DNP IgE to specific BSA-DNP antigen led to a 20% increase of endothelial integrity (p<0.05) after 24 hours, but only in cells pre-incubated with IL-4.CONCLUSIONS:The presence of FcεRI and FcεRII may allow the human vascular endothelium to respond to a specific antigen by increasing its integrity via an IgE-mediated mechanism.
3-Bromopyruvate (3-BrPA) is an halogenated analogue of pyruvic acid known for over four decades as an alkylating agent reacting with thiol groups of many proteins. It enters animal cells like a lactate: via monocarboxylic acid transporters. Increasing interest in this compound, in recent times, is mainly due to hopes associated with its anticancer action. It is based on the impairment of energy metabolism of tumor cells by inhibiting enzymes in the glycolysis pathway (hexokinase II, glyceraldehyde 3-phosphate dehydrogenase, phosphoglycerate kinase) and the oxidative phosphorylation (succinate dehydrogenase). Two cases of clinical application of this compound in the treatment of advanced cancers were reported. By using 3-BrPA, rheumatoid arthritis in SKG mice has been reduced. This compound has also antiparasitic activity: lowers cell viability of Trypanosoma brucei, decreases intracellular proliferation of Toxoplasma gondii and reduces the metabolic activity of Schistosoma mansoni. It also has antifungal properties; particularly it acts strongly on Cryptococcus neoformans, as well as Saccharomyces cerevisiae. An inhibitory effect on bacterial enzymes was also described on: isocitrate lyase from Escherichia coli, Mycobacterium tuberculosis, Pseudomonas indigofera and 2-methylisocitrate lyase, succinate dehydrogenase and acetohydroxylic acid synthase from Escherichia coli. Wherever undesirable (cancer, parasitic) cells differ from normal by more intense glycolysis and higher energy needs, there is a good chance of successful 3-BrPA use. However, this compound acts on all cells and it, therefore, seems that its future as a pharmaceutical is dependent upon the development of appropriate methods for its effective and safe application.
In the search for explanations of diabetes pathomechanisms, especially the development of its vascular complications (micro- and macrovascular ), although current, good metabolic control of diabetes, attention was drawn to the role of epigenetic inheritance associated with epigenetic modifications of histone proteins and DNA in hyperglycemia conditions. This study showed the significant role of DNA methylation and histone epigenetic modifications (a different nature and a different degree) in the transmission of information that is not connected with gene inheritance but concerns the persistent changes induced by hyperglycemia..Attention was paid to the role of DNA methylation of pancreatic cells in the pathogenesis of type 1 diabetes, but also type 2. The important role of DNA methylation changes in a so-called intrauterine growth restriction (IUGR) as reason of subsequent development of diabetes was particularly emphasized. In the pathogenesis of type 2 diabetes and its complications, especially microvascular complications, the greatest share and importance of epigenetic modifications on mitochondrial DNA metylation are the most important. The multidirectionality Complicaand complexity of epigenetic modifications of histone proteins indicate their importance in the development of diabetic disturbances. An especially important role is attributed to methylation and acetylation of histone proteins, in particular on arginine and lysine, whose changes occur most frequently. Moreover, epigenetic modifications of the enzymes, especially methylases, responsible for these processes are the underlying. It has been indicated that the identification of epigenetic differences within the DNA or histone proteins may be a useful prognostic biomarker of susceptibility to the disease development in the future. Moreover, they may become a potential target for future therapeutic interventions for clinical disorders in diabetes.
There is a variety of mechanisms(s) factor(s) that may influence stem cell therapies for heart regeneration. Among the best candidates for stem cell source are: mesenchymal stem cells (also those isolated from adipose tissue), cardiac cell progenitors (CPC) and descendants of iPSC cells. iPSC/s can be potentially beneficial although their pluripotent induction has been still in question due to: low propagation efficacy, danger of genomic integration/instability, biological risk of current vector system teratoma formation etc. which have been discussed in this review. Optimization protocols are required in order to enhance stem cells resistance to pathological conditions that they may encounter in pathological organ and to increase their retention. Combination between gene transfer and stem cell therapy is now more often used in pre-clinical studies with the prospect of subsequent clinical trials. Complementary substances have been contemplated to support stem cell viability (mainly anti-inflammatory and anti- apoptotic agents), which have been tested in animal models with promising results. Integration of nanotechnology both for efficient stem cell imaging as well as with the aim to provide cell supporting scaffolds seem to be inevitable for further development of cellular therapies. The whole organ (heart) reconstruction as well as biodegradable scaffolds and scaffold-free cell sheets have been also outlined.
According to recent reports, bacterial chromosomes exhibit a hierarchical organization. The number of proteins that bind DNA are responsible for local and global organization of the DNA ensuring proper chromosome compaction. Advanced molecular biology techniques combined with high-throughput DNA sequencing methods allow a precise analysis of bacterial chromosome structures on a local and global scale. Methods such as in vivo footprinting and ChIP-seq allow to map binding sites of analyzed proteins in certain chromosomal regions or along the whole chromosome while analysis of the spatial interactions on global scale could be performed by 3C techniques. Additional insight into complex structures created by chromosome-organizing proteins is provided by high-resolution fluorescence microscopy techniques.
A stigma is currently defined as a discrediting mark, biological or social, that sets a person off from others and disrupts interactions with them. People who differ from social norms in some respect are often negatively labeled. A number of medical conditions are recognized at present as stigmatizing their sufferers and certain skin diseases are among them. The article aimed to analyze the current understanding about stigmatization among dermatological patients, especially those with psoriasis. We performed our search on PubMed up to November 2016 and utilized combinations of key phrases containing such words as stigmatization, skin, dermatology, names of various skin conditions (psoriasis, vitiligo, acne, etc.). Following a precise selection process, 58 articles remained. Stigmatization seems to be a common and important problem in dermatology. Psoriasis appears as the most frequently studied skin disease (37.2% of articles). It was followed by vitiligo (13.7%) and leprosy (8.6%). Mainly, the visibility of skin lesions as well as cultural factors contribute to the feeling of stigmatization. There is a need for more research in the field of stigmatization in dermatological conditions and an urgent need for the creation of special anti-stigmatization program/programs for patients suffering from dermatoses.
