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EN
The human digestive system is colonized by a huge number of microorganisms, that are referred to collectively as the gut microbiota. The composition of intestinal microorganisms are shaped from an early life and undergoes constant changes depending on the influence of external factors, such as: type of delivery, feeding the young child, diet in subsequent years of life, pharmaceuticals use, stress, lifestyle or infections and previous inflammation within the digestive tract. Despite transient changes in microbiota composition, the intestinal ecosystem is constantly striving to maintain homeostasis, both qualitative and quantitative, which is fundamental to human health and human development. Microbes present in the intestines are responsible for sealing the intestinal barrier, mucin production, stimulation of the angiogenesis process, supporting digestive processes by fermentation and decomposition of undigested food residues, vitamin production or protection from pathogenic microorganisms. As shown by numerous studies carried out in recent years, intestinal dysbiosis plays a fundamental role in the development of many chronic diseases such as inflammatory bowel disease, diabetes, obesity, celiac disease, connective tissue diseases and others. Insightful understanding of the interactions between microorganisms and the host organisms can provide new information about pathogenesis of diseases as well as new ways to prevent and treat intestinal or systemic disorders. The aim of this work is to review the latest reports on the role of the gastrointestinal microbiome in selected chronic diseases.
EN
 Background: The coexistence of cystic fibrosis (CF) and celiac disease (CD) has been reported. To our knowledge there is no study directly comparing the incidence of CD in CF patients to that in the general population at the same time. There is no published data on genetic predisposition to CD in CF patients either. Therefore, in the present study we aimed to assess the genetic predisposition to CD and its incidence in CF patients comparing it to data from the general population. Patients and methods: Two hundred eighty-two CF patients were enrolled in the study. In 230 CF patients the genetic predisposition to CD (the presence of HLA-DQ2/ DQ8) was assessed. In all CF patients, serological screening for CD was conducted. In patients with positive antiendomysial antibodies (EMA) gastroduenoscopy was offered. Intestinal histology was classified according to modified Marsh criteria. The results of serological CD screening in 3235 Polish schoolchildren and HLA-DQ typing in 200 healthy subjects (HS) were used for comparison. Results: Positive EMA was found in 2.84 % of the studied CF patients. The incidence of proven CD was 2.13 %. The incidence of CD as well as positive serological screening were significantly more frequent in the CF group than in the general population. The frequency of CD-related HLA-DQ alleles in CF and HS did not differ. Conclusions: Genetic predisposition to celiac disease in cystic fibrosis patients is similar to that of the general population. However, our results suggest that cystic fibrosis is a risk factor for celiac disease development.
EN
Autoimmune diseases due to probable common pathogenesis tend to coexist in some patients. Complex clinical presentation with diverse timing of particular symptoms and sophisticated treatment with numerous side effects, may cause diagnostic difficulties, especially in children. The paper presents diagnostic difficulties and pitfalls in a child with Graves' disease, celiac disease and liver function abnormalities.
EN
Loss of homeostasis is a hallmark of malignant tumorigenesis and autoimmune diseases. Recent studies have implicated apoptotic cell death pathways in initiating and propagating autoimmune diseases in susceptible individuals. During malignancy, however, there is an accumulation of cells resistant to apoptosis. Intriguingly, some patients with malignant tumors develop symptoms that cannot be explained solely on the basis of the effects produced by either the primary tumor or its metastases. The mechanisms responsible for these complex symptoms, known as paraneoplastic autoimmunity, remain the focus of investigation.
11
Content available Platelets and the clinical course of Crohn's disease
75%
EN
Background. Crohn’s disease (CD) is a chronic, autoimmune, inflammatory bowel disease (IBD) characterised by periods of exacerbations and remissions. Autoimmune disorders caused by undetermined factors lead to inflammation in the intestinal mucosa. Presently, there is a growing interest in the role of platelets in the assessment of inflammatory lesions in CD. Accordingly, the aim of this study was to answer the question of whether routinely measured platelet indices: concentration of platelets (PLT), the mean platelet volume (MPV), plateletcrit (PCT) could become biomarkers for monitoring the course of CD. Material and methods. In the study programme, there were enrolled 100 patients with a diagnosed CD with a different clinical course, disease location and heterogeneous therapy. In all patients, there were collected blood and stool samples for the assessment of CRP, blood count and fecal calprotectin evaluation. The clinical state of each patient was classified using the Harvey-Bradshaw index. Results. The study showed a positive, statistically significant correlation between fecal calprotectin, CRP, WBC, the Harvey-Bradshaw index and the number of platelets and PCT. Furthermore, the analysis showed a statistically significant negative correlation between MPV and the number of WBC, CRP and fecal calprotectin. Conclusions. Our study showed that platelet indices are a valuable, non-invasive and widely accessible method to assess mucosal healing and the clinical status of the patient.
PL
Wprowadzenie. Choroba Leśniowskiego-Crohna (CD) należy do przewlekłych nieswoistych chorób zapalnych jelit (IBD) o podłożu autoimmunologicznym, przebiegająca z okresami zaostrzeń i remisji. U jej podstaw leżą zaburzenia autoimmunologiczne wywołane przez nieokreślone czynniki, prowadzące do zmian zapalnych w błonie śluzowej jelita. Rośnie zainteresowanie płytkami krwi w aspekcie oceny stanu zaawansowania zmian zapalnych w CD. Celem pracy była odpowiedź na pytanie, czy rutynowo oznaczane w morfologii krwi parametry płytkowe: ilość płytek krwi (PLT), średnia objętość płytek krwi (MPV), płytkokryt (PCT) mogą być wskaźnikami służącymi do monitorowania przebiegu CD. Materiał i metody. D o b adań z akwalifikowano 100 p acjentów o zróżnicowanym p rzebiegu klinicznym, lokalizacji zmian i stosowanej terapii. U wszystkich chorych pobrano krew oraz próbki do stolca celem oznaczenia CRP, morfologii krwi oraz kalprotektyny w kale. Stan kliniczny każdego pacjenta oceniano wykorzystując wskaźnik Harvey- Bradshaw. Wyniki. Wykazano istotnie statystyczną dodatnią korelacje pomiędzy kalprotektyną, CRP, WBC, wskaźnikiem Harvey-Bradshaw oraz ilością płytek krwi i płytkokrytem. Analiza wykazała także istotnie statystyczną ujemną korelację pomiędzy MPV i ilością WBC, CRP oraz kalprotektyną. Wnioski. W naszym badaniu wykazano, że parametry płytkowe mogą stanowić użyteczną, nieinwazyjną i powszechnie dostępną metodę, służącą do oceny gojenia śluzówkowego i stanu klinicznego pacjenta z CD.
12
Content available remote Neutrophil extracellular traps (NETs) - formation and implications
75%
EN
Neutrophils are cells of the immune system which freely circulate in blood vessels and are recruited to the inflammation sites when the human organism responds to microbial infections. One of the mechanisms of neutrophil action is the formation of neutrophil extracellular traps (NETs) The process of NET generation, called netosis, is a specific type of cell death, different from necrosis and apoptosis. NETs are formed by neutrophils upon contact with various bacteria or fungi as well as with activated platelets or under the influence of numerous inflammatory stimuli, and this process is associated with dramatic changes in the morphology of the cells. The main components of NETs, DNA and granular antimicrobial proteins, determine their antimicrobial properties. The pathogens trapped in NETs are killed by oxidative and non-oxidative mechanisms. On the other hand, it was also discovered that chromatin and proteases released into the circulatory system during NET formation can regulate procoagulant and prothrombotic factors and take part in clot formation in blood vessels. NETs have also been detected in lungs where they are involved in chronic inflammation processes in ALI/ARDS patients. Moreover, DNA-proteins complexes have been found in the airway fluids of cystic fibrosis patients where they can increase the viscosity of the sputum and have a negative impact on the lung functions. The DNA-complexed granular proteins and other proteins released by neutrophils during netosis lead to autoimmunity syndromes such as systemic lupus erythematosus (SLE), small-vessel vasculitis (SVV) or autoimmune diseases associated with the formation of autoantibodies against chromatin and neutrophil components. A possible involvement of NETs in metastasis is also considered.
EN
The discovery of cyclosporine A was a milestone in organ transplantation and the treatment of autoimmune diseases. However, developing an efficient oral delivery system for this drug is complicated by its poor biopharmaceutical characteristics (low solubility and permeability) and the need to carefully monitor its levels in the blood. Current research is exploring various approaches, including those based on emulsions, microspheres, nanoparticles, and liposomes. Although progress has been made, none of the formulations is flawless. This review is a brief description of the main pharmaceutical systems and devices that have been described for the oral delivery of cyclosporine A in the context of the physicochemical properties of the drug and the character of its interactions with lipid membranes.
EN
Although autoimmune diseases are relatively common, mechanisms that lead to their development remain largely unknown. Nuclear factor-κB (NF-κB), as a key transcription factor involved in the regulation of immune responses and apoptosis, appears to be a good candidate for studies on the pathogenesis of autoimmunity. This review presents how perturbations of the NF-κB signaling pathway may contribute to self-tolerance failure, initiation of autoimmune inflammatory response as well as its persistent maintenance and therefore to the development of common autoimmune diseases including rheumatoid arthritis, multiple sclerosis, type 1 diabetes mellitus, thyroid autoimmune diseases, systemic lupus erythematosus as well as inflammatory bowel diseases and psoriasis. A special emphasis is put on the genetic variations in the NF-κB related genes and their possible association with susceptibility to autoimmune diseases, as well as on the therapeutic potential of the NF-κB targeted strategies in the treatment of autoimmunity
Open Medicine
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2006
|
tom 1
|
nr 4
313-329
EN
Multiple sclerosis is still a disease without a cure. Although intensive research efforts have led to the development of drugs that modify the activity of the disease, most of them have various side effects and are expensive. At the same time it is becoming apparent that some remedies usually used to treat somatic and psychic disorders also have immunomodulating properties, and may help manage multiple sclerosis and other autoimmune diseases. We describe here the role of the sympathetic nervous system in the neuro-immune interaction in multiple sclerosis and other immune diseases with increased cellular immunity as well as neurochemical disturbances that take place in these disorders.
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