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EN
Objectives. Recent epidemiological studies suggested an association between a poor vitamin D [25(OH)D] status, inflammatory mediators, and rheumatoid arthritis (RA). We have recently proposed that pro-inflammatory interleukin 6 (IL-6) may represent a good marker for disease activity of RA. The aim of this study was to investigate the relationship between serum 25(OH)D levels and disease activity, joint damage, as well as serum IL-6 levels in a Polish RA population. Materials and Methods. Serum 25(OH)D levels were measured in 35 female RA patients and 38 age- and gender-matched healthy controls. Statistical correlations between 25(OH)D levels and the disease activity score 28 (DAS 28), joint damage based on the Steinbrocker criteria, as well as serum IL-6 levels were performed. Results. There was no statistically significant difference between levels of 25(OH)D in RA (16.89±8.57 ng/ml) and healthy controls (14.12±7.51 ng/ml), and the vitamin D deficiency (<20 ng/ml) was found in 71.43% of RA patients and 73.68 % of healthy controls. While vitamin D status did not correlate with DAS 28 (r=0.265, p=0.149) and joint damage based on the Steinbrocker criteria (r=0.367, p=0.065), a positive correlation between 25(OH)D and IL-6 (r=0.537, p=0.002) was observed in RA. Conclusion. Although further studies on a larger group of patients will be needed to confirm the data presented here, it seems that hypovitaminosis D is common in the RA patients and middle-aged non-RA healthy women in the Polish population. 25(OH)D levels were similar in the RA patients and age- and gender-matched healthy controls, and were not associated with joint damage and disease activity in patients.
EN
Interleukin 1 (IL-1) and interleukin 6 (IL-6) are typical examples of multfunctonal pro-infammatory cytokines involved in the regulaton of the immune response, hematopoiesis, and infammaton. Both peripheral and intraventricular administraton of these cytokines causes acute phase symptoms, e.g. fever, actvaton of the hypothalamic-pituitary-adrenal axis and psychological depression. The amygdala belongs to the structures of the limbic system involved in the regulaton of the immune response. Increased actvity of immune system may lead to changes in the role of amygdala, medial prefrontal cortex, anterior cingulate cortex or insula. The aim of the study was to present the mutual interactons between the amygdala and pro-infammatory cytokines such as interleukin-1β (IL-1 beta) and interleukin 6 (IL-6). Most of the data included in this review comes from animal studies.
EN
Inflammation plays an important role in the development of many obesity-related diseases. This study aimed to investigate the effect of ezetimibe on inflammation and myocardial remodeling in obese rats. A rat model of obesity was established, and myocardial damage was examined by transmission electron microscopy and Masson staining. Twenty obese rats were divided into two groups (n=10): obese group and ezetimibe group. Ten SD rats were used as controls. Western blot was performed to monitor the expression of P-p38MAPK and interleukin (IL)-6. Immunohistochemical staining was used to monitor the expression of intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. In the obese rats group, we observed increased inflammatory factors and myocardial hypertrophy. In contrast, the ezetimibe group exhibited decreased expression of inflammatory factors and an improvement in myocardial remodeling compared to the obese group. Mechanistically, we found that ezetimibe decreased P-p38MAPK, IL-6, intercellular adhesion molecule-1, and vascular cell adhesion molecule-1 levels in the hearts of the obese rats. Taken together, these results indicate that ezetimibe may improve myocardial remodeling in obese rats by inhibiting inflammation.
EN
BACKGROUND Series of evidences have shown that interleukin-6 (IL-6) could play an important role in the pathogenesis of colon cancer. Inositol hexaphosphate (IP6) is a naturally occurring polyphosphorylated carbohydrate, found in many plant sources and in certain high-fi ber diets. Over the past few years interest in IP6 has stemmed mostly from its potentially important antineoplastic activity against various types of cancer, including colon cancer. Moreover, it was pointed out that IP6 has ability to act on the host immune functions and infl ammatory processes by controlling the synthesis of cytokines such as IL-6. The aim of this study was to evaluate the infl uence of IP6 on IL-6 secretion by malignant epithelial colorectal Caco-2 cells. MATERIAL AND METHODS The Caco-2 cells were treated with IP6 at the concentrations of 1.0; 2.5; 5.0 mM for 1; 6; 12 and 24 hours. The level of IL-6 was measured by enzyme-linked immunosorbent assay. The concentration of IL-6 was related to the amount of total cell protein which was estimated by the Bradford method (pg/mg). RESULTS It was found that colorectal Caco-2 cells constitutively secreted IL-6 at the constant level during 24 hour culture. IP6 down-regulated IL-6 secretion in a dose and time dependent manner. Conclusion old The present fi ndings demonstrate that IP6 in the lumen of the large intestine may play an immunoregulatory role by inducing changes in IL-6 secretion by epithelial colon cells.
PL
WSTĘP Szereg danych wskazuje, że interleukina-6 (IL-6) może odgrywać potencjalną rolę w patogenezie raka jelita grubego. W ciągu ostatnich lat szczególną uwagę naukowców zwraca aktywność przeciwnowotworowa kwasu fi tynowego (IP6), ufosforylowanego węglowodanu, składnika diety bogatobłonnikowej. Pojawiły się sugestie, że może on modulować przebieg reakcji odpornościowych i stanów zapalnych między innymi poprzez regulację syntezy cytokin takich jak IL-6. Celem pracy była ocena wpływu IP6 na sekrecję IL-6 przez komórki nowotworowe jelita grubego linii Caco-2. MATERIAŁ I METODY Komórki linii Caco-2 eksponowano na działanie IP6 w stężeniach 1,0; 2,5; 5,0 mM przez 1; 6; 12 i 24 godziny. Oznaczenie stężenia IL-6 w hodowlach przeprowadzono przy użyciu testu ELISA, natomiast do oznaczenia stężenia białka zastosowano metodę Bradforda. Stężenie IL-6 wyrażono w pg/mg białka komórek. WYNIKI Stwierdzono, że transformowane komórki nabłonkowe jelita grubego linii Caco-2 wykazują konstytutywną sekrecję IL-6, utrzymującą się na stałym poziomie w czasie trwania doświadczenia. IP6 posiada zdolność do zmniejszania tej sekrecji w sposób zależny od jego stężenia i czasu działania na komórki. WNIOSKI Wyniki badań sugerują, że IP6 obecny w świetle jelita może wywierać efekty immunoregulatorowe związane ze zmianami sekrecji IL-6 w komórkach nabłonka jelitowego.
EN
This work was carried out to investigate the role of Glutathione S-Transferase M1 (GSTM1) null genotype frequency in prognosis of β-thalassemia, and to detect the correlation between GSTM1 null genotype and appearance of cardiac complications in β-thalassemia. Materials and Methods. The studied groups in the present work were divided to three groups (group I: 20 healthy subjects, group II: 56 β-thalassemic patients and group III: 16 β-thalassemic patients with cardiac complications were taken from group II). The measurement of human high sensitive C-reactive protein (hs-CRP) was performed using nephelometry. GSTM1 genotype was detected by Polymerase Chain Reaction (PCR) and cardiac complications were determined by using Echocardiography. Results. A statistically significant increase in hs-CRP and interleukin-6 (IL-6) levels was found in β-thalassemic patients with cardiac complications compared to normal subjects. Results showed no relation between GSTM1 null genotype frequency neither with β-thalassemia nor with cardiac complications appearance, where the interaction between GSTM1 null genotype in β-thalassemic patients with cardiac complications and healthy subjects were insignificant compared to subjects with GSTM1 non-null genotype. Conclusions. GSTM1 null genotype frequency has no role in β-thalassemia or cardiac complications appearance.
EN
Introduction: Chronic obstructive pulmonary disease (COPD) is characterised by the airflow limitation as a consequence of progressive inflammatory response to inhaled noxious particles and gases, particularly cigarette smoke. Three factors play a main role in pathogenesis of the disease: inflammatory process, oxidative stress and imbalance between proteases and antiproteases. Recently there are some evidences that also extrapulmonary changes like cachexia, osteoporosis or depression are associated with COPD. The aim of the study was to access local and systemic inflammation in patients with COPD. Material and methods: The study group consisted of 23 patients with COPD during stable and exacerbation phase of the disease. As a control served 16 asymptomatic smokers. We investigated: 1) concentration of hydrogen peroxide (H2O2) and proinflammatory cytokines like TNF-a and IL-6 in expired breath condensate (EBC); 2) serum levels of TNF-a and IL-6. Results: It was showed that the level of H2O2 in EBC of patients with stable COPD was significantly higher as compared with healthy smokers. Additional significant enhanced in H2O2 exhalation was demonstrated during exacerbation of COPD. There was no difference in IL-6 concentration between the study groups (p>0,05). Discernible level of TNF-a in exhaled air was measured only in those with COPD exacerbation. Exhaled H2O2 correlated with FEV1% predicted value in patients with stable as well as with exacerbation phase of COPD. Also serum levels of TNF-a and IL-6 of patients with stable disease were higher compared to the values of healthy smokers. The serum concentrations of studied cytokines did not change significantly during exacerbation of COPD. Conclusions:Our results demonstrated the occurrence of local oxidative stress in patients with stable COPD. This process significantly increased during exacerbation of the disease. Besides of local reaction in respiratory compartment of patients with stable COPD we revealed systemic inflammatory process measured by serum levels of TNF-a and IL-6. Exhaled H2O2 correlated with lung function (FEV1% pred).
PL
Wstęp: Przewlekłą obturacyjną chorobę płuc (POChP) charakteryzuje ograniczenie przepływu powietrza przez drogi oddechowe będące wynikiem nadmiernej reakcji zapalnej na wdychane pyły i gazy, głównie dym tytoniowy. W patogenezie tej choroby odgrywają rolę trzy czynniki: proces zapalny, stres oksydacyjny oraz zaburzenia równowagi pomiędzy proteinazami i antyproteinazami. W ostatnich latach coraz więcej danych wskazuje na obecność u chorych na POChP zmian pozapłucnych, takich jak wyniszczenie, osteoporoza czy depresja. Celem pracy była ocena stanu zapalnego lokalnego oraz systemowego u chorych na POChP. Materiał i metody: Badania przeprowadzono u 23 chorych na POChP dwukrotnie - w stabilnym okresie choroby oraz w zaostrzeniu. Grupę kontrolną stanowiło 16 asymptomatycznych palaczy papierosów. Analizie poddano: 1) w kondensacie powietrza wydechowego (kpw) stężenie nadtlenku wodoru (H2O2) oraz proza-palnych cytokin TNF-α i IL-6; 2) w surowicy poziom TNF-a i IL-6. Wyniki: Stwierdzono, że u chorych na POChP w okresie stabilnym w kpw poziom H2O2 był znamiennie wyższy niż w grupie kontrolnej osób zdrowych. W trakcie zaostrzenia choroby ulegał on dalszemu wzrostowi (p<0,05). Natomiast stężenie IL-6 w powietrzu wydechowym było w badanych grupach podobne (p>0,05). Mierzalny poziom TNF-α zanotowano jedynie u chorych z zaostrzeniem POChP. Zarówno w okresie stabilnym, jak i w zaostrzeniu choroby poziom H2O2 w kpw korelował z FEV1% wartości należnej. Chorych na stabilną POChP charakteryzowało podwyższone w surowicy zarówno stężenie TNF-α, jak i IL-6 w porównaniu z grupą asymptomatycznych palaczy. W okresie zaostrzenia badane cytokiny nie ulegały istotnym zmianom (p>0,05). Wnioski: U chorych na POChP wykazano obecność lokalnego stresu oksydacyjnego, który w trakcie zaostrzenia choroby ulegał dalszemu znamiennemu nasileniu. Obok reakcji w kompartmencie oddechowym chorzy ze stabilną postacią POChP charakteryzowali się obecnością systemowej reakcji zapalnej mierzonej poziomem TNF-α i IL-6 w surowicy. Poziom nadtlenku wodoru w powietrzu wydechowym korelował z wartościami spirometrycznymi (FEV1% wartości należnej).
EN
Inflammatory response has been recognized as a central feature in the development and progression of atherosclerosis, and VSMCs (Vascular Smooth Muscle Cells) - the main cellular component of media, play an important role in this process. Many reports indicate that the biologically active vitamin D metabolite - 1,25-dihydroxyvitamin D3 (1,25(OH)2D3 = calcitriol), besides its well established role in calcium homeostasis, plays an essential role in the regulation of the inflammation process. The aim of this study was to determine the regulatory effects of calcitriol, applied at two supra-physiological doses (10 nM and 100 nM), in VSMC culture. Secretion of the pro-inflammatory cytokines, IL-6 and TNF-α, was significantly attenuated in calcitriol-treated VSMC culture, but the level of anti-inflammatory TGF-β was generally unchanged. Since in advanced atherosclerosis lesions several cell types, including VSMCs, overproduce the HSP70 chaperone protein, we also checked the effects of calcitriol on its synthesis. The presence of 1,25(OH)2D3 did not affect HSP70 synthesis under physiological conditions but the synthesis of HSP70 in VSMCs exposed to heat shock was significantly inhibited by calcitriol (=100 nM). We observed that 1,25(OH)2D3 induced SOD 1 activity, stimulated the expression of IκB-α, and did not influence the level of NF-κB-p65 in VSMCs. The results of our study suggest that 1,25(OH)2D3 may serve as a natural anti-inflammatory agent and may therefore play a beneficial role in the physiology of VSMC in some contexts of atherosclerosis.
EN
Microglia represent the immune system in the central nervous system. They have long been regarded as as the main aggressor, which induce and support inflammatory and neurodegenerative processes in the central nervous system. The latest studies indicate that they can also play a protective role. In this study we present evidence underlying their anti-inflammatory properties. Microglia can be activated in two different ways and they have two different phenotypes: classical – pro-inflammatory and alternative – anti-inflammatory. The latter is characterized by CD200 expression and fractalkine. Alternatively, the activated microglia also produce pro-inflammatory cytokine. Their influence on the surrounding cells is associated not only with destruction but also with neuroregeneration and myelination. Perhaps the latest reports will draw researchers' attention to new solutions which may be used in the prevention and treatment of the central nervous system diseases through the anti-inflammatory properties of cells which are still seen as inflammatory cells.
PL
Komórki mikrogleju są reprezentantami układu immunologicznego w ośrodkowym układzie nerwowym (OUN). Od dawna były postrzegane jako główny agresor, indukujący i podtrzymujący procesy zapalne i neurodegeneracyjne w OUN. Ostatnie doniesienia naukowe wskazują jednak, że mogą one pełnić istotną rolę ochronną. W niniejszej pracy przedstawiono dowody naukowe, podkreślające ich właściwości przeciwzapalne. Komórki mikrogleju podlegają aktywacji na dwa różne sposoby, co powoduje powstanie dwóch odmiennych fenotypów: klasycznego zapalnego oraz alternatywnego przeciwzapalnego. Ten ostatni charakteryzuje się m.in. ekspresją CD200 oraz fraktalkiny. Alternatywnie aktywowany mikroglej produkuje również cytokiny prozapalne, których wpływ na otaczające komórki nie do końca wiąże się tylko z ich destrukcją, lecz także niejednokrotnie z procesami neuroregeneracji i mielinizacji. Być może przedstawienie najnowszych doniesień skieruje uwagę badaczy na nowe narzędzia mogące znaleźć zastosowanie w zapobieganiu i leczeniu chorób OUN poprzez wykorzystanie przeciwzapalnych właściwości komórek, które wciąż uważa się za komórki prozapalne.
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