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1
Content available remote Inter-α-inhibitor, hyaluronan and inflammation.
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Inter-α-inhibitor is an abundant plasma protein whose physiological function is only now beginning to be revealed. It consists of three polypeptides: two heavy chains and one light chain called bikunin. Bikunin, which has antiproteolytic activity, carries a chondroitin sulphate chain to which the heavy chains are covalently linked. The heavy chains can be transferred from inter-α-inhibitor to hyaluronan molecules and become covalently linked. This reaction seems to be mediated by TSG-6, a protein secreted by various cells upon stimulation by inflammatory cytokines. Inter-α-inhibitor has been shown to be required for the stabilization of the cumulus cell-oocyte complex during the expansion that occurs prior to ovulation. Hyaluronan-linked heavy chains in the extracellular matrix of this cellular complex have recently been shown to be tightly bound to TSG-6. Since TSG-6 binds to hyaluronan, its complex with heavy chains could stabilize the extracellular matrix by cross-linking hyaluronan molecules. Heavy chains linked to hyaluronan molecules have also been found in inflamed tissues. The physiological role of these complexes is not known but there are indications that they might protect hyaluronan against fragmentation by reactive oxygen species. TSG-6 also binds to bikunin thereby enhancing its antiplasmin activity. Taken together, these results suggest that inter-α-inhibitor is an anti-inflammatory agent which is activated by TSG-6.
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One of our study direction is research in the group of compounds affecting the TRPA1 ion channel which can perform an important function in pain (including neuropathic pain) and inflammation for example in asthma and other chronic respiratory diseases. The aim of this study was to evaluate the analgesic and anti-inflammatory activity of two analogues of HC-030031 analogues belonging to nitrogen derivatives of heterocyclic system: xanthine (cmpd 1) and benzimidazole (cmpd 2) with hydrazide and amide moieties respectively In this paper, for two derivatives (cmpd 1 and cmpd 2) potential analgesic and anti-inflammatory/anti-edematous activities were evaluated in animal models of pain in mice (writhing response test, formalin test) and inflammation in rats (carrageenan-induced paw edema test). Both the tested compounds 1 and 2 showed a significant analgesic and anti-inflammatory activity.
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Content available remote Suppressor of cytokine signaling and accelerated atherosclerosis in kidney disease
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The prevalence of cardiovascular disease in patients with renal failure is extremely high and accounts for a large part of the morbidity and mortality. Inflammation participates importantly in host defense against infectious agents and injury, but also contributes to the pathophysiology of many diseases, including cardiovascular atherosclerosis, which is a main problem in patients with renal failure. Recruitment of blood leukocytes to the injured vascular endothelium characterizes the initiation and progression of atherosclerosis and involves many inflammatory mediators, modulated by cells of both innate and adaptive immunity. Excessive inflammatory and immune responses, communicated by these different cell types, are driven by inflammatory cytokines that promote associated tissue damage if cytokine signaling pathways remain unregulated. Thus, pathways capable of suppressing proinflammatory cytokine signaling hold the potential to limit life-threatening cardiovascular events caused by atherogenesis. Suppressor of cytokine signaling (SOCS) are a family of intracellular proteins, several of which have emerged as key physiological regulators of cytokine-mediated homeostasis, including innate and adaptive immunity. Accumulating evidence supports the idea that dysregulation of cytokine signaling by differential SOCS expression is involved in the pathogenesis of various inflammatory, and immunological diseases, including atherosclerosis. Based on recent observations, in which SOCS expression levels are profoundly altered in kidney disease, we discuss the possibilities of SOCS as new intracellular markers of inflammation as well as their potential atherogenic properties in renal failure related cardiovascular disease.
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Ovarian cancer is the most threatening cause of death among gynecologic malignancies and represents the fifth leading cause of death from all cancers for women. Research reveals that ovarian cancer patients exhibit significant immune responses against the tumor. In this review of the current literature chiefly the interaction of ovarian cancer tumor cells and the immune system is discussed. There is increasingly growing evidence that pro-inflammatory cytokines are involved in intricate complex of mechanisms responsible for tumorigenesis, and delicate balance between pro- and anti-inflammatory cytokines is critical for the antitumor host immune response.
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Neutrophils form the first line of host defense against infections that combat pathogens using two major mechanisms, the phagocytosis or the release of neutrophil extracellular traps (NETs). The netosis (NET formation) exerts additional, unfavorable effects on the fitness of host cells and is also involved at the sites of lung infection, increasing the mucus viscosity and in the circulatory system where it can influence the intravascular clot formation. Although molecular mechanisms underlying the netosis are still incompletely understood, a role of NADPH oxidase that activates the production of reactive oxygen species (ROS) during the initiation of NETs has been well documented. Since several commonly used drugs can affects the netosis, our current study was aimed to determine the effects of selected mucolytic, anti-inflammatory and cardiovascular drugs on NET formation, with a special emphasis on ROS production and NADPH oxidase activity. The treatment of neutrophils with N-acetylcysteine, ketoprofen and ethamsylate reduced the production of ROS by these cells in a dose-dependent manner. NET formation was also modulated by selected drugs. N-acetylcysteine inhibited the netosis but in the presence of H2O2 this neutrophil ability was restored, indicating that N-acetylcysteine may influence the NET formation by modulating ROS productivity. The administration of ethamsylate led to a significant reduction in NET formation and this effect was not restored by H2O2 or S. aureus, suggesting the unexpected additional side effects of this drug. Ketoprofen seemed to promote ROS-independent NET release, simultaneously inhibiting ROS production. The results, obtained in this study strongly suggest that the therapeutic strategies applied in many neutrophil-mediated diseases should take into account the NET-associated effects.
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Rheumatoid arthritis (RA) is a systemic autoimmune disease that manifests itself by joint inflammation, swelling, pain, tenderness and may involve extra-articular organs in severe cases. Joint inflammatory lesions are associated with higher temperature due to increased vascularity in the area of inflamed tissues. This papers aimed to identify heat patterns from ROIs to interpret the presence of inflammation in rheumatoid arthritis patients. The thermovisual image sequences were collected from 65 patients with Rheumatoid Arthritis (RA). Infrared images were generated by a thermal scanning camera (FLIR E60bx Systems Inc., USA). Separate recordings of left and right foot temperature changes were performed for 3 minute periods. The temperature measurement was performed at the moment right after cold water immersion (post-cooling temperature) and at the moment after thermal recovery (post-recovery temperature). The recording of 3-minute foot thermal recovery was used for analysis. Automatically identified ROI corresponds to the area of the soft tissues covering cuboid and navicular bone.
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Acute pancreatitis (AP) is associated with the intensive inflammatory response in white blood cells (WBC) and C-reactive protein (CRP). This paper presents the relationship between the CRP plasma concentration and the direct counts of peripheral WBC in AP during the initial five days. The study consisted of 56 patients with AP, 36 patients with mild form of AP and 20 patients with severe form of AP. ABX VegaRetic hematological analyzer was used to perform the count of blood cells, and the immunonephelometric method was performed to measure the CRP concentration levels. AP patients presented with WBC count values in the range of 3.2 − 22.4 × 103/µl and CRP concentration levels in the range 3.3 − 599.8 mg/l. The WBC count correlates with CRP levels during the entire observation period. The relationship of CRP and WBC is expressed in the following regression equation: WBC (103/µl) = 3.66 + 1.40 × logeCRP (mg/l). The highest median neutrophil count (8.15 × 103/µl) was observed on the first day. The count decreased to 5.27 × 103/µl on the fifth day. The most substantial finding in this study involved the values found for the monocytes and CRP (r= 0.53; p<0.001). Day two and day three were the highest (r=0.59, p<0.001). On day two, the regression equation for this relationship is: Monocytes (103/µl) = −0.34 + 0.21 × logeCRP(mg/l). The correlation between direct monocyte count and plasma CRP concentration in AP reflect a CRP-dependent stimulation of IL-6 release from activated blood monocytes.
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Inflammation plays a key role in epithelial ovarian cancer tumorigenesis and progression. The growth and progression of epithelial ovarian cancer may be due to local cytokine-induced immunosu-ppression, which may lead to an immunity impairment. Thus, cytokine antagonism may be an essential factor in the treatment of ovarian cancer. Based on the increased knowledge on the role of the immune system in ovarian cancer, major improvements are to be expected of immunotherapy based treatment of this disease. This article aims to summarize the current literature views on the evidence for a role for chronic inflammation with a specific focus on anti-inflammatory cytokines.
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Content available remote Immunoinflammatory responses in gastrointestinal tract injury and recovery
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Inflammation is a non-specific immune response to infection, irritation or other injury, the key features being redness, warmth, swelling and pain. A number of mediators are released which alter the resistance of mucosa to injury induced by noxious substances. Oxidative stress is a unifying mechanism of injury in many types of disease processes, including gastrointestinal diseases. It has been defined as an imbalance in the activity of pro and antioxidants. Pro-oxidants favour free radical formation while antioxidants inhibit or retard the same. A number of markers of oxidative stress have been identified. This review provides an overview of various mediators of inflammation and oxidative stress, and diverse approaches for prevention and treatment of gastrointestinal inflammation.
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Tissue-specific heterogeneity of endothelial cells, both structural and functional, plays a crucial role in physiologic as well as pathologic processes, including inflammation, autoimmune diseases and tumor metastasis. This heterogeneity primarily results from the differential expression of adhesion molecules that are involved in the interactions between endothelium and circulating immune cells or disseminating tumor cells. Among these molecules present on endothelial cells is hyaluronan (HA), a glycosaminoglycan that contributes to primary (rolling) interactions through binding to its main receptor CD44 expressed on leukocytes and tumor cells. While the regulation of CD44 expression and function on either leukocytes or tumor cells has been well characterized, much less is known about the ability of endothelial cells to express HA on their surface. Therefore, in these studies we analyzed HA levels on tissue-specific endothelium. We used endothelial cell lines of different origin, including lung, skin, gut and lymph nodes that had been established previously as model lines to study interactions between the endothelium and leukocytes/tumor cells. Our results indicate that HA is accumulated on the surface of all endothelial cells examined. Moreover, retention of endogenous HA differs between the lines and may depend on their tissue origin. Analysis of binding of exogenous HA reveals the presence of specific HA binding sites on all endothelial cell lines tested. However, the retention of endogenous HA and the binding of exogenous HA is mediated through a CD44-independent mechanism.
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Content available remote Kinin-generating cellular model obtained from human glioblastoma cell line U-373
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Kinins, a group of important pro-inflammatory peptides, are abundantly found in tissues and biological fluids of cancer patients. Bradykinin, the major representative of kinins, induces vascular permeability and, in consequence, promotes tumor expansion. Additionally, the kinin-induced inflammatory responses, especially those mediated by kinin metabolites without the C-terminal arginine residue, lead to enhanced tumor growth. The present study aimed at analyzing the ability of the human glioblastoma cell line U-373, derived from a malignant tumor, to produce kinin peptides. The proteins involved in kinin generation, i.e., the kininogens and the kallikreins, were shown to be expressed in these cells. Moreover, tumor necrosis factor α, a proinflammatory cytokine that mediates tumorigenesis, was found to enhance the expression of enzymes associated with kinin production. The strong binding of kininogen to the cell surface and the enzymatic degradation of this protein by cells suggest the activation of kinin-generating systems. Indeed, glioblastoma cells, pre-treated with tumor necrosis factor α, released kinin peptides from exogenous kininogen. The expression of kinin receptors in these cells was also shown to increase under the influence of this cytokine. Our results suggest that the human glioblastoma cell line U-373 constitutes a good cellular model that can be helpful in cancer research focused on kinin-induced inflammation. Furthermore, our findings can contribute to new approaches in cancer treatment with the use of kinin receptor antagonists and inhibitors of kinin production.
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Purpose. To determine if the complement system is activated following strenuous eccentrically-biased exercise. Secondly, to determine if complement activation is attenuated (repeated bout effect) following a second bout of the same exercise. Basic procedures. Healthy, active but untrained males performed 2 × 60 min bouts of downhill running, 14 days apart. Samples were taken pre, immediately post (IP), then every hour for twelve hours, and at 24, 48, 72, 96, 120 and 144 h post exercise. Concentrations of C1est, C4, and circulating immune complexes (CIC's) were determined using standardised nephelometery. C6 was determined using radial immunodifusion. The variables were analysed using a repeated measures ANOVA, with significance set at p < 0.05. Main findings. A significant (p < 0.01) run effect was observed for C1est, C4, C6 and CIC's with the concentrations elevated after run 2 compared with run 1. C1est and C4 exhibited significant time effects (p < 0.001). Conclusions. The complement system is activated following a strenuous bout of downhill running. Complement proteins and circulating immune complexes do not exhibit the same traditional ‘repeated bout effect’ as many other common markers of muscle damage/inflammation. The increase in complement proteins following the second bout may indicate enhanced innate immune function and/or an amplification of the immune response to tissue damage through interaction with the adaptive immune system.
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Ground level (tropospheric) ozone, an air pollutant and key ingredient of urban smog, has a negative impact on human health worldwide. Many studies have reported increases in emergency-room visits, hospital admissions, and mortality for patients with these conditions, associated with days of increased ozone. Short-term exposures to ozone irritate the respiratory system and may cause health problems by damaging lung tissue, reducing lung function, increased airway inflammation and making the lungs more sensitive to other irritants. It not only affects people with existing breathing problems, but also can affect healthy children and adults. Persons especially sensitive to ozone exposure are the elderly, infants, children, persons with existing respiratory issues such as diabetes mellitus, asthma or allergies, asthmatics, chronic respiratory patients, pregnant women, smokers, and persons with lung cancer, cardiovascular disease or immune system deficiency. Furthermore, recent research studies suggest that long-term exposure to ozone may be associated with lung cancer. This possibility is expected to be further explored.
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Content available The perplexities of the ZC3H12A self-mRNA regulation
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The mechanisms regulating transcript turnover are key processes in the regulation of gene expression. The list of proteins involved in mRNAs' degradation is still growing, however, the details of RNase-mRNAs interactions are not fully understood. ZC3H12A is a recently discovered inflammation-related RNase engaged in the control of proinflammatory cytokine transcript turnover. ZC3H12A also regulates its own transcript half-live. Here, we studied the details of this regulation. Our results confirm the importance of the 3'UTR in ZC3H12A-dependent ZC3H12A mRNA degradation. We compared the mouse and human stemloop structures present in this region and discovered that the human conserved stem-loop structure is not sufficient for ZC3H12A-dependent degradation. However, this structure is important for the ZC3H12A mRNA post-transcriptional regulation. Our studies emphasize the importance of the neighboring features of the identified stem-loop structure for its biological activity. Removal of this region together with the stem-loop structure greatly inhibits the ZC3H12A regulation of the investigated 3'-untranslated region (3'UTR).
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Metal responsive transcription factor 1 (MTF-1) is a zinc dependent transcription factor which is involved in the regulation of intracellular signaling pathways. MTF-1 regulates the expression of two streams of genes functioning in metal homeostasis and anti-oxidative response. MTF-1 acts in the process of binding of toxic metal ions in the cell, due to the activation of the expression of metallothioneins (MTs). Additionally, MTF-1 regulates transcription of genes involved in the sequestration of zinc and its intracellular transport. Disruption of zinc and MT homeostasis has an indispensable influence on the development of several pathological states. Moreover, by increasing MT activity, MTF-1 can effectively protect cells from oxidative and hypoxic stresses. The mechanism of MTF-1 action in cells includes the regulation of the proper immune response through activation/repression of anti- and pro-inflammatory cytokines. MTF-1 function in immune response is related to nuclear factor-κB (NF-κB) activity. Synthesis of insulin is also related to the activity of this transcription factor and zinc balance. Insulin transport also depends on zinc. In pancreatic β-cells, several types of the zinc transporters are found. Zinc transporters coordinated action is crucial for the synthesis and secretion of insulin. Disturbances in the regulation of signaling pathways connected with MTF-1 function can entail further alterations in zinc intracellular status and this growing imbalance can promote the pathophysiology of degenerative disorders.
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Content available remote Acute Inflammation of the True Cecal Diverticulum - Case Report
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In this case report, we describe a rare event: acute inflammation of the true cecal diverticulum. Emergency surgery enabled proper diagnosis and management of this condition. Diagnostic approaches and the management of this disease are described in detail and based on literature review. In conclusion, pathologies of cecal diverticula should be considered in differential diagnosis of pain in the right iliac fossa.
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Introduction: Erythrocyte sedimentation rate (ESR, in Poland known as OB) and C-reactive protein (CRP) are biomarkers most often used to diagnose and monitor systemic inflammation. However, they are independent markers and have different properties. The aim of this study was to compare the values of specific markers of systemic inflammation such as ESR and CRP in patients hospitalized in the internal wards and suspected of suffering from systemic inflammation. Material and methods: The study group included 187 patients (99 women and 88 men, aged from 20 to 97 years) hospitalized in the internal medicine clinics of the Military Medical Academy University Teaching Hospital - Central Veterans' Hospital in Lodz. Each marker of inflammation, ESR and CRP, were measured in patients’ peripheral blood (ESR) and serum (CRP). Results: For the diagnosis of inflammation there was no significant correlation between CRP and ESR in groups of patients both with mild (CRP > 6.1 – 40 mg/L) and severe (CRP ≥ 40.1) inflammation. However, in persons with highly developed inflammation (ESR ≥ 31 mm/h and CRP ≥ 40.1 mg/L) there was a strong correlation between the mentioned biomarkers (r = 0.9973). Conclusions: The results indicate that CRP and ESR biomarkers are independent parameters that are clinically useful for the diagnosis and monitoring of inflammations. For the diagnosis of acute inflammation the designation of serum CRP is clinically more useful than the measurement of ESR.
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Wstęp: Odczyn opadania krwinek czerwonych (ESR, w Polsce znany pod nazwą odczyn Biernackiego - OB) i stężenie białka C-reaktywnego (CRP) są najczęściej wykorzystywanymi przez lekarzy biomarkerami do rozpoznawania i monitorowania stanu zapalnego ustroju. Jednak są one wskaźnikami niezależnymi i cechują się różnymi własnościami. Celem niniejszej pracy była analiza porównawcza wyników oznaczeń dwóch laboratoryjnych biomarkerów zapalenia: ESR i CRP u pacjentów leczonych na oddziałach internistycznych, u których podejrzewano narastający lub istniejący proces zapalny. Materiał i metody: Badaniem objęto 187 chorych (99 kobiet i 88 mężczyzn, w wieku od 20 do 97 lat) hospitalizowanych w klinikach chorób wewnętrznych Uniwersyteckiego Szpitala Klinicznego im. Wojskowej Akademii Medycznej – Centralnego Szpitala Weteranów w Łodzi. U każdego pacjenta w tym samym czasie wykonano oznaczenie dwóch wskaźników stanu zapalnego: ESR i CRP. Wyniki: Dla rozpoznawania narastającego zapalenia nie wykazano istotnej korelacji między CRP i ESR w grupach pacjentów zarówno o małym (CRP > 6,1 – 40 mg/L), jak i dużym (CRP ≥ 40,1) nasileniu zapalenia. Z drugiej strony, u ludzi z silnie już rozwiniętym zapaleniem (ESR ≥ 31 mm/h i CRP ≥ 40,1 mg/L) zaznaczyła się wysoka korelacja pomiędzy tymi biomarkerami (r = 0,9973). Wnioski: Wyniki wskazują, że analizowane biomarkery CRP i ESR są parametrami niezależnymi i są klinicznie użyteczne w rozpoznawaniu i obserwacji stanów zapalnych. W rozpoznawaniu zapalenia o ostrym przebiegu bardziej użytecznym klinicznie biomarkerem jest stężenie CRP w surowicy niż wartość ESR.
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Despite the emerging evidence suggesting a proatherogenic role of C-reactive protein (CRP) in atherosclerosis, the contribution of CRP in pathogenesis of atherosclerosis and atherothrombosis has not been unequivocally defined. The role of CRP in pathophysiology/pathology seems to largely depend on its structure. Two CRP isoforms, the native pentameric and the modified monomeric one, differ substantially in their physiological functions, which is thought to origin from the considerable structural heterogeneity of the CRP molecule. The present review provides an overview of the experimental evidence with relevance to the clinical role(s) of various CRP isoforms. The biological role of the protein, its structure and distribution are discussed with particular emphasis on the diverse properties of the pentameric and monomeric forms of CRP. Some methodological aspects, related to experimental models and techniques of CRP preparation, are also critically reviewed.
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