Cytokine
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Cytokines are inflammatory mediators of major relevance during sepsis. Recent evidence shows that adipose tissue can produce many distinct cytokines under physiological and pathological conditions, but the role of cytokines produced in adipose tissue was not addressed in sepsis. In the present study the open-flow microperfusion (OFM) technique was used to investigate whether the cytokines produced in subcutaneous adipose tissue (SAT) of patients with severe sepsis correlate with clinical variables. ⋯ Interleukin-1beta, 6 and 8 were higher in SAT than in serum suggesting they were locally produced. Diastolic blood pressure (DBP) negatively correlated with IL-1beta, IL-6 and IL-8 in SAT indicating a possible interaction between adipose tissue inflammation and vascular tone regulation. A multiple regression analysis disclosed that mean DBP was significantly related to IL-6 concentrations in SAT (B=-43.9; R-square=0.82; P=0.002).
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The occurrence of severe sepsis may be associated with deficient pro-inflammatory cytokine production. Transforming growth factor beta-1 (TGFbeta-1) predominantly inhibits inflammation and may simultaneously promote IL-17 production. Interleukin-17 (IL-17) is a recently described pro-inflammatory cytokine, which may be important in auto-immunity and infection. We investigated the hypothesis that the onset of sepsis is related to differential TGFbeta-1 and IL-17 gene expression. ⋯ Down regulation of TGFbeta-1 gene transcription was related to the occurrence of infection but not the onset of sepsis. Interleukin-17 production in PBMC may not be significant in the human host response to infection.
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Radiotherapy (RT) produces oxidative stress and local inflammation. This study aimed at clarifying the role of different cytokines (VEGF, TNFalpha, IL-1beta, IL-6, IL-8, IL-12 and IL-18) in bronchoalveolar lavage (BAL) fluid and in the serum of lung cancer patients at baseline and during RT. Bronchoscopy and BAL were performed on 36 lung cancer patients and 36 controls for diagnosis; patients receiving RT had a second bronchoscopy during RT. ⋯ This study shows that lung cancer is associated with upregulation of IL-6 and IL-8. The increase of BAL fluid IL-6 during RT might be attributed to enhanced RT-related oxidative stress or increased cell death. Serum and BAL fluid IL-8 and serum VEGF might have a prognostic role in survival of lung cancer.
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Endotoxin shock can induce the production of several inflammatory mediators such as TNF-alpha, IL-6, and IL-1beta, leading to multiple organ dysfunction and death. Erythropoietin (EPO) has been found to interact with its receptor (EPO-R), expressed in a wide variety of non-hematopoietic tissues, to induce a range of pleiotropic cytoprotective actions. We investigated the effects of low doses of EPO (300U/kg, intravenous administration) on the physiopathology and cytokine levels in endotoxin shock in conscious rats. ⋯ EPO further increased the markers of organ injury (GOT, GPT, BUN, Cre, LDH, and CPK), inflammatory biomarkers (TNF-alpha, IL-6, and IL-1beta) and did not affect MAP and HR after LPS. EPO disserved endotoxin shock-induced liver, kidney, lung, and small intestine damage in conscious rats. In conclusion, pre-treatment with low doses of EPO increased the release of TNF-alpha, IL-6, and IL-1beta, along with aggravating endotoxin shock-induced markers of organ injury in conscious rats.
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The pathogenesis of rheumatoid arthritis (RA) and psoriatic arthritis (PsA) involves an abnormal chemokine regulation. The chemokine receptor CCR4 is necessary for T cell migration to the skin. We, therefore, studied if CCR4 and its ligand macrophage-derived chemokine (MDC/CCL22) could participate in spreading the disease between skin and joints by examining RA, PsA and osteoarthritis (OA) patients. ⋯ Immunohistochemistry of the RA and OA synovial membrane demonstrated CCR4 to be expressed by mononuclear cells and endothelial cells. Our results show that MDC/CCL22 is present within the synovial membrane of RA and OA patients and in high amount in the synovial fluid of patients with RA and PsA. This will enable migration of CCR4 expressing memory cells supporting that MDC/CCR4 could play a role in attracting skin specific memory T cells to the joints.