brefeldin a/inflammatie

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Brefeldin A reduces tumor necrosis factor-α-stimulated production of inflammatory mediators by suppressing the Akt, mTOR, and NF-κB pathways in human keratinocytes.

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Keratinocytes may play an important role in the pathogenesis of inflammatory skin diseases. Brefeldin A has been shown to attenuate the production and secretion of chemical mediators involved in inflammation and immune responses. However, the effect of brefeldin A on the TNF-α-stimulated production

Endocytic mechanism of internalization of dietary peptide lunasin into macrophages in inflammatory condition associated with cardiovascular disease.

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Cardiovascular disease (CVD) is the leading cause of death in the United States. Diet influences risk factors associated with CVD and atherosclerosis, a major vascular disease that arises from inflammation. Lunasin, a peptide derived from plant foods such as soybeans, contains a unique Arg-Gly-Asp

sCD48 is anti-inflammatory in Staphylococcus aureus Enterotoxin B-induced eosinophilic inflammation.

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Staphylococcus aureus, one of the most important pathogens, is heavily associated with allergy. S. aureus and its toxins interact with eosinophils through CD48, a GPI-anchored receptor important in allergy mainly as expressed by the eosinophils (mCD48). CD48 can exist in a soluble form (sCD48). Our

Brefeldin A inhibits experimentally induced AA amyloidosis.

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OBJECTIVE Brefeldin A, an antibiotic with effects on certain intracellular compartments, was tested on murine secondary AA amyloidosis. Effects on splenic proteoglycan metabolism were analyzed along with plasma serum amyloid A (SAA) levels. METHODS Brefeldin A was administered daily to mice

Serum IL-6, IL-23 profile and Treg/Th17 peripheral cell populations in pediatric patients with inflammatory bowel disease.

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IL-6 and IL-23 are both pleiotropic cytokines involved in the regulation of the immune response, inflammation, and hematopoeisis. They also could mediate effector cells and tolerance mediated by cells with regulatory function. Inflammatory bowel disease (IBD) is associated with a reduced ratio of

Aberrant frequency of IL-10-producing B cells and its association with the balance of Treg/Th17 in children with inflammatory bowel disease.

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Regulatory B cells (Breg) are a distinct B cell subset, which contribute to the pathogenesis of autoimmune disorders. Interleukin-10 (IL-10) plays a pivotal function to Breg. It is well described in adults but little is known in a pediatric population. This study was to investigate the role of

Extracorporeal photopheresis reduces the number of mononuclear cells that produce pro-inflammatory cytokines, when tested ex-vivo.

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Extracorporeal photopheresis (ECP) has been shown to be clinically effective in the treatment of many T cell-mediated conditions. ECP's mechanism of action includes the induction of apoptosis and the release of pro-inflammatory cytokines. Recently, we have observed early lymphoid apoptosis,

Extracellular allograft inflammatory factor-1 (AIF-1) potentiates Th1 cell differentiation and inhibits Treg response in human peripheral blood mononuclear cells from normal subjects.

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We identified the presence of AIF-1 (allograft inflammatory factor-1) in human peripheral blood mononuclear cells (PBMCs) from normal subjects by immunocytological methods. After isolation of different types of mononuclear cells by FACS (Fluorescence-activated cell sorting) with >95% purity, we

Flow cytometric detection of antigen-specific cytokine responses in lung T cells in a murine model of pulmonary inflammation.

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Multiparameter flow cytometry was used to examine the cytokine responses of antigen-specific T lymphocytes isolated from the lungs of antigen-sensitized mice which developed pulmonary inflammation after aerosol challenge with ovalbumin (OA) (OA/OA). Lung T cells were stimulated in vitro with OA and

Role of microtubules in LPS-induced macrophage inflammatory protein-2 production from rat pneumocytes.

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We have recently demonstrated that primary cultured rat pneumocytes produce macrophage inflammatory protein-2 (MIP-2) in response to lipopolysaccharide (LPS) stimulation. In this study, we found that brefeldin A, by blocking anterograde transport from the endoplasmic reticulum (ER) to the Golgi

Sex differences in in vitro pro-inflammatory cytokine production from peripheral blood of multiple sclerosis patients.

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We compared the patterns of the pro-inflammatory cytokines, interferon-gamma (IFN-gamma), interleukin-2 (IL-2) and tumor necrosis factor-alpha (TNF-alpha), and the anti-inflammatory cytokines, interleukin-10 (IL-10) and tumor growth factor-beta (TGF-beta) from peripheral blood of male and female

Amniotic fluid angiopoietin-1, angiopoietin-2, and soluble receptor tunica interna endothelial cell kinase-2 levels and regulation in normal pregnancy and intraamniotic inflammation-induced preterm birth.

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BACKGROUND Angiopoietin-1 (Ang-1) and Ang-2 act selectively on endothelial cells by engaging the Tunica interna endothelial cell kinase-2 (Tie2) receptor. A soluble form of Tie2 (sTie2) blocks angiopoietin bioactivity. OBJECTIVE The aim of the study was to characterize changes and expression

BIG1 controls macrophage pro-inflammatory responses through ARF3-mediated PI(4,5)P2 synthesis.

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Sepsis is caused by a dysregulated host inflammatory response to serious infections resulting in life-threatening organ dysfunction. The high morbidity and mortality make sepsis still a major clinical problem. Here, we investigated the roles of Brefeldin A-inhibited guanine nucleotide-exchange

Prostaglandin E2 negatively regulates the production of inflammatory cytokines/chemokines and IL-17 in visceral leishmaniasis.

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Persistence of intracellular infection depends on the exploitation of factors that negatively regulate the host immune response. In this study, we elucidated the role of macrophage PGE2, an immunoregulatory lipid, in successful survival of Leishmania donovani, causative agent of the fatal visceral

Chemical Inducers of Obesity-Associated Metabolic Stress Activate Inflammation and Reduce Insulin Sensitivity in 3T3-L1 Adipocytes.

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Obesity is accompanied by dyslipidemia, hypoxia, endoplasmic reticulum (ER) stress, and inflammation, representing the major risk factor for the development of insulin resistance (IR) and type 2 diabetes. We modeled these conditions in cultured 3T3-L1 adipocytes and studied their effect on insulin

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