Peritoneal Sclerosis: Role of Plasticizers in Stimulating Interleukin-1 Production

1993 ◽  
Vol 13 (2_suppl) ◽  
pp. 517-519 ◽  
Author(s):  
Agostino Fracasso ◽  
Lorenzo Calo ◽  
Silvano Landini ◽  
Paolo Morachiello ◽  
Flavio Righetto ◽  
...  
Keyword(s):  
Healthy Subjects ◽  
Mononuclear Cells ◽  
Interleukin 1 ◽  
Final Concentration ◽  
The Other ◽  
Fibroblast Proliferation ◽  
Two Cultures

The role of plasticizers (PLS) in inducing water flow inhibition and peritoneal sclerosis has been demonstrated in both In vivo and In vitro studies. Interleukin-1 (IL-1) has been shown to be a regulator of fibroblast proliferation as well as collagenase production. The aim of this study was to evaluate the role of PLS in stimulating mononuclear ce1l1L-1 secretion. Two cultures containing 103 cells/mL were obtained from 14 healthy subjects. One was used as the control, and the other was mixed with diethylhexylphthalate (DEHP) to reach a final concentration of 2.8x10” M. After 4 hours the samples were centrifuged, and the supernatants were tested by radioimmunoassay for IL-1α and IL-1β. The results showed a significant increase In both IL-1α and IL-1 β production In DEHP-stimulated cells in comparIson to the controls: 42.6±15.4 versus 29.3±10 ng/L (p<0.015) for IL-1α. and 153.6±55 versus 113.6±32 ng/L (p<0.03) for IL-1β In conclusion, PLS added to mononuclear cells were able to Induce IL-1 secretion. This mechanism could be responsible, at least in part, for the development of peritoneal sclerosis. Thus the employment of plasticlzer-free bags should be elective in peritoneal dialysis.

scholarly journals The Potential Role of IL1RAP on Tumor Microenvironment-Related Inflammatory Factors in Stomach Adenocarcinoma

2021 ◽  
Vol 20 ◽  
pp. 153303382199528
Author(s):  
Qing Lv ◽  
Qinghua Xia ◽  
Anshu Li ◽  
Zhiyong Wang
Keyword(s):  
Tumor Microenvironment ◽  
Interleukin 1 ◽  
Mrna Level ◽  
Inflammatory Factors ◽  
Stomach Carcinoma ◽  
Downstream Target ◽  
Volume Weight

This study was performed to investigate the role of interleukin-1 receptor accessory protein (IL1RAP) in stomach carcinoma in vitro and in vivo, determine whether IL1RAP knockdown could regulate the development of stomach carcinoma, and elucidate the relationship between IL1RAP knockdown and inflammation by tumor microenvironment-related inflammatory factors in stomach carcinoma. We first used TCGA and GEPIA systems to predict the potential function of IL1RAP. Second, western blot and RT-PCR were used to analyze the expression, or mRNA level, of IL1RAP at different tissue or cell lines. Third, the occurrence and development of stomach carcinoma in vitro and in vivo were observed by using IL1RAP knockdown lentivirus. Finally, the inflammation of stomach carcinoma in vitro and in vivo was observed. Results show that in GEPIA and TCGA systems, IL1RAP expression in STAD tumor tissue was higher than normal, and high expression of IL1RAP in STAD patients had a worse prognostic outcome. Besides, GSEA shown IL1RAP was negative correlation of apopopsis, TLR4 and NF-κB signaling pathway. We also predicted that IL1RAP may related to IL-1 s, IL-33, and IL-36 s in STAD. The IL1RAP expression and mRNA level in tumor, or MGC803, cells were increased. Furthermore, IL1RAP knockdown by lentivirus could inhibit stomach carcinoma development in vitro and in vivo through weakening tumor cell proliferation, migration, invasion, therefore reducing tumor volume, weight, and biomarker levels, and increasing apoptotic level. Finally, we found IL1RAP knockdown could increase inflammation of tumor microenvironment-related inflammatory factors of stomach carcinoma, in vitro and in vivo. Our study demonstrates that IL1RAP is possibly able to regulate inflammation and apoptosis in stomach carcinoma. Furthermore, TLR4, NF-κB, IL-1 s, IL-33, and IL-36 s maybe the downstream target factor of IL1RAP in inflammation. These results may provide a new strategy for stomach carcinoma development by regulating inflammation.

scholarly journals Role of Cathepsin S in Periodontal Inflammation and Infection

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
S. Memmert ◽  
A. Damanaki ◽  
A. V. B. Nogueira ◽  
S. Eick ◽  
M. Nokhbehsaim ◽  
...  
Keyword(s):  
Periodontal Diseases ◽  
Interleukin 1 ◽  
Critical Role ◽  
Gingival Tissue ◽  
Cathepsin S ◽  
Protein Levels ◽  
Periodontal Inflammation

Cathepsin S is a cysteine protease and regulator of autophagy with possible involvement in periodontitis. The objective of this study was to investigate whether cathepsin S is involved in the pathogenesis of periodontal diseases. Human periodontal fibroblasts were cultured under inflammatory and infectious conditions elicited by interleukin-1β and Fusobacterium nucleatum, respectively. An array-based approach was used to analyze differential expression of autophagy-associated genes. Cathepsin S was upregulated most strongly and thus further studied in vitro at gene and protein levels. In vivo, gingival tissue biopsies from rats with ligature-induced periodontitis and from periodontitis patients were also analyzed at transcriptional and protein levels. Multiple gene expression changes due to interleukin-1β and F. nucleatum were observed in vitro. Both stimulants caused a significant cathepsin S upregulation. A significantly elevated cathepsin S expression in gingival biopsies from rats with experimental periodontitis was found in vivo, as compared to that from control. Gingival biopsies from periodontitis patients showed a significantly higher cathepsin S expression than those from healthy gingiva. Our findings provide original evidence that cathepsin S is increased in periodontal cells and tissues under inflammatory and infectious conditions, suggesting a critical role of this autophagy-associated molecule in the pathogenesis of periodontitis.

Vitamin D modulates the expression of HLA-DR and CD38 after in vitro activation of T-cells

2017 ◽  
Vol 29 (3) ◽  
Author(s):  
Simon Villegas-Ospina ◽  
Wbeimar Aguilar-Jimenez ◽  
Sandra M. Gonzalez ◽  
María T. Rugeles
Keyword(s):  
Vitamin D ◽  
Flow Cytometry ◽  
Healthy Subjects ◽  
Mononuclear Cells ◽  
Activation Markers ◽  
Hla Dr ◽  
In Vitro Activation ◽  
Cells Cultured

AbstractObjective:Vitamin D (VitD) is an anti-inflammatory hormone; however, some evidence shows that VitD may induce the expression of activation markers, such as CD38 and HLA-DR. We explored its effect on the expression of these markers on CD4Materials and methods:CD38 and HLA-DR expression was measured by flow cytometry in PHA/IL-2-activated mononuclear cells cultured under VitD precursors: three cholecalciferol (10Results:Cholecalciferol at 10Conclusion:Although no significant correlations were observed in vivo in healthy subjects, VitD treatment in vitro modulated immune activation by increasing the expression of CD38 and decreasing the proliferation of HLA-DR

The effect of a leukodepletion model on the activation stage of platelets

Open Medicine ◽  
2011 ◽  
Vol 6 (2) ◽  
pp. 181-184
Author(s):  
Miodrag Vucic ◽  
Ivan Tijanic ◽  
Nenad Govedarevic ◽  
Lana Macukanovic ◽  
Zoran Pavlovic
Keyword(s):  
Flow Cytometry ◽  
Proinflammatory Cytokines ◽  
Mononuclear Cells ◽  
Buffy Coat ◽  
The Other ◽  
Therapeutic Doses ◽  
Cell Counter ◽  
Automatic Cell Counter

AbstractThe preparation of thrombocyte concentrates with filtration before storage (in-line) makes it possible to avoid the presence of mononuclear cells in the concentrate and proinflammatory cytokines. Therefore, this filtration may result with decreased activation of trombocyte receptors in vitro, which may improve therapeutic efficiancy. Methods. We compared two groups, each with 30 therapeutic doses of concentrated thrombocytes. We prepared the first group using the classic model from the buffy coat and the other with concentrated thrombocyte samples filtrated during sampling, so-called in-line, with the WBC filter Imuflex (Terumo). Mononuclear cells (MNC), thrombocyte, and erythrocyte counts in the units of concentrated thrombocytes were obtained on an automatic cell counter, and we used flow cytometry to measure the expression of surface thrombocyte receptors. The results demonstrated that the trombocytes prepared with pre-storage filtration contained a very low level of mononuclear cells and markedly reduced trombocyte receptors. Conclusion. The number of MNC and expression of surface thrombocyte receptors were markedly lower in the concentrated thrombocyte units prepared with in-line filtration. The thrombocytes prepared in this way contain fewer mononuclear cells, are of higher quality, are more functional, and may produce a better therapeutic effect in vivo.

scholarly journals IL1RAP potentiates multiple oncogenic signaling pathways in AML

2018 ◽  
Vol 215 (6) ◽  
pp. 1709-1727 ◽  
Author(s):  
Kelly Mitchell ◽  
Laura Barreyro ◽  
Tihomira I. Todorova ◽  
Samuel J. Taylor ◽  
Iléana Antony-Debré ◽  
...  
Keyword(s):  
Tyrosine Kinases ◽  
Interleukin 1 ◽  
Oncogenic Signaling ◽  
Genetic Deletion ◽  
Mechanistic Basis ◽  
Oncogenic Signaling Pathways ◽  
Receptor Accessory Protein

The surface molecule interleukin-1 receptor accessory protein (IL1RAP) is consistently overexpressed across multiple genetic subtypes of acute myeloid leukemia (AML) and other myeloid malignancies, including at the stem cell level, and is emerging as a novel therapeutic target. However, the cell-intrinsic functions of IL1RAP in AML cells are largely unknown. Here, we show that targeting of IL1RAP via RNA interference, genetic deletion, or antibodies inhibits AML pathogenesis in vitro and in vivo, without perturbing healthy hematopoietic function or viability. Furthermore, we found that the role of IL1RAP is not restricted to the IL-1 receptor pathway, but that IL1RAP physically interacts with and mediates signaling and pro-proliferative effects through FLT3 and c-KIT, two receptor tyrosine kinases with known key roles in AML pathogenesis. Our study provides a new mechanistic basis for the efficacy of IL1RAP targeting in AML and reveals a novel role for this protein in the pathogenesis of the disease.

Anionic and cationic exchange mechanisms in the skin of anurans, with special reference to Leptodactylidae in vivo

1971 ◽  
Vol 262 (842) ◽  
pp. 163-174 ◽  
Keyword(s):  
Transport Mechanism ◽  
Selective Inhibition ◽  
The Other ◽  
Sodium Absorption ◽  
Experimental Conditions ◽  
Net Flux ◽  
Cationic Exchange

In several species of anurans, the in vivo skin has been shown to absorb Na + and Cl - independently from dilute external solutions. That the mechanism for sodium absorption is different from that of chloride absroption is born out by the following: (1) Either of these ions is absorbed without an accompanying ion when this latter is impermeant. (2) From NaCl solutions there can be an unequal absorption of sodium and chloride. (3) A selective inhibition of the absorption of one of the ions can be produced experimentally, while the net flux of the other remains unchanged. In all these situations, the absorbed ion has to be exchanged against an endogenous ion of the same charge. In Calyptocephalella gayi , H + and HCO - 3 are exchanged against sodium and chloride respectively. A comparison of the relationships between H + excretion and Na + absorption in vivo skins and shortcircuited in vitro skins shows that in the latter no H + excretion occurs, only the Na + transport being maintained under these experimental conditions. From this, one must conclude that the active Na + transport is the motive factor of the transport mechanism. H + excretion by the in vivo skin plays the role of physiologically short-circuiting the Na + transport.

Interleukin 1 induces renal CD44 expression in vivo and in vitro: role of the transcription factor Egr-1

Nephrology ◽  
2002 ◽  
Vol 7 (3) ◽  
pp. 136-144
Author(s):  
Kazunori Takazoe ◽  
Rita Foti ◽  
Lynette A Hurst ◽  
Hui Y Lan ◽  
Robert C Atkins ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Interleukin 1 ◽  
Cd44 Expression

scholarly journals Role of interleukin-1 and tumour necrosis factor in leukocyte recruitment to acute dermal inflammation

1992 ◽  
Vol 1 (5) ◽  
pp. 347-353 ◽  
Author(s):  
Andrew C. Issekutz ◽  
Nancy Lopes ◽  
Thomas B. Issekutz
Keyword(s):  
Monoclonal Antibody ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
E Coli ◽  
Tnf Α ◽  
Lps Activation ◽  
Necrosis Factor

The cytokines IL-1 and TNF-α are involved in inflammation and their production is stimulated by various agents, especially endotoxin (LPS). Here, using the human IL-1 receptor antagonist (IL-1RA) and a new monoclonal antibody (mAb 7F11) to rabbit TNF, the role of endogenous IL-l and TNF production in acute (3h) leukocyte (PMNL) recruitment to dermal inflammation in rabbits has been studied. IL-1RA inhibited by 27% the PMNL accumulation in reactions induced by killed Escherichia coli (p < 0.05) but not by LPS. The monoclonal antibody to TNF inhibited by 27% and 38% (p < 0.002) the PMNL accumulation in LPS and E. coli reactions respectively, but a combination of the mAb with IL-1RA was not more effective. Treatment of human umbilical vein endothelium with LPS for 3 h activated endothelium to induce PMNL transendothelial migration in vitro, which was not inhibited by IL-1RA, antibody to TNF-α, IL-1 or to IL-8. In conclusion, TNF and IL-1 may partially mediate acute PMNL infiltration in vivo to LPS and Gram negative bacteria, but there is a major IL-1/TNF independent mechanism, at least in dermal inflammation, which may be due to direct LPS activation of the microvasculature or perhaps the generation of cytokines other than IL-1 and TNF.

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