scholarly journals Candesartan reduces the innate immune response to lipopolysaccharide in human monocytes

2009 ◽  
Vol 27 (12) ◽  
pp. 2365-2376 ◽  
Author(s):  
Ignacio M Larrayoz ◽  
Tao Pang ◽  
Julius Benicky ◽  
Jaroslav Pavel ◽  
Enrique Sánchez-Lemus ◽  
...  
2012 ◽  
Vol 207 (6) ◽  
pp. 947-956 ◽  
Author(s):  
Andrew W. Chung ◽  
Peter A. Sieling ◽  
Mirjam Schenk ◽  
Rosane M. B. Teles ◽  
Stephan R. Krutzik ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Tiziana Ada Renzi ◽  
Marcello Rubino ◽  
Laura Gornati ◽  
Cecilia Garlanda ◽  
Massimo Locati ◽  
...  

A proper regulation of the innate immune response is fundamental to keep the immune system in check and avoid a chronic status of inflammation. As they act as negative modulators of TLR signaling pathways, miRNAs have been recently involved in the control of the inflammatory response. However, their role in the context of endotoxin tolerance is just beginning to be explored. We here show that miR-146b is upregulated in human monocytes tolerized by LPS, IL-10, or TGFβpriming and demonstrate that its transcription is driven by STAT3 and RUNX3, key factors downstream of IL-10 and TGFβsignaling. Our study also found that IFNγ, known to revert LPS tolerant state, inhibits miR-146b expression. Finally, we provide evidence that miR-146b levels have a profound effect on the tolerant state, thus candidating miR-146b as a molecular mediator of endotoxin tolerance.


2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Nicholas E. Ilott ◽  
James A. Heward ◽  
Benoit Roux ◽  
Eleni Tsitsiou ◽  
Peter S. Fenwick ◽  
...  

Abstract Early reports indicate that long non-coding RNAs (lncRNAs) are novel regulators of biological responses. However, their role in the human innate immune response, which provides the initial defence against infection, is largely unexplored. To address this issue, here we characterize the long non-coding RNA transcriptome in primary human monocytes using RNA sequencing. We identify 76 enhancer RNAs (eRNAs), 40 canonical lncRNAs, 65 antisense lncRNAs and 35 regions of bidirectional transcription (RBT) that are differentially expressed in response to bacterial lipopolysaccharide (LPS). Crucially, we demonstrate that knockdown of nuclear-localized, NF-κB-regulated, eRNAs (IL1β-eRNA) and RBT (IL1β-RBT46) surrounding the IL1β locus, attenuates LPS-induced messenger RNA transcription and release of the proinflammatory mediators, IL1β and CXCL8. We predict that lncRNAs can be important regulators of the human innate immune response.


2014 ◽  
Vol 5 (1) ◽  
Author(s):  
Sarah Kim ◽  
Jessica Becker ◽  
Matthias Bechheim ◽  
Vera Kaiser ◽  
Mahdad Noursadeghi ◽  
...  

2015 ◽  
Vol 29 (3) ◽  
pp. 119-129 ◽  
Author(s):  
Richard J. Stevenson ◽  
Deborah Hodgson ◽  
Megan J. Oaten ◽  
Luba Sominsky ◽  
Mehmet Mahmut ◽  
...  

Abstract. Both disgust and disease-related images appear able to induce an innate immune response but it is unclear whether these effects are independent or rely upon a common shared factor (e.g., disgust or disease-related cognitions). In this study we directly compared these two inductions using specifically generated sets of images. One set was disease-related but evoked little disgust, while the other set was disgust evoking but with less disease-relatedness. These two image sets were then compared to a third set, a negative control condition. Using a wholly within-subject design, participants viewed one image set per week, and provided saliva samples, before and after each viewing occasion, which were later analyzed for innate immune markers. We found that both the disease related and disgust images, relative to the negative control images, were not able to generate an innate immune response. However, secondary analyses revealed innate immune responses in participants with greater propensity to feel disgust following exposure to disease-related and disgusting images. These findings suggest that disgust images relatively free of disease-related themes, and disease-related images relatively free of disgust may be suboptimal cues for generating an innate immune response. Not only may this explain why disgust propensity mediates these effects, it may also imply a common pathway.


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