Being perceived accurately is associated with better inflammatory regulation in adolescents

2014 ◽  
Author(s):  
Lauren J. Human ◽  
Meanne Chan ◽  
Anita DeLongis ◽  
Laura Roy ◽  
Gregory E. Miller ◽  
...  
Keyword(s):  
Inflammatory Regulation

scholarly journals Genetic Correction of IL-10RB Deficiency Reconstitutes Anti-Inflammatory Regulation in iPSC-Derived Macrophages

2021 ◽  
Vol 11 (3) ◽  
pp. 221
Author(s):  
Dirk Hoffmann ◽  
Johanna Sens ◽  
Sebastian Brennig ◽  
Daniel Brand ◽  
Friederike Philipp ◽  
...  
Keyword(s):  
Disease Modeling ◽  
Integration Site ◽  
Cytokine Secretion ◽  
Cytokine Signaling ◽  
Stat3 Phosphorylation ◽  
Tnf Α ◽  
Socs3 Expression ◽  
Healthy Control ◽  
Anti Inflammatory ◽  
Inflammatory Regulation

Patient material from rare diseases such as very early-onset inflammatory bowel disease (VEO-IBD) is often limited. The use of patient-derived induced pluripotent stem cells (iPSCs) for disease modeling is a promising approach to investigate disease pathomechanisms and therapeutic strategies. We successfully developed VEO-IBD patient-derived iPSC lines harboring a mutation in the IL-10 receptor β-chain (IL-10RB) associated with defective IL-10 signaling. To characterize the disease phenotype, healthy control and VEO-IBD iPSCs were differentiated into macrophages. IL-10 stimulation induced characteristic signal transducer and activator of transcription 3 (STAT3) and suppressor of cytokine signaling 3 (SOCS3) downstream signaling and anti-inflammatory regulation of lipopolysaccharide (LPS)-mediated cytokine secretion in healthy control iPSC-derived macrophages. In contrast, IL-10 stimulation of macrophages derived from patient iPSCs did not result in STAT3 phosphorylation and subsequent SOCS3 expression, recapitulating the phenotype of cells from patients with IL-10RB deficiency. In line with this, LPS-induced cytokine secretion (e.g., IL-6 and tumor necrosis factor-α (TNF-α)) could not be downregulated by exogenous IL-10 stimulation in VEO-IBD iPSC-derived macrophages. Correction of the IL-10RB defect via lentiviral gene therapy or genome editing in the adeno-associated virus integration site 1 (AAVS1) safe harbor locus led to reconstitution of the anti-inflammatory response. Corrected cells showed IL-10RB expression, IL-10-inducible phosphorylation of STAT3, and subsequent SOCS3 expression. Furthermore, LPS-mediated TNF-α secretion could be modulated by IL-10 stimulation in gene-edited VEO-IBD iPSC-derived macrophages. Our established disease models provide the opportunity to identify and validate new curative molecular therapies and to investigate phenotypes and consequences of additional individual IL-10 signaling pathway-dependent VEO-IBD mutations.

scholarly journals The Inflammatory Regulation of TRPA1 Expression in Human A549 Lung Epithelial Cells

2021 ◽  
pp. 102059
Author(s):  
Samu Luostarinen ◽  
Mari Hämäläinen ◽  
Noriyuki Hatano ◽  
Katsuhiko Muraki ◽  
Eeva Moilanen
Keyword(s):  
Epithelial Cells ◽  
Lung Epithelial Cells ◽  
Lung Epithelial ◽  
Inflammatory Regulation ◽  
Human A549 ◽  
A549 Lung

scholarly journals Theophylline improves lipopolysaccharide-induced alveolarization arrest through inflammatory regulation

2014 ◽  
Vol 10 (1) ◽  
pp. 269-275 ◽  
Author(s):  
HUA HE ◽  
FEI CHEN ◽  
WENSI NI ◽  
JIANHUI LI ◽  
YONGJUN ZHANG
Keyword(s):  
Inflammatory Regulation

scholarly journals Inflammatory Regulation of Valvular Remodeling: The Good(?), the Bad, and the Ugly

2011 ◽  
Vol 2011 ◽  
pp. 1-13 ◽  
Author(s):  
Gretchen J. Mahler ◽  
Jonathan T. Butcher
Keyword(s):  
Heart Valve ◽  
Cell Biology ◽  
Heart Valves ◽  
Valve Disease ◽  
Heart Valve Disease ◽  
Inflammatory Signaling ◽  
Current State ◽  
Valve Remodeling ◽  
Inflammatory Regulation ◽  
Key Questions

Heart valve disease is unique in that it affects both the very young and very old, and does not discriminate by financial affluence, social stratus, or global location. Research over the past decade has transformed our understanding of heart valve cell biology, yet still more remains unclear regarding how these cells respond and adapt to their local microenvironment. Recent studies have identified inflammatory signaling at nearly every point in the life cycle of heart valves, yet its role at each stage is unclear. While the vast majority of evidence points to inflammation as mediating pathological valve remodeling and eventual destruction, some studies suggest inflammation may provide key signals guiding transient adaptive remodeling. Though the mechanisms are far from clear, inflammatory signaling may be a previously unrecognized ally in the quest for controlled rapid tissue remodeling, a key requirement for regenerative medicine approaches for heart valve disease. This paper summarizes the current state of knowledge regarding inflammatory mediation of heart valve remodeling and suggests key questions moving forward.

Influence of silver speciation on the inflammatory regulation of AgNPs anchoring onto titania nanotubes

2020 ◽  
Vol 194 ◽  
pp. 111199
Author(s):  
Congling Yang ◽  
Ziquan Wang ◽  
Ke Huang ◽  
Jie Weng ◽  
Jianxin Wang ◽  
...  
Keyword(s):  
Titania Nanotubes ◽  
Inflammatory Regulation

scholarly journals Asymptomatic SARS-CoV-2 infection: Is it all about being refractile to innate immune sensing of viral spare-parts? – Clues from exotic animal reservoirs

2020 ◽  
Author(s):  
Esaki M Shankar ◽  
Karlhans F Che ◽  
Yean K Yong ◽  
A S Smiline Girija ◽  
Vijayakumar Velu ◽  
...  
Keyword(s):  
Spare Parts ◽  
Viral Control ◽  
Evolutionary Advantage ◽  
Exotic Animal ◽  
Rate Of Recovery ◽  
Immune Sensing ◽  
Inflammatory Regulation ◽  
Innate Immune Sensing ◽  
Animal Reservoirs

Abstract A vast proportion of coronavirus disease 2019 (COVID-19) individuals remain asymptomatic and can shed severe acute respiratory syndrome (SARS-CoV) type 2 virus to transmit the infection, which also explains the exponential increase in the number of COVID-19 cases globally. Furthermore, the rate of recovery rates from clinical COVID-19 in certain pockets of the globe is surprisingly high. Based on published reports and available literature, here, we speculated a few immunovirological mechanisms as to why a vast majority of individuals remain asymptomatic similar to exotic animal (bats and pangolins) reservoirs that remain refractile to disease development despite carrying a huge load of diverse insidious viral species, and whether such evolutionary advantage would unveil therapeutic strategies against human COVID-19 infection. Understanding the unique mechanisms that exotic animal species employ to achieve viral control, as well as inflammatory regulation, appears to hold key clues to the development of therapeutic versatility against COVID-19.

scholarly journals Sildenafil (Viagra) Protective Effects on Neuroinflammation: The Role of iNOS/NO System in an Inflammatory Demyelination Model

2013 ◽  
Vol 2013 ◽  
pp. 1-11 ◽  
Author(s):  
Catarina Raposo ◽  
Ana Karolina de Santana Nunes ◽  
Rayana Leal de Almeida Luna ◽  
Shyrlene Meiry da Rocha Araújo ◽  
Maria Alice da Cruz-Höfling ◽  
...  
Keyword(s):  
Neuroprotective Effect ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Wild Type ◽  
Glutathione S Transferase ◽  
Cox 2 ◽  
Inflammatory Regulation ◽  
Inos Inhibition ◽  
Inflammatory Effect

We recently demonstrated that sildenafil reduces the expression of cytokines, COX-2, and GFAP in a demyelinating model induced in wild-type (WT) mice. Herein, the understandings of the neuroprotective effect of sildenafil and the mediation of iNOS/NO system on inflammatory demyelination induced by cuprizone were investigated. The cerebella of iNOS−/−mice were examined after four weeks of treatment with cuprizone alone or combined with sildenafil. Cuprizone increased GFAP, Iba-1, TNF-α, COX-2, IL-1β, and IFN-γexpression, decreased expression of glutathione S-transferase pi (GSTpi), and damaged myelin in iNOS−/−mice. Sildenafil reduced Iba-1, IFN-γ, and IL-1βlevels but had no effect on the expression of GFAP, TNF-α, and COX-2 compared to the cuprizone group. Sildenafil elevated GSTpi levels and improved the myelin structure/ultrastructure. iNOS−/−mice suffered from severe inflammation following treatment with cuprizone, while WT mice had milder inflammation, as found in the previous study. It is possible that inflammatory regulation through iNOS-feedback is absent in iNOS−/−mice, making them more susceptible to inflammation. Sildenafil has at least a partial anti-inflammatory effect through iNOS inhibition, as its effect on iNOS−/−mice was limited. Further studies are required to explain the underlying mechanism of the sildenafil effects.

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