scholarly journals Cardiac regeneration in the axolotl is unaffected by alterations in leukocyte numbers induced by lipopolysaccharide and prednisolone

2021 ◽  
Vol 14 (1) ◽  
Author(s):  
Kathrine Pedersen ◽  
Rikke Kongsgaard Rasmussen ◽  
Anita Dittrich ◽  
Henrik Lauridsen

Abstract Objective Cardiac regeneration in the axolotl has been found to rely on the innate immune system, and especially macrophages have been demonstrated to play a vital role in regulating the regenerative process. In this study we wanted to induce a pro- and anti-inflammatory milieu in the axolotl during heart regeneration to test the resilience of the regenerative response. Results This was induced via repeated intrapericardial injections of lipopolysaccharide or prednisolone during a 40-day regeneration period in order to challenge the presumably fine-tuned inflammatory response that normally facilitates regeneration. We observed a local and systemic leucocyte response to pro- and anti-inflammatory stimulation, but we found cardiac regeneration to be structurally and functionally unaffected.

2014 ◽  
Vol 5 (3) ◽  
pp. 517-520 ◽  
Author(s):  
Roderick Williams ◽  
Gerald Münch ◽  
Erika Gyengesi ◽  
Louise Bennett

Bacopa monnieri(L., BM) is a traditional Ayurvedic medicinal herb recognised for its efficacy in relieving acute pain and inflammation, as related to selective inhibition of cyclo-oxygenase-2 (COX-2) enzyme and consequent reduction in COX-2-mediated prostanoid mediators. Anti-inflammatory activity of BM might also account for its benefits in cognition.


PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0241224
Author(s):  
Soohan Jung ◽  
Jaehee Park ◽  
Kwang Suk Ko

Prohibitin 1 (Phb1) is a pleiotropic protein with multiple functions in mammalian cells including cell cycle regulation and mitochondrial protein stabilization. It has been proposed as a potential therapeutic target for a variety of diseases including inflammatory diseases. In this study, we investigated the potential immune-modulatory functions of Phb1 and anti-inflammatory properties of S-adenosylmethionine (SAMe) using macrophages, which play a major role in the innate immune system. The results showed that expressions of Phb1 mRNA and protein were reduced in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells (p<0.05). Phb1 knockdown further ameliorated the mRNA expression of pro- and anti-inflammatory cytokines such as TNF-α, IL-1α, IL-1β, IL-6, and IL10 in LPS-stimulated RAW 264.7 cells. SAMe significantly attenuated LPS-induced inflammatory responses such as IL-1β, IL-10, Nos2, and NO production in the presence of siPhb1. Luciferase reporter assay was conducted to determine the mechanisms underlying the effects of Phb1 and SAMe on the immune system. The luciferase activity of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) was significantly increased in LPS-treated RAW 264.7 cells. In addition, the luciferase reporter assay showed increased NF-κB activation in Phb1 knockdown RAW 264.7 cells (p<0.1) and SAMe treatment attenuated the NF-κB luciferase activity in Phb1 knockdown RAW 264.7 cells. Based on the results, we concluded that Phb1 possibly modulates the inflammatory response whereas SAMe has an anti-inflammatory effect on Phb1 knockdown macrophage cells. Furthermore, Phb1 expression level has potential properties of affecting on innate immune system by modulating the NF-κB signaling pathway.


PPAR Research ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-20 ◽  
Author(s):  
Amanda Croasdell ◽  
Parker F. Duffney ◽  
Nina Kim ◽  
Shannon H. Lacy ◽  
Patricia J. Sime ◽  
...  

The resolution of inflammation is an active and dynamic process, mediated in large part by the innate immune system. Resolution represents not only an increase in anti-inflammatory actions, but also a paradigm shift in immune cell function to restore homeostasis. PPARγ, a ligand activated transcription factor, has long been studied for its anti-inflammatory actions, but an emerging body of literature is investigating the role of PPARγand its ligands (including thiazolidinediones, prostaglandins, and oleanolic acids) in all phases of resolution. PPARγcan shift production from pro- to anti-inflammatory mediators by neutrophils, platelets, and macrophages. PPARγand its ligands further modulate platelet and neutrophil function, decreasing trafficking, promoting neutrophil apoptosis, and preventing platelet-leukocyte interactions. PPARγalters macrophage trafficking, increases efferocytosis and phagocytosis, and promotes alternative M2 macrophage activation. There are also roles for this receptor in the adaptive immune response, particularly regarding B cells. These effects contribute towards the attenuation of multiple disease states, including COPD, colitis, Alzheimer’s disease, and obesity in animal models. Finally, novel specialized proresolving mediators—eicosanoids with critical roles in resolution—may act through PPARγmodulation to promote resolution, providing another exciting area of therapeutic potential for this receptor.


2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Onkar P. Kulkarni ◽  
Julia Lichtnekert ◽  
Hans-Joachim Anders ◽  
Shrikant R. Mulay

Inflammation is a response to infections or tissue injuries. Inflammation was once defined by clinical signs, later by the presence of leukocytes, and nowadays by expression of “proinflammatory” cytokines and chemokines. But leukocytes and cytokines often have rather anti-inflammatory, proregenerative, and homeostatic effects. Is there a need to redefine “inflammation”? In this review, we discuss the functions of “inflammatory” mediators/regulators of the innate immune system that determine tissue environments to fulfill the need of the tissue while regaining homeostasis after injury.


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