scholarly journals The Immune System in Tissue Environments Regaining Homeostasis after Injury: Is “Inflammation” Always Inflammation?

2016 ◽  
Vol 2016 ◽  
pp. 1-9 ◽  
Author(s):  
Onkar P. Kulkarni ◽  
Julia Lichtnekert ◽  
Hans-Joachim Anders ◽  
Shrikant R. Mulay
Keyword(s):  
Immune System ◽  
Proinflammatory Cytokines ◽  
Inflammatory Mediators ◽  
Innate Immune System ◽  
Clinical Signs ◽  
Innate Immune ◽  
Cytokines And Chemokines ◽  
Anti Inflammatory ◽  
Tissue Injuries

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.

Bacopamonnieri (L.) exerts anti-inflammatory effects on cells of the innate immune system in vitro

2014 ◽  
Vol 5 (3) ◽  
pp. 517-520 ◽  
Author(s):  
Roderick Williams ◽  
Gerald Münch ◽  
Erika Gyengesi ◽  
Louise Bennett
Keyword(s):  
Immune System ◽  
Acute Pain ◽  
Innate Immune System ◽  
Selective Inhibition ◽  
Innate Immune ◽  
Inflammatory Activity ◽  
Consequent Reduction ◽  
Cox 2 ◽  
Anti Inflammatory

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.

scholarly journals Untangling the Web of Systemic Autoinflammatory Diseases

2014 ◽  
Vol 2014 ◽  
pp. 1-15 ◽  
Author(s):  
Donato Rigante ◽  
Giuseppe Lopalco ◽  
Antonio Vitale ◽  
Orso Maria Lucherini ◽  
Francesco Caso ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Immune System ◽  
Proinflammatory Cytokines ◽  
Innate Immune System ◽  
Tumor Necrosis ◽  
Interleukin 1 ◽  
Innate Immune ◽  
Autoinflammatory Diseases ◽  
Necrosis Factor ◽  
The Web

The innate immune system is involved in the pathophysiology of systemic autoinflammatory diseases (SAIDs), an enlarging group of disorders caused by dysregulated production of proinflammatory cytokines, such as interleukin-1βand tumor necrosis factor-α, in which autoreactive T-lymphocytes and autoantibodies are indeed absent. A widely deranged innate immunity leads to overactivity of proinflammatory cytokines and subsequent multisite inflammatory symptoms depicting various conditions, such as hereditary periodic fevers, granulomatous disorders, and pyogenic diseases, collectively described in this review. Further research should enhance our understanding of the genetics behind SAIDs, unearth triggers of inflammatory attacks, and result in improvement for their diagnosis and treatment.

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
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Cardiac Regeneration ◽  
Vital Role ◽  
Regenerative Process ◽  
Innate Immune ◽  
Heart Regeneration ◽  
Regeneration Period ◽  
Anti Inflammatory ◽  
Inflammatory Milieu

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.

scholarly journals Lipopolysaccharide-induced innate immune responses are exacerbated by Prohibitin 1 deficiency and mitigated by S-adenosylmethionine in murine macrophages

PLoS ONE ◽  
2020 ◽  
Vol 15 (11) ◽  
pp. e0241224
Author(s):  
Soohan Jung ◽  
Jaehee Park ◽  
Kwang Suk Ko
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Luciferase Activity ◽  
Innate Immune ◽  
Raw 264.7 Cells ◽  
Luciferase Reporter ◽  
Raw 264.7 ◽  
Reporter Assay ◽  
Anti Inflammatory ◽  
Prohibitin 1

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.

scholarly journals Review on Treatment of Gout & Hyperuricemia

1970 ◽  
Vol 29 (2) ◽  
pp. 85-95 ◽  
Author(s):  
MR Chowdhury ◽  
MM Hassan ◽  
F Hakim ◽  
SA Haq
Keyword(s):  
Uric Acid ◽  
Immune System ◽  
Proinflammatory Cytokines ◽  
Inflammatory Reaction ◽  
Innate Immune System ◽  
Innate Immune ◽  
Monosodium Urate ◽  
Novel Treatments ◽  
Local Inflammatory Reaction ◽  
Msu Crystals

In the last few decades, both hyperuricemia and gout have increased markedly. Recent studies show new concept into the transporters that handle uric acid in the kidney as well as possible links between these transporters & hyperuricemia. There are changes in the treatment of established hyperuricemia. Febuxostat and PEGuricase are two novel treatments that have been evaluated and shown to be highly effective in the management of hyperuricemia. Monosodium urate (MSU) crystals are the inducers of inflammation. Within the joint, they trigger a local inflammatory reaction, neutrophil recruitment, and the production of proinflammatory cytokines as well as other inflammatory mediators. The uptake of MSU crystals by monocytes involves interactions with components of the innate immune system. The inflammatory effects of MSU are IL-1-dependent and can be blocked by IL-1 inhibitors. These advances in the understanding of hyperuricemia and gout provide new therapeutic targets for the future. DOI: http://dx.doi.org/10.3329/jbcps.v29i2.7953 (J Bangladesh Coll Phys Surg 2011; 29: 85-95)

scholarly journals PPARγand the Innate Immune System Mediate the Resolution of Inflammation

PPAR Research ◽  
2015 ◽  
Vol 2015 ◽  
pp. 1-20 ◽  
Author(s):  
Amanda Croasdell ◽  
Parker F. Duffney ◽  
Nina Kim ◽  
Shannon H. Lacy ◽  
Patricia J. Sime ◽  
...  
Keyword(s):  
Immune System ◽  
Innate Immune System ◽  
Cell Function ◽  
Immune Cell ◽  
Therapeutic Potential ◽  
Adaptive Immune Response ◽  
Innate Immune ◽  
M2 Macrophage ◽  
Resolution Of Inflammation ◽  
Anti Inflammatory

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.

scholarly journals NLRP3 Inflammasome in the Pathophysiology of Hemorrhagic Stroke: A Review

2019 ◽  
Vol 17 (7) ◽  
pp. 582-589 ◽  
Author(s):  
Yujie Luo ◽  
Cesar Reis ◽  
Sheng Chen
Keyword(s):  
Immune System ◽  
Brain Injury ◽  
Nlrp3 Inflammasome ◽  
Innate Immune System ◽  
Hemorrhagic Stroke ◽  
Innate Immune ◽  
High Morbidity ◽  
Pyrin Domain ◽  
Cytokines And Chemokines

Hemorrhagic stroke is a devastating disease with high morbidity and mortality. There is still a lack of effective therapeutic approach. The recent studies have shown that the innate immune system plays a significant role in hemorrhagic stroke. Microglia, as major components in innate immune system, are activated and then can release cytokines and chemokines in response to hemorrhagic stroke, and ultimately led to neuroinflammation and brain injury. The NOD-like receptor family, pyrin domain containing 3 (NLRP3) inflammasome is predominantly released by microglia and is believed as the main contributor of neuroinflammation. Several studies have focused on the role of NLRP3 inflammasome in hemorrhagic stroke-induced brain injury, however, the specific mechanism of NLRP3 activation and regulation remains unclear. This review summarized the mechanism of NLRP3 activation and its role in hemorrhagic stroke and discussed the translational significance.

Sign in / Sign up

Export Citation Format

Share Document