scholarly journals Sirtuins and Sepsis: Cross Talk between Redox and Epigenetic Pathways

Antioxidants ◽  
2021 ◽  
Vol 11 (1) ◽  
pp. 3
Author(s):  
Anugraha Gandhirajan ◽  
Sanjoy Roychowdhury ◽  
Vidula Vachharajani
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Compensatory Mechanism ◽  
Inflammatory Phase ◽  
Epigenetic Programming ◽  
Secondary Infections ◽  
The Us ◽  
Anti Oxidant ◽  
Anti Inflammatory ◽  
Sepsis And Septic Shock

Sepsis and septic shock are the leading causes of death among hospitalized patients in the US. The immune response in sepsis transitions from a pro-inflammatory and pro-oxidant hyper-inflammation to an anti-inflammatory and cytoprotective hypo-inflammatory phase. While 1/3rd sepsis-related deaths occur during hyper-, a vast majority of sepsis-mortality occurs during the hypo-inflammation. Hyper-inflammation is cytotoxic for the immune cells and cannot be sustained. As a compensatory mechanism, the immune cells transition from cytotoxic hyper-inflammation to a cytoprotective hypo-inflammation with anti-inflammatory/immunosuppressive phase. However, the hypo-inflammation is associated with an inability to clear invading pathogens, leaving the host susceptible to secondary infections. Thus, the maladaptive immune response leads to a marked departure from homeostasis during sepsis-phases. The transition from hyper- to hypo-inflammation occurs via epigenetic programming. Sirtuins, a highly conserved family of histone deacetylators and guardians of homeostasis, are integral to the epigenetic programming in sepsis. Through their anti-inflammatory and anti-oxidant properties, the sirtuins modulate the immune response in sepsis. We review the role of sirtuins in orchestrating the interplay between the oxidative stress and epigenetic programming during sepsis.

scholarly journals The immune response of T cells and therapeutic targets related to regulating the levels of T helper cells after ischaemic stroke

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Tian-Yu Lei ◽  
Ying-Ze Ye ◽  
Xi-Qun Zhu ◽  
Daniel Smerin ◽  
Li-Juan Gu ◽  
...  
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Immune System ◽  
Immune Responses ◽  
Ischaemic Stroke ◽  
Immune Cells ◽  
Tissue Injury ◽  
Recovery Period ◽  
Vital Functions ◽  
Anti Inflammatory

AbstractThrough considerable effort in research and clinical studies, the immune system has been identified as a participant in the onset and progression of brain injury after ischaemic stroke. Due to the involvement of all types of immune cells, the roles of the immune system in stroke pathology and associated effects are complicated. Past research concentrated on the functions of monocytes and neutrophils in the pathogenesis of ischaemic stroke and tried to demonstrate the mechanisms of tissue injury and protection involving these immune cells. Within the past several years, an increasing number of studies have elucidated the vital functions of T cells in the innate and adaptive immune responses in both the acute and chronic phases of ischaemic stroke. Recently, the phenotypes of T cells with proinflammatory or anti-inflammatory function have been demonstrated in detail. T cells with distinctive phenotypes can also influence cerebral inflammation through various pathways, such as regulating the immune response, interacting with brain-resident immune cells and modulating neurogenesis and angiogenesis during different phases following stroke. In view of the limited treatment options available following stroke other than tissue plasminogen activator therapy, understanding the function of immune responses, especially T cell responses, in the post-stroke recovery period can provide a new therapeutic direction. Here, we discuss the different functions and temporal evolution of T cells with different phenotypes during the acute and chronic phases of ischaemic stroke. We suggest that modulating the balance between the proinflammatory and anti-inflammatory functions of T cells with distinct phenotypes may become a potential therapeutic approach that reduces the mortality and improves the functional outcomes and prognosis of patients suffering from ischaemic stroke.

scholarly journals Immune cells as targets for cardioprotection: new players and novel therapeutic opportunities

2019 ◽  
Vol 115 (7) ◽  
pp. 1117-1130 ◽  
Author(s):  
Ioanna Andreadou ◽  
Hector A Cabrera-Fuentes ◽  
Yvan Devaux ◽  
Nikolaos G Frangogiannis ◽  
Stefan Frantz ◽  
...  
Keyword(s):  
Heart Failure ◽  
Inflammatory Reaction ◽  
Immune Cells ◽  
Cell Response ◽  
Immune Cell ◽  
Left Ventricular ◽  
Lymphoid Cells ◽  
Inflammatory Phase ◽  
Anti Inflammatory ◽  
Immune Cell Response

Abstract New therapies are required to reduce myocardial infarct (MI) size and prevent the onset of heart failure in patients presenting with acute myocardial infarction (AMI), one of the leading causes of death and disability globally. In this regard, the immune cell response to AMI, which comprises an initial pro-inflammatory reaction followed by an anti-inflammatory phase, contributes to final MI size and post-AMI remodelling [changes in left ventricular (LV) size and function]. The transition between these two phases is critical in this regard, with a persistent and severe pro-inflammatory reaction leading to adverse LV remodelling and increased propensity for developing heart failure. In this review article, we provide an overview of the immune cells involved in orchestrating the complex and dynamic inflammatory response to AMI—these include neutrophils, monocytes/macrophages, and emerging players such as dendritic cells, lymphocytes, pericardial lymphoid cells, endothelial cells, and cardiac fibroblasts. We discuss potential reasons for past failures of anti-inflammatory cardioprotective therapies, and highlight new treatment targets for modulating the immune cell response to AMI, as a potential therapeutic strategy to improve clinical outcomes in AMI patients. This article is part of a Cardiovascular Research Spotlight Issue entitled ‘Cardioprotection Beyond the Cardiomyocyte’, and emerged as part of the discussions of the European Union (EU)-CARDIOPROTECTION Cooperation in Science and Technology (COST) Action, CA16225.

scholarly journals Characterization of Cytokines and Proliferation Marker Ki67 in Cleft Affected Lip Tissue

Medicina ◽  
2019 ◽  
Vol 55 (9) ◽  
pp. 518 ◽  
Author(s):  
Pilmane ◽  
Sidhoma ◽  
Akota ◽  
Kazoka
Keyword(s):  
Immune Response ◽  
Connective Tissue ◽  
Cleft Lip ◽  
Cellular Proliferation ◽  
Tissue Response ◽  
Compensatory Mechanism ◽  
Strong Positive Correlation ◽  
Proliferation Marker ◽  
Significant Difference ◽  
Anti Inflammatory

Background and objectives: Cleft lip palate takes the second place among all anomalies. The complex appearance of cytokines and proliferation markers has still not been clarified despite their possible crucial role in cleft tissue. Therefore, the aim of work was the detection of appearance of pro- and anti-inflammatory cytokines and proliferation marker Ki67, and their inter-correlations in cleft affected lip (CAL). Materials and Methods: The lip material was obtained from 16 children aged before primary dentition during plastic surgery. Control was obtained from 7 non-CAL oral tissue. Tissues were stained for IL-1, IL-4, IL-6, IL-8, IL-10 and Ki67 immunohistochemically. Non-parametric statistic, Mann–Whitney and Spearman’s coefficient were used. Results: All cytokines positive cells were observed more into the epithelium. Statistically significant difference was seen between epithelial IL-1, IL-10, IL-8 and Ki67 positive cells and IL-10-, IL-4-containing connective tissue cells in comparison to the control. Strong positive correlation was detected in CAL epithelium between IL-10 and IL-8, IL-10 and IL-4, IL-10 and IL-1, IL-1 and IL-8, IL-1 and IL-4, IL-4 and IL-8, IL-8 and Ki67, IL-10 and Ki67, but moderate—in connective tissue between IL-1 and IL-10, IL-1 and IL-4. Conclusion: The CAL epithelium is the main source for the interleukins. Rich similar expression of IL-1 and IL-10 suggests the balance between pro-and anti-inflammatory tissue response on basis of dysregulated tissue homeostasis (increase of IL-8). The correlations between the different ILs -1, -4, -8, -10 in CAL epithelium seem to indicate the self-protection compensatory mechanism for intensification of local inflammatory-immune response without involvement of IL-6. The correlations between Ki67 and cytokines indicate the involvement of IL-8 and IL-10 in stimulation of cellular proliferation. IL-4 and IL-10 expression from CAL connective tissue simultaneously to IL-1, IL-4 and IL-10 inter-correlations there suggests the intensification of local immune response regulated probably by main pro-inflammatory cytokine—IL-1.

scholarly journals Cytokines in Sepsis: Potent Immunoregulators and Potential Therapeutic Targets—An Updated View

2013 ◽  
Vol 2013 ◽  
pp. 1-16 ◽  
Author(s):  
Wibke Schulte ◽  
Jürgen Bernhagen ◽  
Richard Bucala
Keyword(s):  
Septic Shock ◽  
Immune Response ◽  
Intensive Care ◽  
Defense Mechanisms ◽  
Causes Of Death ◽  
Current Knowledge ◽  
The Other ◽  
Anti Inflammatory ◽  
Pleiotropic Regulators ◽  
Sepsis And Septic Shock

Sepsis and septic shock are among the leading causes of death in intensive care units worldwide. Numerous studies on their pathophysiology have revealed an imbalance in the inflammatory network leading to tissue damage, organ failure, and ultimately, death. Cytokines are important pleiotropic regulators of the immune response, which have a crucial role in the complex pathophysiology underlying sepsis. They have both pro- and anti-inflammatory functions and are capable of coordinating effective defense mechanisms against invading pathogens. On the other hand, cytokines may dysregulate the immune response and promote tissue-damaging inflammation. In this review, we address the current knowledge of the actions of pro- and anti-inflammatory cytokines in sepsis pathophysiology as well as how these cytokines and other important immunomodulating agents may be therapeutically targeted to improve the clinical outcome of sepsis.

scholarly journals Tablet Swasvin D Vyro (Virofight) - A Proven Solution for any Viral Infection, Immunity and Inflammation

2020 ◽  
pp. 7-12
Author(s):  
Dr. Smita Naram ◽  
Dr. Deepak Mahajan ◽  
Dr. Hemang Parekh ◽  
Dr. Ronak Naik
Keyword(s):  
Immune Response ◽  
Immune Modulation ◽  
Viral Infections ◽  
First Response ◽  
Therapeutic Measures ◽  
Anti Oxidant ◽  
Infected Cells ◽  
Anti Inflammatory ◽  
Work Done

Viral infections commonly affect both the respiratory tract, upper and lower. The first response of the immune system to the infection is Inflammation. This inflammation is produced by eicosanoids and cytokines, which are released by injured or infected cells. The immune modulation with Ayurvedic formulations as a possible therapeutic measures is need of the hour nowadays. The ancient Indian medicinal system of Ayurveda has a scope of treating many diseases by the theory of Rasayana, in other terms called preparations from plant or herbal source, including immune modulatory properties. In this article, we want to validate immunemodulatory, anti-inflammatory anti-viral role of Tablet Swasvin D vyro (Virofight) with the reference of some previous work done. In conclusion, we can say that Swasvin D vyro (Virofight) tablet is the best effective immune-modulatory, as it augments the cell-mediated as well as humeral mediated immune response, it is antiviral as it can inhibit replication of several viruses. It is anti-inflammatory by inhibiting various cytokine producing pathways, it has anti-oxidant and antiulcer properties.

scholarly journals Ghrelin as an Anti-Sepsis Peptide: Review

2021 ◽  
Vol 11 ◽  
Author(s):  
Nimisha Mathur ◽  
Syed F. Mehdi ◽  
Manasa Anipindi ◽  
Monowar Aziz ◽  
Sawleha A. Khan ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Immune Response ◽  
Immune Responses ◽  
Immune Cells ◽  
Inflammatory Agent ◽  
Wide Range ◽  
Inflammatory Processes ◽  
Anti Inflammatory ◽  
Preclinical Animal Models ◽  
Stimulation Of

Sepsis continues to produce widespread inflammation, illness, and death, prompting intensive research aimed at uncovering causes and therapies. In this article, we focus on ghrelin, an endogenous peptide with promise as a potent anti-inflammatory agent. Ghrelin was discovered, tracked, and isolated from stomach cells based on its ability to stimulate release of growth hormone. It also stimulates appetite and is shown to be anti-inflammatory in a wide range of tissues. The anti-inflammatory effects mediated by ghrelin are a result of both the stimulation of anti-inflammatory processes and an inhibition of pro-inflammatory forces. Anti-inflammatory processes are promoted in a broad range of tissues including the hypothalamus and vagus nerve as well as in a broad range of immune cells. Aged rodents have reduced levels of growth hormone (GH) and diminished immune responses; ghrelin administration boosts GH levels and immune response. The anti-inflammatory functions of ghrelin, well displayed in preclinical animal models of sepsis, are just being charted in patients, with expectations that ghrelin and growth hormone might improve outcomes in patients with sepsis.

scholarly journals A novel definition and treatment of hyperinflammation in COVID-19 based on purinergic signalling

2021 ◽  
Author(s):  
Djo Hasan ◽  
Atsuko Shono ◽  
Coenraad K. van Kalken ◽  
Peter J. van der Spek ◽  
Eric P. Krenning ◽  
...  
Keyword(s):  
Adverse Effects ◽  
Immune Cells ◽  
Purinergic Receptors ◽  
Atp Release ◽  
The Body ◽  
Purinergic Signalling ◽  
Cytokine Storm ◽  
Secondary Infections ◽  
Half Maximal Effective Concentration ◽  
Anti Inflammatory

AbstractHyperinflammation plays an important role in severe and critical COVID-19. Using inconsistent criteria, many researchers define hyperinflammation as a form of very severe inflammation with cytokine storm. Therefore, COVID-19 patients are treated with anti-inflammatory drugs. These drugs appear to be less efficacious than expected and are sometimes accompanied by serious adverse effects. SARS-CoV-2 promotes cellular ATP release. Increased levels of extracellular ATP activate the purinergic receptors of the immune cells initiating the physiologic pro-inflammatory immune response. Persisting viral infection drives the ATP release even further leading to the activation of the P2X7 purinergic receptors (P2X7Rs) and a severe yet physiologic inflammation. Disease progression promotes prolonged vigorous activation of the P2X7R causing cell death and uncontrolled ATP release leading to cytokine storm and desensitisation of all other purinergic receptors of the immune cells. This results in immune paralysis with co-infections or secondary infections. We refer to this pathologic condition as hyperinflammation. The readily available and affordable P2X7R antagonist lidocaine can abrogate hyperinflammation and restore the normal immune function. The issue is that the half-maximal effective concentration for P2X7R inhibition of lidocaine is much higher than the maximal tolerable plasma concentration where adverse effects start to develop. To overcome this, we selectively inhibit the P2X7Rs of the immune cells of the lymphatic system inducing clonal expansion of Tregs in local lymph nodes. Subsequently, these Tregs migrate throughout the body exerting anti-inflammatory activities suppressing systemic and (distant) local hyperinflammation. We illustrate this with six critically ill COVID-19 patients treated with lidocaine.

Day‐7 embryos generate an anti‐inflammatory immune response in peripheral blood immune cells in superovulated cows

2018 ◽  
Vol 81 (2) ◽  
pp. e13069 ◽  
Author(s):  
Anup K. Talukder ◽  
Mohammad B. Rashid ◽  
Toshiro Takedomi ◽  
Satoru Moriyasu ◽  
Kazuhiko Imakawa ◽  
...  
Keyword(s):  
Immune Response ◽  
Immune Cells ◽  
Peripheral Blood ◽  
Inflammatory Immune Response ◽  
Anti Inflammatory

scholarly journals Possible Role of Pineal and Extra-Pineal Melatonin in Surveillance, Immunity, and First-Line Defense

2021 ◽  
Vol 22 (22) ◽  
pp. 12143
Author(s):  
Regina P. Markus ◽  
Kassiano S. Sousa ◽  
Sanseray da Silveira Cruz-Machado ◽  
Pedro A. Fernandes ◽  
Zulma S. Ferreira
Keyword(s):  
Immune Response ◽  
Inflammatory Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Whole Body ◽  
Pineal Melatonin ◽  
Inflammatory Phase ◽  
Cellular Debris ◽  
Anti Inflammatory

Melatonin is a highly conserved molecule found in prokaryotes and eukaryotes that acts as the darkness hormone, translating environmental lighting to the whole body, and as a moderator of innate and acquired defense, migration, and cell proliferation processes. This review evaluates the importance of pineal activity in monitoring PAMPs and DAMPs and in mounting an inflammatory response or innate immune response. Activation of the immune–pineal axis, which coordinates the pro-and anti-inflammatory phases of an innate immune response, is described. PAMPs and DAMPs promote the immediate suppression of melatonin production by the pineal gland, which allows leukocyte migration. Monocyte-derived macrophages, important phagocytes of microbes, and cellular debris produce melatonin locally and thereby initiate the anti-inflammatory phase of the acute inflammatory response. The role of locally produced melatonin in organs that directly contact the external environment, such as the skin and the gastrointestinal and respiratory tracts, is also discussed. In this context, as resident macrophages are self-renewing cells, we explore evidence indicating that, besides avoiding overreaction of the immune system, extra-pineal melatonin has a fundamental role in the homeostasis of organs and tissues.

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