scholarly journals The Role of gp130 Cytokines in Tuberculosis

Cells ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 2695
Author(s):  
Kristina Ritter ◽  
Jasmin Rousseau ◽  
Christoph Hölscher
Keyword(s):  
Inflammatory Diseases ◽  
Therapeutic Approaches ◽  
Duration Of Treatment ◽  
Common Receptor ◽  
Promising Target ◽  
Increased Risk ◽  
The Common ◽  
Combine Administration ◽  
Cytokine Networks

Protective immune responses to Mycobacterium tuberculosis (Mtb) infection substantially depend on a delicate balance within cytokine networks. Thus, immunosuppressive therapy by cytokine blockers, as successfully used in the management of various chronic inflammatory diseases, is often connected with an increased risk for tuberculosis (TB) reactivation. Hence, identification of alternative therapeutics which allow the treatment of inflammatory diseases without compromising anti-mycobacterial immunity remains an important issue. On the other hand, in the context of novel therapeutic approaches for the management of TB, host-directed adjunct therapies, which combine administration of antibiotics with immunomodulatory drugs, play an increasingly important role, particularly to reduce the duration of treatment. In both respects, cytokines/cytokine receptors related to the common receptor subunit gp130 may serve as promising target candidates. Within the gp130 cytokine family, interleukin (IL)-6, IL-11 and IL-27 are most explored in the context of TB. This review summarizes the differential roles of these cytokines in protection and immunopathology during Mtb infection and discusses potential therapeutic implementations with respect to the aforementioned approaches.

Out of tune: Perceptions of, engagement with, and responses to mental health interventions by professional popular musicians—A scoping review

2021 ◽  
pp. 030573562110194
Author(s):  
Amy Visser ◽  
Megan Lee ◽  
Timothy Barringham ◽  
Nasim Salehi
Keyword(s):  
Mental Health ◽  
Scoping Review ◽  
Distinct Group ◽  
Well Being ◽  
Health Interventions ◽  
Therapeutic Approaches ◽  
Increased Risk ◽  
Mental Health Interventions ◽  
Industry Peers

Professional popular musicians are at increased risk of psychological distress, substance use problems, and suicide, yet little evidence is available on effective psychotherapeutic practices to address these issues. This scoping review aims to understand how professional popular musicians perceive, engage with, and respond to mental health interventions. Four databases were searched, garnering a total of 310 articles. Of these, six met inclusion criteria. Four thematic categories were explored: (1) amenability of professional popular musicians to particular therapeutic approaches; (2) attribution of treatment outcomes to tailored approaches; (3) professional popular musicians’ perceived barriers to treatment; and (4) recommendations for treatment approaches. The scoping review supports the importance of considering the characteristics of professional popular musicians as a distinct group with unique well-being needs, challenges, and strengths. There is a clear preference for tailored, affordable, and accessible approaches that consider the uniquities of musicianship and the need to explore the role of nonclinical support, such as friends, family, and industry peers.

scholarly journals Role of the IL33 and IL1RL1 pathway in the pathogenesis of Immunoglobulin A vasculitis

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Diana Prieto-Peña ◽  
Sara Remuzgo-Martínez ◽  
Fernanda Genre ◽  
Verónica Pulito-Cueto ◽  
Belén Atienza-Mateo ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Disease Onset ◽  
Immunoglobulin A ◽  
Genetic Network ◽  
Signalling Pathway ◽  
Immune Mediated ◽  
Increased Risk ◽  
Genotype And Allele Frequencies ◽  
Immunoglobulin A Vasculitis

AbstractCytokines signalling pathway genes are crucial factors of the genetic network underlying the pathogenesis of Immunoglobulin-A vasculitis (IgAV), an inflammatory vascular condition. An influence of the interleukin (IL)33- IL1 receptor like (IL1RL)1 signalling pathway on the increased risk of several immune-mediated diseases has been described. Accordingly, we assessed whether the IL33-IL1RL1 pathway represents a novel genetic risk factor for IgAV. Three tag polymorphisms within IL33 (rs3939286, rs7025417 and rs7044343) and three within IL1RL1 (rs2310173, rs13015714 and rs2058660), that also were previously associated with several inflammatory diseases, were genotyped in 380 Caucasian IgAV patients and 845 matched healthy controls. No genotypes or alleles differences were observed between IgAV patients and controls when IL33 and IL1RL1 variants were analysed independently. Likewise, no statistically significant differences were found in IL33 or IL1RL1 genotype and allele frequencies when IgAV patients were stratified according to the age at disease onset or to the presence/absence of gastrointestinal (GI) or renal manifestations. Similar results were disclosed when IL33 and IL1RL1 haplotypes were compared between IgAV patients and controls and between IgAV patients stratified according to the clinical characteristics mentioned above. Our results suggest that the IL33-IL1RL1 signalling pathway does not contribute to the genetic network underlying IgAV.

scholarly journals Targeting Hedgehog Signalling through the Ubiquitylation Process: The Multiple Roles of the HECT-E3 Ligase Itch

Cells ◽  
2019 ◽  
Vol 8 (2) ◽  
pp. 98 ◽  
Author(s):  
Paola Infante ◽  
Ludovica Lospinoso Severini ◽  
Flavia Bernardi ◽  
Francesca Bufalieri ◽  
Lucia Di Marcotullio
Keyword(s):  
E3 Ligase ◽  
Multiple Roles ◽  
Post Translational Modification ◽  
Therapeutic Approaches ◽  
Cellular Functions ◽  
Hedgehog Signalling ◽  
Promising Target ◽  
Important Pathway ◽  
Multiple Levels

Hedgehog signalling (Hh) is a developmental conserved pathway strongly involved in cancers when deregulated. This important pathway is orchestrated by numerous regulators, transduces through distinct routes and is finely tuned at multiple levels. In this regard, ubiquitylation processes stand as essential for controlling Hh pathway output. Although this post-translational modification governs proteins turnover, it is also implicated in non-proteolytic events, thereby regulating the most important cellular functions. The HECT E3 ligase Itch, well known to control immune response, is emerging to have a pivotal role in tumorigenesis. By illustrating Itch specificities on Hh signalling key components, here we review the role of this HECT E3 ubiquitin ligase in suppressing Hh-dependent tumours and explore its potential as promising target for innovative therapeutic approaches.

scholarly journals Myeloperoxidase Modulates Hydrogen Peroxide Mediated Cellular Damage in Murine Macrophages

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1255
Author(s):  
Chaorui Guo ◽  
Inga Sileikaite ◽  
Michael J. Davies ◽  
Clare L. Hawkins
Keyword(s):  
Hydrogen Peroxide ◽  
Hypochlorous Acid ◽  
Cell Function ◽  
Inflammatory Diseases ◽  
Innate Immune ◽  
Cellular Damage ◽  
Enzymatic System ◽  
Therapeutic Approaches ◽  
Macrophage Cell

Myeloperoxidase (MPO) is involved in the development of many chronic inflammatory diseases, in addition to its key role in innate immune defenses. This is attributed to the excessive production of hypochlorous acid (HOCl) by MPO at inflammatory sites, which causes tissue damage. This has sparked wide interest in the development of therapeutic approaches to prevent HOCl-induced cellular damage including supplementation with thiocyanate (SCN−) as an alternative substrate for MPO. In this study, we used an enzymatic system composed of glucose oxidase (GO), glucose, and MPO in the absence and presence of SCN−, to investigate the effects of generating a continuous flux of oxidants on macrophage cell function. Our studies show the generation of hydrogen peroxide (H2O2) by glucose and GO results in a dose- and time-dependent decrease in metabolic activity and cell viability, and the activation of stress-related signaling pathways. Interestingly, these damaging effects were attenuated by the addition of MPO to form HOCl. Supplementation with SCN−, which favors the formation of hypothiocyanous acid, could reverse this effect. Addition of MPO also resulted in upregulation of the antioxidant gene, NAD(P)H:quinone acceptor oxidoreductase 1. This study provides new insights into the role of MPO in the modulation of macrophage function, which may be relevant to inflammatory pathologies.

scholarly journals Autophagy Intertwines with Different Diseases—Recent Strategies for Therapeutic Approaches

Diseases ◽  
2019 ◽  
Vol 7 (1) ◽  
pp. 15 ◽  
Author(s):  
Janani Ramesh ◽  
Larance Ronsard ◽  
Anthony Gao ◽  
Bhuvarahamurthy Venugopal
Keyword(s):  
Inflammatory Diseases ◽  
Therapeutic Strategies ◽  
Open Reading Frames ◽  
Signaling Cascades ◽  
Progression Rate ◽  
Therapeutic Approaches ◽  
Genes Encoding ◽  
Novel Therapeutic Strategies ◽  
Reading Frames

Autophagy is a regular and substantial “clear-out process” that occurs within the cell and that gets rid of debris that accumulates in membrane-enclosed vacuoles by using enzyme-rich lysosomes, which are filled with acids that degrade the contents of the vacuoles. This machinery is well-connected with many prevalent diseases, including cancer, HIV, and Parkinson’s disease. Considering that autophagy is well-known for its significant connections with a number of well-known fatal diseases, a thorough knowledge of the current findings in the field is essential in developing therapies to control the progression rate of diseases. Thus, this review summarizes the critical events comprising autophagy in the cellular system and the significance of its key molecules in manifesting this pathway in various diseases for down- or upregulation. We collectively reviewed the role of autophagy in various diseases, mainly neurodegenerative diseases, cancer, inflammatory diseases, and renal disorders. Here, some collective reports on autophagy showed that this process might serve as a dual performer: either protector or contributor to certain diseases. The aim of this review is to help researchers to understand the role of autophagy-regulating genes encoding functional open reading frames (ORFs) and its connection with diseases, which will eventually drive better understanding of both the progression and suppression of different diseases at various stages. This review also focuses on certain novel therapeutic strategies which have been published in the recent years based on targeting autophagy key proteins and its interconnecting signaling cascades.

scholarly journals MPNs as Inflammatory Diseases: The Evidence, Consequences, and Perspectives

2015 ◽  
Vol 2015 ◽  
pp. 1-16 ◽  
Author(s):  
Hans Carl Hasselbalch ◽  
Mads Emil Bjørn
Keyword(s):  
Chronic Inflammation ◽  
Residual Disease ◽  
Inflammatory Diseases ◽  
Myeloproliferative Neoplasms ◽  
Clonal Evolution ◽  
Increased Risk ◽  
Comorbidity Burden ◽  
To Come ◽  
New Treatment

In recent years the evidence is increasing that chronic inflammation may be an important driving force for clonal evolution and disease progression in the Philadelphia-negative myeloproliferative neoplasms (MPNs), essential thrombocythemia (ET), polycythemia vera (PV), and myelofibrosis (MF). Abnormal expression and activity of a number of proinflammatory cytokines are associated with MPNs, in particular MF, in which immune dysregulation is pronounced as evidenced by dysregulation of several immune and inflammation genes. In addition, chronic inflammation has been suggested to contribute to the development of premature atherosclerosis and may drive the development of other cancers in MPNs, both nonhematologic and hematologic. The MPN population has a substantial inflammation-mediated comorbidity burden. This review describes the evidence for considering the MPNs as inflammatory diseases,A Human Inflammation Model of Cancer Development, and the role of cytokines in disease initiation and progression. The consequences of this model are discussed, including the increased risk of second cancers and other inflammation-mediated diseases, emphasizing the urgent need for rethinking our therapeutic approach. Early intervention with interferon-alpha2, which as monotherapy has been shown to be able to induce minimal residual disease, in combination with potent anti-inflammatory agents such as JAK-inhibitors is foreseen as the most promising new treatment modality in the years to come.

scholarly journals Neuroprotective activity of orexin system in ischemic stroke

2018 ◽  
Vol 17 (2) ◽  
pp. 4-11
Author(s):  
I. A. Filchenko ◽  
Yu. V. Sviryaev ◽  
T. D. Vlasov
Keyword(s):  
Ischemic Stroke ◽  
Brain Damage ◽  
Neuroprotective Activity ◽  
Therapeutic Approaches ◽  
Common Features ◽  
Protective Potential ◽  
New Methods ◽  
New Therapeutic Approaches ◽  
The Common

The protective potential of orexin system is a field of interest in the search of the new methods to diminish brain damage in ischemic stroke. The cytoprotective potential of orexins in hypoxic damage is associated with their antioxidant, anti-inflammatory and anti-apoptotic properties and with their ability to activate proliferation and normalize metabolism. Even though today little is known about the role of orexins in memory and pain in ischemic stroke, the common features of the pathogenesis of these disruptions and the mechanisms of orexin-associated protection could suggest the opportunity to use of orexins for correction of these complications following ischemic stroke. Further studies of the orexin-associated neuroprotection could become the further step on the way to the new therapeutic approaches in ischemic stroke.

scholarly journals Osteoclasts contribute to early development of chronic inflammation by promoting dysregulated hematopoiesis and myeloid skewing

2020 ◽  
Author(s):  
Maria-Bernadette Madel ◽  
Lidia Ibáñez ◽  
Thomas Ciucci ◽  
Julia Halper ◽  
Majlinda Topi ◽  
...  
Keyword(s):  
Inflammatory Diseases ◽  
Myeloid Differentiation ◽  
Chronic Colitis ◽  
Therapeutic Blockade ◽  
Hematopoietic Stem ◽  
Chronic Inflammatory Diseases ◽  
Promising Target ◽  
Proliferation And Differentiation ◽  
Early Phases

ABSTRACTIncreased myelopoiesis is a hallmark of many chronic inflammatory diseases. However, the mechanisms involved in the myeloid skewing of hematopoiesis upon inflammation are still incompletely understood. Here, we identify an unexpected role of bone-resorbing osteoclasts in promoting hematopoietic stem cell (HSC) proliferation and differentiation towards myeloipoiesis in the early phases of chronic colitis. RNAseq analysis revealed that osteoclasts in colitis differ from control ones and overexpress genes involved in the remodeling of HSC niches. We showed that colitic osteoclasts modulate the interaction of HSCs with their niche and promote myeloid differentiation. Increased osteoclast activity was correlated with an augmentation of myelopoiesis in patients with chronic colitis. Therapeutic blockade of osteoclasts reduced HSC proliferation and myeloid skewing and resulted in a decreased inflammation and severity of colitis. Together, these data identify osteoclasts as potent regulators of HSCs and promising target in chronic colitis.

Neuroprotection for Spine Surgery

2017 ◽  
Author(s):  
Jess W. Brallier ◽  
Jonathan S. Gal
Keyword(s):  
Evoked Potentials ◽  
Spine Surgery ◽  
Motor Evoked Potentials ◽  
Neurologic Injury ◽  
Arterial Blood ◽  
Increased Risk ◽  
Physiologic Parameter ◽  
The Common ◽  
Transcranial Motor Evoked Potentials

Perioperative neurologic injury related to spine surgery, albeit rare, can result in devastating functional loss. As the number of spine operations has increased, so has the need for strategies designed to avoid and protect against such injury. This chapter reviews the common etiologies of neurologic deficits secondary to spine surgery and the factors that place patients at increased risk for developing these complications. The use of intraoperative neuromonitoring, including somatosensory evoked potentials (SSEPs), electromyography (EMG), and transcranial motor evoked potentials (TcMEPs), to detect surgical trespass of neuronal elements is also reviewed. The authors also summarize the role of physiologic parameter optimization, including mean arterial blood pressure and body temperature, and pharmacologic interventions, should an injury occur. Current practice guidelines for preventing and managing perioperative neurologic injury are described.

Chronic Inflammatory Diseases and Atherosclerotic Cardiovascular Disease: Innocent Bystanders or Partners in Crime?

2018 ◽  
Vol 24 (3) ◽  
pp. 281-290 ◽  
Author(s):  
Peter Riis Hansen
Keyword(s):  
Risk Factors ◽  
Cardiovascular Disease ◽  
Inflammatory Diseases ◽  
Atherosclerotic Cardiovascular Disease ◽  
Cvd Risk Factors ◽  
Cvd Risk ◽  
Chronic Inflammatory Diseases ◽  
Increased Risk ◽  
Shared Risk

Inflammation plays a significant role in atherosclerosis and cardiovascular disease (CVD). Patients with chronic inflammatory diseases are at increased risk of CVD, but it is debated whether this association is causal or dependent on shared risk factors, other exposures, genes, and/or inflammatory pathways. The current review summarizes epidemiological, clinical, and experimental data supporting the role of shared inflammatory mechanisms between atherosclerotic CVD and rheumatoid arthritis, psoriasis, inflammatory bowel disease, and periodontitis, respectively, and provides insights to future prospects in this area of research. Awareness of the role of inflammation in CVD in patients with chronic inflammatory diseases and the potential for anti-inflammatory therapy, e.g., with tumor necrosis factor-α inhibitors, to also reduce atherosclerotic CVD has evolved into guideline- based recommendations. These include regular CVD risk assessment, aggressive treatment of traditional CVD risk factors, and recognition of reduced CVD as an added benefit of strict inflammatory disease control. At present, chronic inflammatory diseases would appear to qualify as partners in crime and not merely innocent bystanders to CVD. However, definite incremental contributions of inflammation versus effects of the complex interplay with other CVD risk factors may never be fully elucidated and for the foreseeable future, inflammation is posed to maintain its current position as both a marker and a maker of CVD, with clinical utility both for identification of patient at risk of CVD and as target for therapy to reduce CVD.

Sign in / Sign up

Export Citation Format

Share Document