scholarly journals Emerging Role of Eosinophils in Resolution of Arthritis

2021 ◽  
Vol 12 ◽  
Author(s):  
Yi Qin ◽  
Hui-Zhi Jin ◽  
Yu-Jing Li ◽  
Zhu Chen
Keyword(s):  
Minor Component ◽  
Chronic Inflammatory Disease ◽  
Specific Population ◽  
Resolution Of Inflammation ◽  
Effector Cells ◽  
Current Therapies ◽  
A Minor ◽  
End Stage ◽  
Pro Inflammatory Cytokines

Eosinophils are a minor component of circulating granulocytes, which are classically viewed as end-stage effector cells in host defense against helminth infection and promoting allergic responses. However, a growing body of evidence has emerged showing that eosinophils are versatile leukocytes acting as an orchestrator in the resolution of inflammation. Rheumatoid arthritis (RA) is the most common chronic inflammatory disease characterized by persistent synovitis that hardly resolves spontaneously. Noteworthy, a specific population of eosinophils, that is, regulatory eosinophils (rEos), was identified in the synovium of RA patients, especially in disease remission. Mechanistically, the rEos in the synovium display a unique pro-resolving signature that is distinct from their counterpart in the lung. Herein, we summarize the latest understanding of eosinophils and their emerging role in promoting the resolution of arthritis. This knowledge is crucial to the design of new approaches to rebalancing immune homeostasis in RA, considering that current therapies are centered on inhibiting pro-inflammatory cytokines and mediators rather than fostering the resolution of inflammation.

The Emergence of Bone Technologies at the End of the Pleistocene in Southeast Asia: Regional and Evolutionary Implications

2012 ◽  
Vol 22 (1) ◽  
pp. 37-56 ◽  
Author(s):  
Ryan J. Rabett ◽  
Philip J. Piper
Keyword(s):  
Early Modern ◽  
Large Scale ◽  
Minor Component ◽  
Modern Human ◽  
Small Element ◽  
Adaptive Process ◽  
Long Time ◽  
One Step ◽  
A Minor

For many decades Palaeolithic research viewed the development of early modern human behaviour as largely one of progress down a path towards the ‘modernity’ of the present. The European Palaeolithic sequence — the most extensively studied — was for a long time the yard-stick against which records from other regions were judged. Recent work undertaken in Africa and increasingly Asia, however, now suggests that the European evidence may tell a story that is more parochial and less universal than previously thought. While tracking developments at the large scale (the grand narrative) remains important, there is growing appreciation that to achieve a comprehensive understanding of human behavioural evolution requires an archaeologically regional perspective to balance this.One of the apparent markers of human modernity that has been sought in the global Palaeolithic record, prompted by finds in the European sequence, is innovation in bonebased technologies. As one step in the process of re-evaluating and contextualizing such innovations, in this article we explore the role of prehistoric bone technologies within the Southeast Asian sequence, where they have at least comparable antiquity to Europe and other parts of Asia. We observe a shift in the technological usage of bone — from a minor component to a medium of choice — during the second half of the Last Termination and into the Holocene. We suggest that this is consistent with it becoming a focus of the kinds of inventive behaviour demanded of foraging communities as they adapted to the far-reaching environmental and demographic changes that were reshaping this region at that time. This record represents one small element of a much wider, much longerterm adaptive process, which we would argue is not confined to the earliest instances of a particular technology or behaviour, but which forms part of an on-going story of our behavioural evolution.

Vagus Nerve Stimulation

2018 ◽  
Vol 3 (2) ◽  
pp. 54-58
Author(s):  
Eric J. Yang ◽  
Sahil Sekhon ◽  
Kristen M. Beck ◽  
Isabelle M. Sanchez ◽  
Tina Bhutani ◽  
...  
Keyword(s):  
Psoriatic Arthritis ◽  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Vagus Nerve Stimulation ◽  
Animal Studies ◽  
Chronic Inflammatory Disease ◽  
Inflammatory Processes ◽  
Current Therapies ◽  
Inflammatory Bowel

Treatments for psoriasis and psoriatic arthritis have progressed at a rapid rate over the past 20 years, but treating patients with recalcitrant disease still remains a difficult task. Current therapies for these diseases involve topical agents, phototherapy, and systemic immunosuppression. However, the role of the nervous system in psoriasis and psoriatic arthritis remains largely unexplored. Recent animal studies and clinical trials have demonstrated that vagus nerve stimulation can decrease inflammatory processes in rheumatoid arthritis and inflammatory bowel disease. In this article, we outline the existing knowledge of the nervous system’s role in chronic inflammatory disease and discuss how these findings could be utilized in the future for treatment of psoriasis and psoriatic arthritis.

scholarly journals Central-pair microtubular complex of Chlamydomonas flagella: polypeptide composition as revealed by analysis of mutants.

1981 ◽  
Vol 91 (1) ◽  
pp. 69-76 ◽  
Author(s):  
G M Adams ◽  
B Huang ◽  
G Piperno ◽  
D J Luck
Keyword(s):  
Minor Component ◽  
Cellular Growth ◽  
Two Dimensional ◽  
Wild Type ◽  
Beta Tubulin ◽  
Central Pair ◽  
Electrophoresis System ◽  
A Minor ◽  
Dimensional Electrophoresis

Four mutants of Chlamydomonas reinhardtii representing independent gene loci have been shown to lack totally (pf-18, pf-19, and pf-15) or nearly totally (pf-20) the central microtubular pair complex in isolated axonemal preparations. Analysis of 35S-labeled axonemal proteins, using two methods of electrophoresis, reveals that all four mutants lack or are markedly deficient in 18 polypeptides, ranging in molecular weight from 360,000 to 20,000, that are regularly present in wild-type axonemes. Analyses of axonemal proteins labeled by cellular growth on 32P-labeled medium indicates that a subset of 8 of the 18 polypeptides are phosphorylated. Mutant and wild-type axonemes and flagella have been analyzed for their content of tubulin subunits using a high resolution two-dimensional electrophoresis system combined with agarose gel overlays containing either anti-alpha or anti-beta tubulin sera prepared from Chlamydomonas tubulins. The immunoprecipitates identify two major alpha tubulins, a major beta tubulin, and a minor component which is also precipitated by the anti-beta serum. None of these tubulins shows a specific defect in mutant axonemes, nor do the tubulin polypeptides show altered two-dimensional map positions in the mutant flagella. The 18 polypeptides provide a useful signature for identifying other mutants affecting the central-pair microtubular complex. Such mutants could be useful in defining the structural or functional role of these polypeptides in the central microtubules. Efforts to obtain additional central-pair mutants based on the motility phenotype of the four mutants analyzed here have yielded mutants which are allelic to three of the four mutants.

scholarly journals Interleukin-35 inhibited production of histamine and pro-inflammatory cytokines through suppression MAPKs pathway in HMC-1 cells

2020 ◽  
Author(s):  
Tao Chen ◽  
Lixin Fu ◽  
Qiaomei Sun ◽  
Peimei Zhou ◽  
Zai-pei Guo
Keyword(s):  
Immune Response ◽  
Inflammatory Cytokine ◽  
Human Mast Cell ◽  
Rt Pcr ◽  
Effector Cells ◽  
Response System ◽  
Mast Cell Line ◽  
Anti Inflammatory Cytokine ◽  
Pro Inflammatory Cytokines

Abstract Background: IL-35 is a newly anti-inflammatory cytokine which belong to the IL-12 family. Mast cells, as one of the major effector cells in the immune response system, play important roles in the pathogenesis of chronic spontaneous urticarial (CSU). The aim of our study is to explore the inhibited role of IL-35 in HMC-1. Methods: The effects of IL-35 on cell proliferation, cytokine expression and histamine release in human mast cell line (HMC­1) were investigated by CCK8, ELISA or RT-PCR. The phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells were detected by Western Blot.Results: We found that IL-35 significantly inhibited the proliferation of HMC-1 cells stimulated by PMA and A23187. IL-35 also down-regulates the released of histamine and the mRNA expression of IL-6 and IL-17 in activated HMC-1. Furthermore, IL-35 markedly inhibited the phosphorylation of ERK1/2, p38 and JNK1/2, in PMA and A23187 induced HMC-1 cells. Conclusions: This study provides first observations on the inhibitory and anti-inflammtory effect of IL-35 on activated HMC-1 cells. We suggest that IL35 may play an inhibited role in the pathogenesis of CSU.

Role of ATP-sensitive K+ channels in CGRP-induced dilatation of basilar artery in vivo

1993 ◽  
Vol 265 (2) ◽  
pp. H581-H585 ◽  
Author(s):  
T. Kitazono ◽  
D. D. Heistad ◽  
F. M. Faraci
Keyword(s):  
Basilar Artery ◽  
Minor Component ◽  
K Channels ◽  
Cranial Window ◽  
Calcitonin Gene ◽  
A Minor ◽  
Oxide Synthase ◽  
Camp Levels

Stimulation of adenylate cyclase appears to activate ATP-sensitive K+ channels in the basilar artery. We tested the hypothesis that calcitonin gene-related peptide (CGRP), which increases intracellular adenosine 3',5'-cyclic monophosphate (cAMP) levels, activates ATP-sensitive K+ channels and thereby causes vasodilatation. Using a cranial window in anesthetized rats, we examined responses of the basilar artery to CGRP in vivo. We also examined responses of the artery to another vasoactive peptide, vasoactive intestinal peptide (VIP). Topical application of CGRP (10(-11) to 10(-8) M) increased diameter of the basilar artery. Responses of the basilar artery to CGRP were almost abolished by a CGRP1 receptor antagonist, CGRP-(8-37). Vasodilatation in response to VIP was much smaller than that produced by CGRP. Dilator responses of the basilar artery to 10(-9) and 10(-8) M CGRP were inhibited by glibenclamide (10(-6) M), a selective inhibitor of ATP-sensitive K+ channels, by 69 +/- 19 and 41 +/- 9%, respectively. NG-nitro-L-arginine methyl ester (10(-5) M), an inhibitor of nitric oxide synthase, did not attenuate dilator response to 10(-8) M CGRP but inhibited responses to 10(-9) M CGRP by 34 +/- 12%. Indomethacin did not alter dilator responses to CGRP. These findings suggest that a minor component of CGRP-induced dilatation of the basilar artery is mediated by endothelium-derived relaxing factor. Vasodilatation in response to CGRP appears to be mediated primarily by direct activation of CGRP1 receptors on vascular muscle.(ABSTRACT TRUNCATED AT 250 WORDS)

Biochemical studies on haemoglobin variants of the irus macaque

1966 ◽  
Vol 165 (999) ◽  
pp. 224-244 ◽  
Keyword(s):  
Minor Component ◽  
Starch Gel Electrophoresis ◽  
Red Cell ◽  
Alkaline Ph ◽  
Peptide Analysis ◽  
Simian Malaria ◽  
Starch Gel ◽  
A Minor ◽  
Recombination Experiments

Haemolysates from 202 M . irus , imported mainly from Thailand and Vietnam, were examined by starch-gel electrophoresis. In addition to the normal haemoglobin, Hb-A mi , two major haemoglobin variants designated as Hb-P mi and Hb-Q mi and two minor components were found. Hb-P mi , which occurred in 12% of the sample, forms molecular aggregates, especially when released from the red cell. Peptide analysis showed that it differs from Hb-A mi in the absence of peptides α .TP III and α -Tp IV. Sera from animals with this haemoglobin in their red cells show two haeme-positive bands in addition to the usual single haptoglobin band; this pattern can be produced in the sera of some animals which do not possess it, by addition of Hb-P mi . Hb-Q mi , which occurred in 24% of the animals, migrates anodally to Hb-A mi at alkaline pH and does not form aggregates. It is found in two ranges of concentration when present with Hb-A mi . It was shown by recombination experiments to have normal β Ami -chains. The sample was polymorphic for a minor component which was shown to have normal β Ami chains. Some animals have two major haemoglobins and also this minor component and therefore possesses three different non- β -chains. It is suggested that the minor component is the product of a mutated duplicate of the α -locus. The population genetics of these variant haemoglobins and the possible selective role of simian malaria are discussed.

scholarly journals Complement Activation Selectively Potentiates the Pathogenicity of the IgG2b and IgG3 Isotypes of a High Affinity Anti-Erythrocyte Autoantibody

2002 ◽  
Vol 195 (6) ◽  
pp. 665-672 ◽  
Author(s):  
Samareh Azeredo da Silveira ◽  
Shuichi Kikuchi ◽  
Liliane Fossati-Jimack ◽  
Thomas Moll ◽  
Takashi Saito ◽  
...  
Keyword(s):  
Affinity Maturation ◽  
Minor Role ◽  
Binding Affinities ◽  
Effector Cells ◽  
High Affinity ◽  
Erythrocyte Binding ◽  
Igg Isotypes ◽  
A Minor

By generating four IgG isotype-switch variants of the high affinity 34–3C anti-erythrocyte autoantibody, and comparing them to the IgG variants of the low affinity 4C8 anti-erythrocyte autoantibody that we have previously studied, we evaluated in this study how high affinity binding to erythrocytes influences the pathogenicity of each IgG isotype in relation to the respective contributions of Fcγ receptor (FcγR) and complement. The 34–3C autoantibody opsonizing extensively circulating erythrocytes efficiently activated complement in vivo (IgG2a = IgG2b > IgG3), except for the IgG1 isotype, while the 4C8 IgG autoantibody failed to activate complement. The pathogenicity of the 34–3C autoantibody of IgG2b and IgG3 isotypes was dramatically higher (>200-fold) than that of the corresponding isotypes of the 4C8 antibody. This enhanced activity was highly (IgG2b) or totally (IgG3) dependent on complement. In contrast, erythrocyte-binding affinities only played a minor role in in vivo hemolytic activities of the IgG1 and IgG2a isotypes of 34–3C and 4C8 antibodies, where complement was not or only partially involved, respectively. The remarkably different capacities of four different IgG isotypes of low and high affinity anti-erythrocyte autoantibodies to activate FcγR-bearing effector cells and complement in vivo demonstrate the role of autoantibody affinity maturation and of IgG isotype switching in autoantibody-mediated pathology.

scholarly journals The Role of Chemokines and Chemokine Receptors in Diabetic Nephropathy

2020 ◽  
Vol 21 (9) ◽  
pp. 3172 ◽  
Author(s):  
Ting-Ting Chang ◽  
Jaw-Wen Chen
Keyword(s):  
Diabetic Nephropathy ◽  
End Stage Renal Disease ◽  
Chemokine Receptors ◽  
Potential Role ◽  
Chronic Inflammatory Disease ◽  
Direct Effects ◽  
Stage Renal Disease ◽  
End Stage ◽  
Kidney Function Decline

Kidney function decline is one of the complications of diabetes mellitus and may be indicated as diabetic nephropathy (DN). DN is a chronic inflammatory disease featuring proteinuria and a decreasing glomerular filtration rate. Despite several therapeutic options being currently available, DN is still the major cause of end-stage renal disease. Accordingly, widespread innovation is needed to improve outcomes in patients with DN. Chemokines and their receptors are critically involved in the inflammatory progression in the development of DN. Although recent studies have shown multiple pathways related to the chemokine system, the specific and direct effects of chemokines and their receptors remain unclear. In this review, we provide an overview of the potential role and mechanism of chemokine systems in DN proposed in recent years. Chemokine system-related mechanisms may provide potential therapeutic targets in DN.

scholarly journals Escherichia coli as a platform for the study of phosphoinositide biology

2019 ◽  
Vol 5 (3) ◽  
pp. eaat4872 ◽  
Author(s):  
Sergio Botero ◽  
Rachel Chiaroni-Clarke ◽  
Sanford M. Simon
Keyword(s):  
Escherichia Coli ◽  
Minor Component ◽  
Signaling Cascades ◽  
Membrane Biology ◽  
E Coli ◽  
A Minor ◽  
Phosphatidylinositol 4

Despite being a minor component of cells, phosphoinositides are essential for eukaryotic membrane biology, serving as markers of organelle identity and involved in several signaling cascades. Their many functions, combined with alternative synthesis pathways, make in vivo study very difficult. In vitro studies are limited by their inability to fully recapitulate the complexities of membranes in living cells. We engineered the biosynthetic pathway for the most abundant phosphoinositides into the bacterium Escherichia coli, which is naturally devoid of this class of phospholipids. These modified E. coli, when grown in the presence of myo-inositol, incorporate phosphatidylinositol (PI), phosphatidylinositol-4-phosphate (PI4P), phosphatidylinositol-4,5-bisphosphate (PIP2), and phosphatidylinositol-3,4,5-trisphosphate (PIP3) into their plasma membrane. We tested models of biophysical mechanisms with these phosphoinositides in a living membrane, using our system to evaluate the role of PIP2 in nonconventional protein export of human basic fibroblast growth factor 2. We found that PI alone is sufficient for the process.

scholarly journals Activation of Adenoviral Gene Expression by Protein IX Is Not Required for Efficient Virus Replication

2004 ◽  
Vol 78 (10) ◽  
pp. 5032-5037 ◽  
Author(s):  
Kathy L. Sargent ◽  
Robert A. Meulenbroek ◽  
Robin J. Parks
Keyword(s):  
Minor Component ◽  
Transient Transfection ◽  
Minimal Effect ◽  
Protein Coding ◽  
Coding Sequences ◽  
Late Genes ◽  
Viral Promoters ◽  
Protein Ix ◽  
A Minor

ABSTRACT The adenovirus (Ad) protein IX (pIX) is a minor component of the Ad capsid and is in part responsible for virion stability; virions lacking pIX are heat labile and lose their infectivity if the DNA content is greater than ∼35 kb. More recently, pIX has been identified as a transcriptional activator and, in transient-transfection assays, was shown to enhance expression from the E1A, E4, and major late Ad promoters by as much as 70-fold. In this study, we examined the role of pIX's ability to activate transcription during Ad replication. In transient-transfection assays, pIX had a minimal effect on expression from the E1A promoter, increasing expression by only 1.4-fold. We used helper-dependent Ad vectors, which had all Ad protein coding sequences deleted with the exception of E1A and which had capsids that either contained or lacked pIX, to show that pIX derived from decapsidation of the infecting virion does not influence expression of E1A. Similarly, expression of pIX from the Ad genome did not alter the expression levels of E1A. Viruses that had pIX deleted showed a threefold reduction in virus yield and expression of late genes compared to those of a similar virus which encoded pIX. This phenotype could not be rescued by growing the virus in cells which constitutively express pIX. Our results indicate that, although pIX can affect transcription from a variety of viral promoters, it does not appear to play a significant role in activation of Ad promoters during normal Ad replication.

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