Database : MEDLINE
Search on : autoimmune and diseases [Words]
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[PMID]: 29524883
[Au] Autor:Luo L; Gao Y; Yang C; Shao Z; Wu X; Li S; Xiong L; Chen C
[Ad] Address:Department of Otolaryngology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China.
[Ti] Title:Halofuginone attenuates intervertebral discs degeneration by suppressing collagen I production and inactivating TGFß and NF-кB pathway.
[So] Source:Biomed Pharmacother;101:745-753, 2018 Mar 07.
[Is] ISSN:1950-6007
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Most low back pain is caused by intervertebral discs (IVD) degeneration, a disease that prevalence is increasing with age. Halofuginone, an analog of ferbrifugine isolated from plant Dichroa febrifuga, has drawn much attention in recent years for the wide range of bioactivities in malaria, cancer, fibrotic and autoimmune diseases. In this study, we evaluated the benefit effects of halofuginone in IVD degeneration treatment in a validated rabbit puncture model. Halofuginone treatment could attenuate disc degeneration by suppressing the decrease of discs height and nucleus pulposus signal strength. Besides, halofuginone treatment could suppress mRNA and protein expression of collagen I in nucleus pulposus. This might possibly due to the inactivation of transform growth factor-ß (TGFß) signal pathway by down-regulating p-Samd3 and up-regulating inhibitory Smad7. Then, we evaluated the effects of halofuginone treatment on nuclear factor of kappa B (NF-κB) signal pathway and its downstream pro-inflammatory cytokines. The level of p-p65 and p-IκBα was down-regulated in halofuginone treated group, indicating the inactivation of NF-κB signal pathway. The mRNA expression of interleukin 1ß (IL-1ß), tumor necrosis factor α (TNF-α), interleukin 6 (IL-6) and interleukin 8 (IL-8) was decreased in nucleus pulposus too, indicating the down-regulation of pro-inflammatory cytokines. In conclusion, halofuginone treatment could attenuate IVD degeneration and this was possibly due to suppressing of collagen I production and inactivation of TGFß and NF-κB signal pathway in nucleus pulposus of degenerated discs. These results suggest that halofuginone has the potential for IVD degeneration treatment, but more research is needed to validate this.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  2 / 119510 MEDLINE  
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[PMID]: 29524758
[Au] Autor:Shahmohammadi S; Sahraian MA; Shahmohammadi A; Doosti R; Zare-Mirzaie A; Naser Moghadasi A
[Ad] Address:MS Research Center, Neuroscience Institute, Tehran University of Medical Sciences, Tehran, Iran.
[Ti] Title:A presentation of ulcerative colitis after rituximab therapy in a patient with multiple sclerosis and literature review.
[So] Source:Mult Scler Relat Disord;22:22-26, 2018 Mar 01.
[Is] ISSN:2211-0356
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Multiple sclerosis (MS) is one of the most important demyelinating diseases that affects the central nervous system. Its treatment often involves a long-term disease modifying therapy. According to some studies, the prevalence of autoimmune disorders, such as autoimmune hepatitis (AIH) and ulcerative colitis (UC) is higher in MS patients than in the normal population. There are also few studies that have reported the onset of UC after rituximab therapy. The present study presents a report of a 31-years old female patient suffering from aggressive multiple sclerosis, which developed into autoimmune hepatitis during the MS therapy. Thereafter, she received rituximab for the treating both MS and AIH. One week after the third cycle of rituximab (6 doses of 1000 mg), she experienced abdominal pain, fever, and severe bloody diarrhea; finally, she was diagnosed with ulcerative colitis (UC). It seems that the administration of certain immunomodulators or immunosuppressive drugs may have a main role in the exacerbation of some autoimmune diseases.
[Pt] Publication type:JOURNAL ARTICLE; REVIEW
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  3 / 119510 MEDLINE  
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[PMID]: 29524647
[Au] Autor:Zhao M; Wu J; Li X; Gao Y
[Ad] Address:Department of Laboratory Medicine, Beijing Hospital, National Center of Gerontology, Beijing, China; Department of Pathophysiology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences, School of Basic Medicine, Peking Union Medical College, Beijing, China.
[Ti] Title:Urinary candidate biomarkers in an experimental autoimmune myocarditis rat model.
[So] Source:J Proteomics;, 2018 Mar 07.
[Is] ISSN:1876-7737
[Cp] Country of publication:Netherlands
[La] Language:eng
[Ab] Abstract:Urine is a better source than plasma for biomarker studies, as it can accumulate all changes in the body. Various candidate urinary biomarkers of physiological condition, kidney disease and even brain dysfunction, have been detected in urine; however, urine has rarely been used to reflect cardiac diseases. In this study, urine at day 0, 14, 21 and 28 were collected from the myosin-induced autoimmune myocarditis rat models. The candidate urinary biomarkers were then characterized using the isobaric tandem mass tag labeling approach coupled with offline two-dimensional reverse-phase liquid chromatography and high-resolution mass spectrometry. Compared with controls, forty-six urinary proteins were significantly changed in the myocarditis rats; among them, ten had previously been associated with myocarditis, twelve corresponding gene products had annotated as mainly cardiovascular network genes by the Ingenuity Pathway Analysis, four urinary proteins were validated by western blot, thirteen were reported in previous urine proteome studies of other diseases and twenty-six were reported the first time to be related to myocarditis. SIGNIFICANCE: This is the first study to use isobaric tandem mass tag labeling approach in the urine proteome analysis of experimental autoimmune myocarditis. These findings may provide clues for the pathogenesis of myocarditis. And the study showed that urine can be a good source of myocarditis biomarkers.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

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[PMID]: 29524589
[Au] Autor:Sigaux J; Biton J; André E; Semerano L; Boissier MC
[Ad] Address:Inserm UMR 1125, 74, rue Marcel Cachin, 93017, Bobigny, France; Sorbonne Paris Cité - Université Paris 13, 74, rue Marcel Cachin 93017, Bobigny, France; Service de Rhumatologie, Assistance Publique-Hôpitaux de Paris (AP-HP) Groupe hospitalier Avicenne -Jean Verdier- René Muret, 125, rue de Stalingra
[Ti] Title:Air Pollution as a Determinant of Rheumatoid Arthritis.
[So] Source:Joint Bone Spine;, 2018 Mar 07.
[Is] ISSN:1778-7254
[Cp] Country of publication:France
[La] Language:eng
[Ab] Abstract:Pollution has long been incriminated in many cardiovascular and respiratory diseases. More recently, studies evaluated the potential role for particulate pollutants in autoimmune diseases, including rheumatoid arthritis (RA). The incidence of RA was found to be higher in urban areas. Living near air pollution emitters was associated with higher risks of developing RA and of producing RA-specific autoantibodies. Nevertheless, no strong epidemiological evidence exists to link one or more specific air pollution particles to RA. The presence in the bronchi of lymphoid satellite islands (inducible bronchus-associated lymphoid tissue, iBALT) is strongly associated with both inflammatory lung disease and RA-associated lung disease. Diesel exhaust particles can stimulate iBALT formation. The induction by air pollution of an inflammatory environment with high citrullination levels in the lung may induce iBALT formation, thereby causing a transition toward a more specific immune response via the production of anti-citrullinated peptide antibodies. Air pollution not only triggers innate immune responses at the molecular level, increasing the levels of proinflammatory cytokines and reactive oxygen species, but is also involved in adaptive immune responses. Thus, via the aryl hydrocarbon receptor (AHR), diesel exhaust particles can trigger a T-cell switch to the Th17 profile. Finally, in the murine collagen-induced arthritis model, animals whose lymphocytes lack the AHR develop milder arthritis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  5 / 119510 MEDLINE  
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[PMID]: 29500307
[Au] Autor:Maryanovich M; Takeishi S; Frenette PS
[Ad] Address:Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461.
[Ti] Title:Neural Regulation of Bone and Bone Marrow.
[So] Source:Cold Spring Harb Perspect Med;, 2018 Mar 02.
[Is] ISSN:2157-1422
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Bones provide both skeletal scaffolding and space for hematopoiesis in its marrow. Previous work has shown that these functions were tightly regulated by the nervous system. The central and peripheral nervous systems tightly regulate compact bone remodeling, its metabolism, and hematopoietic homeostasis in the bone marrow (BM). Accumulating evidence indicates that the nervous system, which fine-tunes inflammatory responses and alterations in neural functions, may regulate autoimmune diseases. Neural signals also influence the progression of hematological malignancies such as acute and chronic myeloid leukemias. Here, we review the interplay of the nervous system with bone, BM, and immunity, and discuss future challenges to target hematological diseases through modulation of activity of the nervous system.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher

  6 / 119510 MEDLINE  
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[PMID]: 29476963
[Au] Autor:Klasen C; Ziehm T; Huber M; Asare Y; Kapurniotu A; Shachar I; Bernhagen J; El Bounkari O
[Ad] Address:Department of Vascular Biology, Institute for Stroke and Dementia Research (ISD), Klinikum der Universität München, Ludwig-Maximilians-University of Munich (LMU), Feodor-Lynen-Straße 17, D-81377 Munich, Germany.
[Ti] Title:LPS-mediated cell surface expression of CD74 promotes the proliferation of B cells in response to MIF.
[So] Source:Cell Signal;46:32-42, 2018 Feb 21.
[Is] ISSN:1873-3913
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Macrophage migration inhibitory factor (MIF) is a chemokine-like inflammatory cytokine, which plays a pivotal role in the pathogenesis of inflammatory and cardiovascular diseases as well as cancer. We previously identified MIF as a novel B cell chemokine that promotes B cell migration through non-cognate interaction with the CXC chemokine receptor CXCR4 and CD74, the surface form of MHC class II invariant chain. In this study, we have analyzed the regulation of the MIF receptors under inflammatory conditions by investigating the impact of lipopolysaccharide (LPS), tumor necrosis factor-α (TNF-α) and interleukin-1ß (IL-1ß) on CD74 and CXCR4 expression in B lymphocytes. We found that both LPS and TNF-α stimulation of primary B cells and the human B myeloma cell line RPMI-8226 enhanced protein expression as well as mRNA levels of CD74 in a time- and dose-dependent manner. By contrast, no effect on CXCR4 expression was observed. Selective inhibition of IκBα phosphorylation significantly attenuated LPS-induced expression of CD74, suggesting the contribution of NF-κB signaling pathways to the regulation of CD74 expression. Importantly, individual or simultaneous blockade of MIF or CD74 using specific neutralizing antibodies markedly affected B cell proliferation after LPS exposure. Taken together, our findings unveil a connection between the pro-proliferative activity of MIF/CD74 signaling in B cells and inflammation, offering novel target mechanisms in inflammatory cardiovascular or autoimmune pathogenesis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher

  7 / 119510 MEDLINE  
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[PMID]: 29362796
[Au] Autor:Bouillon K; Bertrand M; Bader G; Lucot JP; Dray-Spira R; Zureik M
[Ad] Address:Department of Epidemiology of Health Products, French National Agency for Medicines and Health Products Safety (ANSM), Saint-Denis, France.
[Ti] Title:Association of Hysteroscopic vs Laparoscopic Sterilization With Procedural, Gynecological, and Medical Outcomes.
[So] Source:JAMA;319(4):375-387, 2018 01 23.
[Is] ISSN:1538-3598
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Importance: Safety of hysteroscopic sterilization has been recently questioned following reports of general symptoms such as allergy, tiredness, and depression in addition to associated gynecological results such as pelvic pain, perforation of fallopian tubes or uterus, and unwanted pregnancy. Objective: To compare the risk of reported adverse events between hysteroscopic and laparoscopic sterilization. Design, Setting, and Participants: French nationwide cohort study using the national hospital discharge database linked to the health insurance claims database. Women aged 30 to 54 years receiving a first hysteroscopic or laparoscopic sterilization between 2010 and 2014 were included and were followed up through December 2015. Exposures: Hysteroscopic sterilization vs laparoscopic sterilization. Main Outcomes and Measures: Risks of procedural complications (surgical and medical) and of gynecological (sterilization failure that includes salpingectomy, second sterilization procedure, or pregnancy; pregnancy; reoperation) and medical outcomes (all types of allergy; autoimmune diseases; thyroid disorder; use of analgesics, antimigraines, antidepressants, benzodiazepines; outpatient visits; sickness absence; suicide attempts; death) that occurred within 1 and 3 years after sterilization were compared using inverse probability of treatment-weighted Cox models. Results: Of the 105 357 women included (95.5% of eligible participants; mean age, 41.3 years [SD, 3.7 years]), 71 303 (67.7% ) underwent hysteroscopic sterilization, and 34 054 (32.3%) underwent laparoscopic sterilization. During the hospitalization for sterilization, risk of surgical complications for hysteroscopic sterilization was lower: 0.13% for hysteroscopic sterilization vs 0.78% for laparoscopic sterilization (adjusted risk difference [RD], -0.64; 95% CI, -0.67 to -0.60) and was lower for medical complications: 0.06% vs 0.11% (adjusted RD, -0.05; 95% CI, -0.08 to -0.01). During the first year after sterilization, 4.83% of women who underwent hysteroscopic sterilization had a higher risk of sterilization failure than the 0.69% who underwent laparoscopic sterilization (adjusted hazard ratio [HR], 7.11; 95% CI, 5.92 to 8.54; adjusted RD, 4.23 per 100 person-years; 95% CI, 3.40 to 5.22). Additionally, 5.65% of women who underwent hysteroscopic sterilization required gynecological reoperation vs 1.76% of women who underwent laparoscopic sterilization (adjusted HR, 3.26; 95% CI, 2.90 to 3.67; adjusted RD, 4.63 per 100 person-years; 95% CI, 3.38 to 4.75); these differences persisted after 3 years, although attenuated. Hysteroscopic sterilization was associated with a lower risk of pregnancy within the first year of the procedure but was not significantly associated with a difference in risk of pregnancy by the third year (adjusted HR, 1.04; 95% CI, 0.83-1.30; adjusted RD, 0.01 per 100 person-years; 95% CI, -0.04 to 0.07). Risks of medical outcomes were not significantly increased with hysteroscopic sterilization compared with laparoscopic sterilization. Conclusions and Relevance: Among women undergoing first sterilization, the use of hysteroscopic sterilization was significantly associated with higher risk of gynecological complications over 1 year and over 3 years than was laparoscopic sterilization. Risk of medical outcomes was not significantly increased over 1 year or over 3 years. These findings do not support increased medical risks associated with hysteroscopic sterilization.
[Mh] MeSH terms primary: Hysteroscopy/adverse effects
Laparoscopy/adverse effects
Postoperative Complications/etiology
Sterilization, Tubal/methods
[Mh] MeSH terms secundary: Adult
Cohort Studies
Female
France
Humans
Middle Aged
Postoperative Complications/epidemiology
Pregnancy
Pregnancy, Unplanned
Reoperation/statistics & numerical data
Sterilization, Tubal/adverse effects
Treatment Failure
[Pt] Publication type:COMPARATIVE STUDY; JOURNAL ARTICLE; OBSERVATIONAL STUDY
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[Js] Journal subset:AIM; IM
[Da] Date of entry for processing:180125
[St] Status:MEDLINE
[do] DOI:10.1001/jama.2017.21269

  8 / 119510 MEDLINE  
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[PMID]: 29341591
[Au] Autor:Nemmara VV; Subramanian V; Muth A; Mondal S; Salinger AJ; Maurais AJ; Tilvawala R; Weerapana E; Thompson PR
[Ad] Address:Department of Biochemistry and Molecular Pharmacology, UMass Medical School , 364 Plantation Street, Worcester, Massachusetts 01605, United States.
[Ti] Title:The Development of Benzimidazole-Based Clickable Probes for the Efficient Labeling of Cellular Protein Arginine Deiminases (PADs).
[So] Source:ACS Chem Biol;, 2018 Feb 01.
[Is] ISSN:1554-8937
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:Citrullination is the post-translational hydrolysis of peptidyl-arginines to form peptidyl-citrulline, a reaction that is catalyzed by the protein arginine deiminases (PADs), a family of calcium-regulated enzymes. Aberrantly increased protein citrullination is associated with a slew of autoimmune diseases (e.g., rheumatoid arthritis (RA), multiple sclerosis, lupus, and ulcerative colitis) and certain cancers. Given the clear link between increased PAD activity and human disease, the PADs are therapeutically relevant targets. Herein, we report the development of next generation cell permeable and "clickable" probes (BB-Cl-Yne and BB-F-Yne) for covalent labeling of the PADs both in vitro and in cell-based systems. Using advanced chemoproteomic technologies, we also report the off targets of both BB-Cl-Yne and BB-F-Yne. The probes are highly specific for the PADs, with relatively few off targets, especially BB-F-Yne, suggesting the preferential use of the fluoroacetamidine warhead in next generation irreversible PAD inhibitors. Notably, these compounds can be used in a variety of modalities, including the identification of off targets of the parent compounds and as activity-based protein profiling probes in target engagement assays to demonstrate the efficacy of PAD inhibitors.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:Publisher
[do] DOI:10.1021/acschembio.7b00957

  9 / 119510 MEDLINE  
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[PMID]: 29228214
[Au] Autor:Kim RY; Mangu D; Hoffman AS; Kavosh R; Jung E; Itoh N; Voskuhl R
[Ad] Address:Multiple Sclerosis Program, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
[Ti] Title:Oestrogen receptor β ligand acts on CD11c+ cells to mediate protection in experimental autoimmune encephalomyelitis.
[So] Source:Brain;141(1):132-147, 2018 01 01.
[Is] ISSN:1460-2156
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Oestrogen treatments are neuroprotective in a variety of neurodegenerative disease models. Selective oestrogen receptor modifiers are needed to optimize beneficial effects while minimizing adverse effects to achieve neuroprotection in chronic diseases. Oestrogen receptor beta (ERβ) ligands are potential candidates. In the multiple sclerosis model chronic experimental autoimmune encephalomyelitis, ERβ-ligand treatment is neuroprotective, but mechanisms underlying this neuroprotection remain unclear. Specifically, whether there are direct effects of ERβ-ligand on CD11c+ microglia, myeloid dendritic cells or macrophages in vivo during disease is unknown. Here, we generated mice with ERβ deleted from CD11c+ cells to show direct effects of ERβ-ligand treatment in vivo on these cells to mediate neuroprotection during experimental autoimmune encephalomyelitis. Further, we use bone marrow chimeras to show that ERβ in peripherally derived myeloid cells, not resident microglia, are the CD11c+ cells mediating this protection. CD11c+ dendritic cell and macrophages isolated from the central nervous system of wild-type experimental autoimmune encephalomyelitis mice treated with ERβ-ligand expressed less iNOS and T-bet, but more IL-10, and this treatment effect was lost in mice with specific deletion of ERβ in CD11c+ cells. Also, we extend previous reports of ERβ-ligand’s ability to enhance remyelination through a direct effect on oligodendrocytes by showing that the immunomodulatory effect of ERβ-ligand acting on CD11c+ cells is necessary to permit the maturation of oligodendrocytes. Together these results demonstrate that targeting ERβ signalling pathways in CD11c+ myeloid cells is a novel strategy for regulation of the innate immune system in neurodegenerative diseases. To our knowledge, this is the first report showing how direct effects of a candidate neuroprotective treatment on two distinct cell lineages (bone marrow derived myeloid cells and oligodendrocytes) can have complementary neuroprotective effects in vivo.awx315media15688130498001.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1712
[Cu] Class update date: 180311
[Lr] Last revision date:180311
[St] Status:In-Data-Review
[do] DOI:10.1093/brain/awx315

  10 / 119510 MEDLINE  
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[PMID]: 29524279
[Au] Autor:Dumas M; Hua C; Hotz C; Velter C; Duong TA; Maraffi T; Ortonne N; Hüe S; Fardet L; de Prost N; Wolkenstein P; Ingen-Housz-Oro S; Chosidow O
[Ad] Address:Dermatology department, AP-HP, Henri Mondor hospital, Créteil, France.
[Ti] Title:Epidermal necrolysis and autoimmune diseases: two more observations supporting the concept that "toxic" epidermal necrolysis can be "non-toxic".
[So] Source:J Eur Acad Dermatol Venereol;, 2018 Mar 10.
[Is] ISSN:1468-3083
[Cp] Country of publication:England
[La] Language:eng
[Ab] Abstract:Toxic epidermal necrolysis (TEN, Lyell syndrome) and Stevens-Johnson syndrome are severe cutaneous adverse reactions to drugs characterized by epidermal necrolysis (EN). However, in 15% of cases, no causative drug is identified. In these cases, other triggers such as Mycoplasma pneumoniae have been described. Furthermore, the role of lupus as triggering factor has been suggested. We report 2 cases of EN without any drug causality, revealing autoimmune diseases as a cause. This article is protected by copyright. All rights reserved.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:Publisher
[do] DOI:10.1111/jdv.14935


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