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https://www.readbyqxmd.com/read/29451482/-nuclear-sequestration-of-alarmins-as-%C3%A3-new-adenoviral-strategy-to-escape-from-innate-immunity
#1
Amandine Tisserand, Asma Boumbar, Karim Benihoud
No abstract text is available yet for this article.
February 2018: Médecine Sciences: M/S
https://www.readbyqxmd.com/read/29449623/targeted-disruption-of-the-inos-gene-improves-adipose-tissue-inflammation-and-fibrosis-in-leptin-deficient-ob-ob-mice-role-of-tenascin-c
#2
S Becerril, A Rodríguez, V Catalán, L Méndez-Giménez, B Ramírez, N Sáinz, M Llorente, X Unamuno, J Gómez-Ambrosi, G Frühbeck
BACKGROUND/OBJECTIVES: Obesity is related to a dynamic extracellular matrix (ECM) remodeling, which involves the synthesis and degradation of different proteins, such as tenascin C (TNC) in the adipose tissue (AT). Given the functional relationship between leptin and inducible nitric oxide synthase (iNOS), our aim was to analyze the impact of the absence of the iNOS gene in AT inflammation and ECM remodeling in ob/ob mice. SUBJECTS/METHODS: The expression of genes involved in inflammation and ECM remodeling was evaluated in 10-week-old male double knockout (DBKO) mice simultaneously lacking the ob and iNOS genes as well as in ob/ob mice classified into three groups [control, leptin-treated (1 mg kg -1 day -1 ) and pair-fed]...
February 15, 2018: International Journal of Obesity: Journal of the International Association for the Study of Obesity
https://www.readbyqxmd.com/read/29436517/endogenous-il-33-contributes-to-kidney-ischemia-reperfusion-injury-as-an-alarmin
#3
Maroua Ferhat, Aurélie Robin, Sébastien Giraud, Sandra Sena, Jean-Michel Goujon, Guy Touchard, Thierry Hauet, Jean-Philippe Girard, Jean-Marc Gombert, André Herbelin, Antoine Thierry
Inflammation is a prominent feature of ischemia-reperfusion injury (IRI), which is characterized by leukocyte infiltration and renal tubular injury. However, signals that initiate these events remain poorly understood. We examined the role of the nuclear alarmin IL-33 in tissue injury and innate immune response triggered by experimental kidney ischemia-reperfusion. In wild-type mice, we found that IL-33 was constitutively expressed throughout the kidney in peritubular and periglomerular spaces, mainly by microvascular endothelial cells, from which it was released immediately during IRI...
February 7, 2018: Journal of the American Society of Nephrology: JASN
https://www.readbyqxmd.com/read/29431205/non-ige-mediated-mast-cell-activation
#4
REVIEW
Frank A Redegeld, Yingxin Yu, Sangeeta Kumari, Nicolas Charles, Ulrich Blank
Mast cells (MCs) are innate immune cells that are scattered in tissues throughout the organism being particularly abundant at sites exposed to the environment such as the skin and mucosal surfaces. Generally known for their role in IgE-mediated allergies, they have also important functions in the maintenance of tissue integrity by constantly sensing their microenvironment for signals by inflammatory triggers that can comprise infectious agents, toxins, hormones, alarmins, metabolic states, etc. When triggered their main function is to release a whole set of inflammatory mediators, cytokines, chemokines, and lipid products...
March 2018: Immunological Reviews
https://www.readbyqxmd.com/read/29427515/injury-repair-inflammation-and-metaplasia-in-the-stomach
#5
Anne R Meyer, James R Goldenring
The development of intestinal-type gastric cancer is preceded by the emergence of metaplastic cell lineages in the gastric mucosa. In particular, intestinal metaplasia and spasmolytic polypeptide-expressing metaplasia (SPEM) have been associated with the pathological progression to intestinal-type gastric cancer. The development of SPEM represents a physiological response to damage that recruits reparative cells to sites of mucosal injury. Metaplastic cell lineages are characterized by mucus secretion, adding a protective barrier to the epithelium...
February 10, 2018: Journal of Physiology
https://www.readbyqxmd.com/read/29426321/systemic-autoinflammation-with-intractable-epilepsy-managed-with-interleukin-1-blockade
#6
Allen D DeSena, Thuy Do, Grant S Schulert
BACKGROUND: Autoinflammatory disorders are distinguished by seemingly random episodes of systemic hyperinflammation, driven in particular by IL-1. Recent pre-clinical work has shown a key role for IL-1 in epilepsy in animal models, and therapies for autoinflammation including IL-1 blockade are proposed for refractory epilepsy. CASE PRESENTATION: Here, we report an adolescent female with signs of persistent systemic inflammation and epilepsy unresponsive to multiple anti-epileptic drugs (AED)...
February 9, 2018: Journal of Neuroinflammation
https://www.readbyqxmd.com/read/29416668/molecular-mechanisms-of-cardioprotective-effects-mediated-by-transplanted-cardiac-ckit-cells-through-the-activation-of-an-inflammatory-hypoxia-dependent-reparative-response
#7
Giovanni Puddighinu, Domenico D'Amario, Eleonora Foglio, Melissa Manchi, Andrea Siracusano, Elena Pontemezzo, Martina Cordella, Francesco Facchiano, Laura Pellegrini, Antonella Mangoni, Marco Tafani, Filippo Crea, Antonia Germani, Matteo Antonio Russo, Federica Limana
The regenerative effects of cardiac ckit+ stem cells (ckit+CSCs) in acute myocardial infarction (MI) have been studied extensively, but how these cells exert a protective effect on cardiomyocytes is not well known. Growing evidences suggest that in adult stem cells injury triggers inflammatory signaling pathways which control tissue repair and regeneration. Aim of the present study was to determine the mechanisms underlying the cardioprotective effects of ckit+CSCs following transplantation in a murine model of MI...
January 2, 2018: Oncotarget
https://www.readbyqxmd.com/read/29399438/type-2-cytokine-responses-regulating-immunity-to-helminth-parasites-and-allergic-inflammation
#8
Everett K Henry, Juan M Inclan-Rico, Mark C Siracusa
Purpose of Review: It is well established that T helper type 2 (TH 2) immune responses are necessary to provide protection against helminth parasites but also to promote the detrimental inflammation associated with allergies and asthma. Given the importance of type 2 immunity and inflammation, many studies have focused on better understanding the factors that regulate TH 2 cell development and activation. As a result, significant progress has been made in understanding the signaling pathways and molecular events necessary to promote TH 2 cell polarization...
December 2017: Current Pharmacology Reports
https://www.readbyqxmd.com/read/29395576/reduced-hmgb1-suppresses-poly-i-c-induced-inflammation-in-keratinocytes
#9
Hideki Mori, Masamoto Murakami, Teruko Tsuda, Kenji Kameda, Ryo Utsunomiya, Kana Masuda, Ken Shiraishi, Xiuju Dai, Mikiko Tohyama, Hiroki Nakaoka, Koji Sayama
BACKGROUND: High mobility group box 1 (HMGB1) is a nuclear protein that stabilizes DNA and facilitates gene transcription. Additionally, cell stress or death induces the release of HMGB1 outside the cell membrane, where HMGB1 functions as an alarmin, causing an inflammatory response in combination with other cytokines, damage-associated molecular patterns (DAMPs), and pathogen-associated molecular patterns (PAMPs). OBJECTIVE: To evaluate the effect of reduced-HMGB1 (previously termed chemoattractive-HMGB1) on polyinosine-polycytidylic acid [poly(I:C)]-induced inflammation in normal human keratinocytes (NHKs)...
January 29, 2018: Journal of Dermatological Science
https://www.readbyqxmd.com/read/29379874/behavioral-changes-in-mice-lacking-interleukin-33
#10
Eisuke Dohi, Eric Y Choi, Indigo V L Rose, Akiho S Murata, Sharon Chow, Minae Niwa, Shin-Ichi Kano
Interleukin (IL)-33 is a member of the IL-1 family of cytokines. IL-33 is expressed in nuclei and secreted as alarmin upon cellular damage to deliver a danger signal to the surrounding cells. Previous studies showed that IL-33 is expressed in the brain and that it is involved in neuroinflammatory and neurodegenerative processes in both humans and rodents. Nevertheless, the role of IL-33 in physiological brain function and behavior remains unclear. Here, we have investigated the behaviors of mice lacking IL-33 (Il33-/- mice)...
November 2017: ENeuro
https://www.readbyqxmd.com/read/29371576/innate-immunity-to-mucosal-candida-infections
#11
REVIEW
Akash Verma, Sarah L Gaffen, Marc Swidergall
Mucosal epithelial tissues are exposed to high numbers of microbes, including commensal fungi, and are able to distinguish between those that are avirulent and those that cause disease. Epithelial cells have evolved multiple mechanisms to defend against colonization and invasion by Candida species. The interplay between mucosal epithelial tissues and immune cells is key for control and clearance of fungal infections. Our understanding of the mucosal innate host defense system has expanded recently with new studies bringing to light the importance of epithelial cell responses, innate T cells, neutrophils, and other phagocytes during Candida infections...
October 31, 2017: Journal of Fungi (Basel, Switzerland)
https://www.readbyqxmd.com/read/29366121/the-alarmin-complex-s100a8-9-as-a-potential-therapeutic-target-after-myocardial-infarction
#12
Goran Marinkovic, Laura Winkler, Lisa Kefene, Jan Nilsson, Stefan Jovinge, Alexandru Schiopu
No abstract text is available yet for this article.
August 2017: Atherosclerosis
https://www.readbyqxmd.com/read/29339456/parp-inhibition-prevents-ethanol-induced-neuroinflammatory-signaling-and-neurodegeneration-in-adult-age-rat-brain-slice-cultures
#13
Nuzhath F Tajuddin, Hee-Yong Kim, Michael A Collins
Utilizing rat adult-age hippocampal-entorhinal cortical (HEC) slice cultures we examined the role of poly [ADP-ribose] polymerase (PARP) in binge ethanol's brain inflammatory and neurodegenerative mechanisms. Activated by DNA strand breaks, PARP (principally PARP1 in brain) promotes DNA repair via poly [ADP-ribose] (PAR) products, but PARP overactivation triggers regulated neuronal necrosis, e.g., parthanatos. Previously we found that brain PARP1 levels were upregulated by neurotoxic ethanol binges in adult rats and HEC slices, and PARP inhibitor PJ34 abrogated slice neurodegeneration...
January 16, 2018: Journal of Pharmacology and Experimental Therapeutics
https://www.readbyqxmd.com/read/29321391/-prothymosin%C3%AE-as-a-neuroprotective-damps-alarmins-molecule
#14
Hiroshi Ueda, Shiori Maeda
Prothymosin alpha (ProTα) has been identified as an anti-necrotic factor from the conditioned medium of primary cultured of rat cortical neurons under the serum-free starving condition. ProTα is released in a non-vesicular manner from neurons or astrocytes by the help of cargo protein S100A13. Thus released ProTα is found to have robustness roles in the brain under the condition of neuronal necrosis or apoptosis. ProTα inhibits necrosis by plasma membrane-translocation of glucose transporters endocytosed by ischemia/starving stress, through an activation of unidentified G protein-coupled receptor and protein kinase Cβ...
2018: Nihon Yakurigaku Zasshi. Folia Pharmacologica Japonica
https://www.readbyqxmd.com/read/29312829/formononetin-inhibits-lipopolysaccharide-induced-release-of-high-mobility-group-box-1-by-upregulating-sirt1-in-a-ppar%C3%AE-dependent-manner
#15
Jung Seok Hwang, Eun Sil Kang, Sung Gu Han, Dae-Seog Lim, Kyung Shin Paek, Chi-Ho Lee, Han Geuk Seo
Background: The release of high mobility group box 1 (HMGB1) induced by inflammatory signals acts as a cellular alarmin to trigger a chain of inflammatory responses. Although the inflammatory actions of HMGB1 are well studied, less is known about the therapeutic agents that can impede its release. This study investigated whether the isoflavonoid formononetin can modulate HMGB1 release in cellular inflammatory responses. Methods: RAW264.7 murine macrophages were exposed to lipopolysaccharide (LPS) in the presence or absence of formononetin...
2018: PeerJ
https://www.readbyqxmd.com/read/29309756/dichotomous-function-of-il-33-in-health-and-disease-from-biology-to-clinical-implications
#16
REVIEW
Harald Braun, Inna S Afonina, Christina Mueller, Rudi Beyaert
Interleukin (IL)-33 is a cytokine that is released from epithelial and endothelial cells at barrier surfaces upon tissue stress or damage to operate as an alarmin. IL-33 has been primarily implicated in the induction of T helper (Th) 2 type immune responses. Therefore, IL-33 has attracted a lot of interest as a potential therapeutic target in asthma and other allergic diseases. Over the years, it has become clear that IL-33 has a much broader activity and also contributes to Th1 immunity, expanding the possibilities for therapeutic modulation of IL-33 activity to multiple inflammatory diseases...
February 2018: Biochemical Pharmacology
https://www.readbyqxmd.com/read/29305434/modulation-of-the-il-33-il-13-axis-in-obesity-by-il-13r%C3%AE-2
#17
Jennifer Duffen, Melvin Zhang, Katherine Masek-Hammerman, Angela Nunez, Agnes Brennan, Jessica E C Jones, Jeffrey Morin, Karl Nocka, Marion Kasaian
In obesity, IL-13 overcomes insulin resistance by promoting anti-inflammatory macrophage differentiation in adipose tissue. Endogenous IL-13 levels can be modulated by the IL-13 decoy receptor, IL-13Rα2, which inactivates and depletes the cytokine. In this study, we show that IL-13Rα2 is markedly elevated in adipose tissues of obese mice. Mice deficient in IL-13Rα2 had high expression of IL-13 response markers in adipose tissue, consistent with increased IL-13 activity at baseline. Moreover, exposure to the type 2 cytokine-inducing alarmin, IL-33, enhanced serum and tissue IL-13 concentrations and elevated tissue eosinophils, macrophages, and type 2 innate lymphoid cells...
January 5, 2018: Journal of Immunology: Official Journal of the American Association of Immunologists
https://www.readbyqxmd.com/read/29282039/plasma-levels-of-alarmin-hnps-1-3-associate-with-lung-dysfunction-after-cardiac-surgery-in-children
#18
XiWang Liu, QiXing Chen, YuJia Luo, YaoQin Hu, DengMing Lai, XiaoLe Zhang, XiangHong Zhang, JianGen Yu, XiangMing Fang, Qiang Shu
BACKGROUND: Early onset of lung injury is considerable common after cardiac surgery and is associated with increasing in morbidity and mortality, but current clinical predictors for the occurrence of this complication always have limited positive warning value. This study aimed to evaluate whether elevated plasma levels of human neutrophil peptides (HNPs) 1-3 herald impaired lung function in infants and young children after cardiac surgery necessitating cardiopulmonary bypass (CPB). METHODS: Consecutive children younger than 3 years old who underwent cardiac surgery were prospectively enrolled...
December 28, 2017: BMC Pulmonary Medicine
https://www.readbyqxmd.com/read/29262324/caspase-1-engagement-and-tlr-induced-c-flip-expression-suppress-asc-caspase-8-dependent-apoptosis-by-inflammasome-sensors-nlrp1b-and-nlrc4
#19
Nina Van Opdenbosch, Hanne Van Gorp, Maarten Verdonckt, Pedro H V Saavedra, Nathalia M de Vasconcelos, Amanda Gonçalves, Lieselotte Vande Walle, Dieter Demon, Magdalena Matusiak, Filip Van Hauwermeiren, Jinke D'Hont, Tino Hochepied, Stefan Krautwald, Thirumala-Devi Kanneganti, Mohamed Lamkanfi
The caspase activation and recruitment domain (CARD)-based inflammasome sensors NLRP1b and NLRC4 induce caspase-1-dependent pyroptosis independent of the inflammasome adaptor ASC. Here, we show that NLRP1b and NLRC4 trigger caspase-8-mediated apoptosis as an alternative cell death program in caspase-1-/- macrophages and intestinal epithelial organoids (IECs). The caspase-8 adaptor FADD was recruited to ASC specks, which served as cytosolic platforms for caspase-8 activation and NLRP1b/NLRC4-induced apoptosis...
December 19, 2017: Cell Reports
https://www.readbyqxmd.com/read/29261777/self-extracellular-rna-acts-in-synergy-with-exogenous-danger-signals-to-promote-inflammation
#20
Frederik Noll, Jonas Behnke, Silke Leiting, Kerstin Troidl, Gustavo Teixeira Alves, Holger Müller-Redetzky, Klaus T Preissner, Silvia Fischer
Self-extracellular RNA (eRNA), released from stressed or injured cells upon various pathological situations such as ischemia-reperfusion-injury, has been shown to act as an alarmin by inducing procoagulatory and proinflammatory responses. In particular, M1-polarization of macrophages by eRNA resulted in the expression and release of a variety of cytokines, including tumor necrosis factor (TNF)-α or interleukin-6 (IL-6). The present study now investigates in which way self-eRNA may influence the response of macrophages towards various Toll-like receptor (TLR)-agonists...
2017: PloS One
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