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Book: Therapeutic targets in airway inflammation

Eissa, N. Tony

(Lung biology in health and disease ; 177)

2003

Author's details	ed. by N. Tony Eissa
Series title	Lung biology in health and disease ; 177
Collection
Keywords	Asthma ; Respiratory Tract Diseases ; Inflammation ; Respiratory Tract Diseases / physiopathology ; Technology, Pharmaceutical ; Immunotherapy ; Atemwegsinfektion ; Pharmakotherapie
Subject	Arzneimitteltherapie ; Arzneitherapie ; Medikamentöse Therapie ; Respiratorische Infektionskrankheit
Language	English
Size	XXXI, 957 S. : Ill., graph. Darst.
Publisher	Dekker
Publishing place	New York u.a.
Publishing country	United States
Document type	Book
HBZ-ID	HT013737186
ISBN	0-8247-0956-X ; 978-0-8247-0956-3
Database	Catalogue ZB MED Medicine, Health

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Article ; Online: Autophagy in Pulmonary Innate Immunity.

Rao, Lang / Eissa, N Tony

Journal of innate immunity

2019 Volume 12, Issue 1, Page(s) 21–30

Abstract: Autophagy is a major intracellular digestion system that delivers cytoplasmic components for degradation and recycling. In this capacity, autophagy plays an important role in maintaining cellular homeostasis by mediating the degradation of cellular ... ...

Abstract	Autophagy is a major intracellular digestion system that delivers cytoplasmic components for degradation and recycling. In this capacity, autophagy plays an important role in maintaining cellular homeostasis by mediating the degradation of cellular macromolecules and dysfunctional organelles and regeneration of nutrients for cell growth. Autophagy is important in innate immunity, as it is responsible for the clearance of various pathogens. Deficiency of intracellular autophagy can result in exaggerated activation of the inflammasome. The latter is an innate immune complex that senses diverse pathogen-associated or danger-associated molecular patterns and activates the expression of inflammatory cytokines. In autophagy-deficient cells, accumulation of damaged organelles, misfolded proteins, and reactive oxygen species contribute to inflammasome activation. The lung is continuously exposed to pathogens from the environment, rendering it vulnerable to infection. The lung innate immune cells act as a crucial initial barrier against the continuous threat from pathogens. In this review, we will summarize recent findings on the regulation of autophagy and its inter-action with innate immunity, focusing on the lung.
MeSH term(s)	Animals ; Autophagy/immunology ; Homeostasis ; Host-Pathogen Interactions ; Humans ; Immunity, Innate ; Inflammasomes/immunology ; Lung/immunology ; Pneumonia/immunology ; Reactive Oxygen Species/metabolism
Chemical Substances	Inflammasomes ; Reactive Oxygen Species
Language	English
Publishing date	2019-04-24
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000497414
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Article ; Online: The exosome in lung diseases: Message in a bottle.

Eissa, N Tony

The Journal of allergy and clinical immunology

2013 Volume 131, Issue 3, Page(s) 904–905

MeSH term(s)	Asthma/genetics ; Exosomes/genetics ; Female ; Humans ; Male ; MicroRNAs/analysis
Chemical Substances	MicroRNAs
Language	English
Publishing date	2013-03
Publishing country	United States
Document type	Comment ; Editorial
ZDB-ID	121011-7
ISSN	1097-6825 ; 1085-8725 ; 0091-6749
ISSN (online)	1097-6825 ; 1085-8725
ISSN	0091-6749
DOI	10.1016/j.jaci.2013.01.021
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Article: Autophagy in Pulmonary Innate Immunity

Rao, Lang / Eissa, N. Tony

Journal of Innate Immunity

2019 Volume 12, Issue 1, Page(s) 21–30

Institution	Department of Medicine, Baylor College of Medicine, Houston, Texas, USA
Abstract	Autophagy is a major intracellular digestion system that delivers cytoplasmic components for degradation and recycling. In this capacity, autophagy plays an important role in maintaining cellular homeostasis by mediating the degradation of cellular macromolecules and dysfunctional organelles and regeneration of nutrients for cell growth. Autophagy is important in innate immunity, as it is responsible for the clearance of various pathogens. Deficiency of intracellular autophagy can result in exaggerated activation of the inflammasome. The latter is an innate immune complex that senses diverse pathogen-associated or danger-associated molecular patterns and activates the expression of inflammatory cytokines. In autophagy-deficient cells, accumulation of damaged organelles, misfolded proteins, and reactive oxygen species contribute to inflammasome activation. The lung is continuously exposed to pathogens from the environment, rendering it vulnerable to infection. The lung innate immune cells act as a crucial initial barrier against the continuous threat from pathogens. In this review, we will summarize recent findings on the regulation of autophagy and its interaction with innate immunity, focusing on the lung.
Keywords	Autophagy ; Inflammasome ; Pathogen ; Innate immunity and pulmonary inflammation
Language	English
Publishing date	2019-04-24
Publisher	S. Karger AG
Publishing place	Basel, Switzerland
Document type	Article
Note	Review Article ; This article is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (CC BY-NC-ND).
ZDB-ID	2454158-8
ISSN	1662-8128 ; 1662-811X
ISSN (online)	1662-8128
ISSN	1662-811X
DOI	10.1159/000497414
Database	Karger publisher's database

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Article ; Online: p38 MAPK Activity Is Required to Prevent Hyperactivation of NLRP3 Inflammasome.

Shin, Jin Na / Rao, Lang / Sha, Youbao / Abdel Fattah, Elmoataz / Hyser, Joseph / Eissa, N Tony

Journal of immunology (Baltimore, Md. : 1950)

2021 Volume 207, Issue 2, Page(s) 661–670

Abstract: Inflammation contributes to the pathogenesis and morbidity of wide spectrum of human diseases. The inflammatory response must be actively controlled to prevent bystander damage to tissues. Yet, the mechanisms controlling excessive inflammatory responses ... ...

Abstract	Inflammation contributes to the pathogenesis and morbidity of wide spectrum of human diseases. The inflammatory response must be actively controlled to prevent bystander damage to tissues. Yet, the mechanisms controlling excessive inflammatory responses are poorly understood. NLRP3 inflammasome plays an important role in innate immune response to cellular infection or stress. Its activation must be tightly regulated because uncontrolled inflammasome activation is associated with a number of human diseases. p38 MAPK signaling plays an essential role in the regulation of inflammation. The role of p38 MAPK in inflammatory response associated with the expression of proinflammatory molecules is known. However, the anti-inflammatory functions of p38 MAPK are largely unknown. In this study, we show that pharmacologic inhibition or genetic deficiency of p38 MAPK leads to hyperactivation of NLRP3 inflammasome, resulting in enhanced Caspase 1 activation and IL-1β and IL-18 production. The deficiency of p38 MAPK activity induced an increase of cytosolic Ca
MeSH term(s)	Animals ; Cell Line ; HEK293 Cells ; Humans ; Immunity, Innate/physiology ; Inflammasomes/metabolism ; Inflammation/metabolism ; Interleukin-1beta/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; NLR Family, Pyrin Domain-Containing 3 Protein/metabolism ; Reactive Oxygen Species/metabolism ; Sepsis/metabolism ; Shock, Septic/metabolism ; Signal Transduction/physiology ; p38 Mitogen-Activated Protein Kinases/metabolism
Chemical Substances	Inflammasomes ; Interleukin-1beta ; NLR Family, Pyrin Domain-Containing 3 Protein ; Nlrp3 protein, mouse ; Reactive Oxygen Species ; p38 Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2021-06-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.2000416
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Article ; Online: Autophagy as a Stress Response Pathway in the Immune System.

Bhattacharya, Abhisek / Eissa, N Tony

International reviews of immunology

2015 Volume 34, Issue 5, Page(s) 382–402

Abstract: Macroautophagy, hereafter, referred to as autophagy, has long been regarded as a housekeeping pathway involved in intracellular degradation and energy recycling. These housekeeping and homeostatic functions are especially important during cellular stress, ...

Abstract	Macroautophagy, hereafter, referred to as autophagy, has long been regarded as a housekeeping pathway involved in intracellular degradation and energy recycling. These housekeeping and homeostatic functions are especially important during cellular stress, such as periods of nutrient deprivation. However, importance of autophagy extends far beyond its degradative functions. Recent evidence shows that autophagy plays an essential role in development, organization and functions of the immune system, and defects in autophagy lead to several diseases, including cancer and autoimmunity. In the immune system, autophagy is important in regulation of the innate and adaptive immune responses. This review focuses on the roles of autophagy in the adaptive immune system. We first introduce the autophagy pathway and provide a brief description of the major molecular players involved in autophagy. We then discuss the importance of autophagy as a stress integrator mechanism and provide relevant examples of this role of autophagy in adaptive immune cells. Then we proceed to describe how autophagy regulates development, activation and functions of different adaptive immune cells. In these contexts, we mention both degradative and non-degradative roles of autophagy, and illustrate their importance. We also discuss role of autophagy in antigen presenting cells, which play critical roles in the activation of adaptive immune cells. Further, we describe how autophagy regulates functions of different adaptive immune cells during infection, inflammation and autoimmunity.
MeSH term(s)	Adaptive Immunity/immunology ; Antigen-Presenting Cells/immunology ; Autoimmune Diseases/immunology ; Autophagy/immunology ; Homeostasis/immunology ; Humans ; Immune System/immunology ; Immunity, Innate/immunology ; Inflammation/immunology ; Neoplasms/immunology ; Stress, Physiological/immunology
Language	English
Publishing date	2015
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	632825-8
ISSN	1563-5244 ; 1545-5858 ; 0883-0185
ISSN (online)	1563-5244 ; 1545-5858
ISSN	0883-0185
DOI	10.3109/08830185.2014.999156
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Article: The E3 ubiquitin ligase STUB1 regulates autophagy and mitochondrial biogenesis by modulating TFEB activity.

Rao, Lang / Sha, Youbao / Eissa, N Tony

Molecular & cellular oncology

2017 Volume 4, Issue 6, Page(s) e1372867

Abstract: TFEB is a master regulator for transcription of genes involved in autophagy, lysosome and mitochondrial biogenesis. Activity of TFEB is inhibited upon its phosphorylation. STUB1, a chaperone-dependent E3 ubiquitin ligase, modulates TFEB activity by ... ...

Abstract	TFEB is a master regulator for transcription of genes involved in autophagy, lysosome and mitochondrial biogenesis. Activity of TFEB is inhibited upon its phosphorylation. STUB1, a chaperone-dependent E3 ubiquitin ligase, modulates TFEB activity by preferentially targeting inactive phosphorylated TFEB for degradation by the ubiquitin proteasome pathway. Thus, the ubiquitin-proteasome pathway participates in regulating autophagy and lysosomal functions by regulating the activity of TFEB.
Language	English
Publishing date	2017-09-28
Publishing country	United States
Document type	Journal Article
ISSN	2372-3556
ISSN	2372-3556
DOI	10.1080/23723556.2017.1372867
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Article: Autophagy and autoimmunity crosstalks.

Bhattacharya, Abhisek / Eissa, N Tony

Frontiers in immunology

2013 Volume 4, Page(s) 88

Abstract: Autophagy, initially viewed as a conserved bulk-degradation mechanism, has emerged as a central player in a multitude of immune functions. Autophagy is important in host defense against intracellular and extracellular pathogens, metabolic syndromes, ... ...

Abstract	Autophagy, initially viewed as a conserved bulk-degradation mechanism, has emerged as a central player in a multitude of immune functions. Autophagy is important in host defense against intracellular and extracellular pathogens, metabolic syndromes, immune cell homeostasis, antigen processing and presentation, and maintenance of tolerance. The observation that the above processes are implicated in triggering or exacerbating autoimmunity raises the possibility that autophagy is involved in mediating autoimmune processes, either directly or as a consequence of innate or adaptive functions mediated by the pathway. Genome-wide association studies have shown association between single nucleotide polymorphisms (SNPs) in autophagy related gene 5 (Atg5), and Atg16l1 with susceptibility to systemic lupus erythematosus (SLE) and Crohn's disease, respectively. Enhanced expression of Atg5 was also reported in blood of mice with experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS), and in T cells isolated from blood or brain tissues from patients with active relapse of MS. This review explores the roles of autophagy pathway in the innate and adaptive immune systems on regulating or mediating the onset, progression, or exacerbation of autoimmune processes.
Language	English
Publishing date	2013-04-15
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2013.00088
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Article ; Online: Combination of esomeprazole and pirfenidone enhances antifibrotic efficacy in vitro and in a mouse model of TGFβ-induced lung fibrosis.

Ebrahimpour, Afshin / Ahir, Manisha / Wang, Min / Jegga, Anil G / Bonnen, Mark D / Eissa, N Tony / Montesi, Sydney B / Raghu, Ganesh / Ghebre, Yohannes T

Scientific reports

2022 Volume 12, Issue 1, Page(s) 20668

Abstract: Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease of unknown etiology. Currently, pirfenidone and nintedanib are the only FDA-approved drugs for the treatment of IPF and are now the standard of care. This is a significant step ... ...

Abstract	Idiopathic pulmonary fibrosis (IPF) is a progressive and fatal lung disease of unknown etiology. Currently, pirfenidone and nintedanib are the only FDA-approved drugs for the treatment of IPF and are now the standard of care. This is a significant step in slowing down the progression of the disease. However, the drugs are unable to stop or reverse established fibrosis. Several retrospective clinical studies indicate that proton pump inhibitors (PPIs; FDA-approved to treat gastroesophageal reflux) are associated with favorable outcomes in patients with IPF, and emerging preclinical studies report that PPIs possess antifibrotic activity. In this study, we evaluated the antifibrotic efficacy of the PPI esomeprazole when combined with pirfenidone in vitro and in vivo. In cell culture studies of IPF lung fibroblasts, we assessed the effect of the combination on several fibrosis-related biological processes including TGFβ-induced cell proliferation, cell migration, cell contraction, and collagen production. In an in vivo study, we used mouse model of TGFβ-induced lung fibrosis to evaluate the antifibrotic efficacy of esomeprazole/pirfenidone combination. We also performed computational studies to understand the molecular mechanisms by which esomeprazole and/or pirfenidone regulate lung fibrosis. We found that esomeprazole significantly enhanced the anti-proliferative effect of pirfenidone and favorably modulated TGFβ-induced cell migration and contraction of collagen gels. We also found that the combination significantly suppressed collagen production in response to TGFβ in comparison to pirfenidone monotherapy. In addition, our animal study demonstrated that the combination therapy effectively inhibited the differentiation of lung fibroblasts into alpha smooth muscle actin (αSMA)-expressing myofibroblasts to attenuate the progression of lung fibrosis. Finally, our bioinformatics study of cells treated with esomeprazole or pirfenidone revealed that the drugs target several extracellular matrix (ECM) related pathways with esomeprazole preferentially targeting collagen family members while pirfenidone targets the keratins. In conclusion, our cell biological, computational, and in vivo studies show that the PPI esomeprazole enhances the antifibrotic efficacy of pirfenidone through complementary molecular mechanisms. This data supports the initiation of prospective clinical studies aimed at repurposing PPIs for the treatment of IPF and other fibrotic lung diseases where pirfenidone is prescribed.
MeSH term(s)	Animals ; Mice ; Esomeprazole/pharmacology ; Transforming Growth Factor beta ; Prospective Studies ; Retrospective Studies ; Proton Pump Inhibitors/pharmacology ; Idiopathic Pulmonary Fibrosis/drug therapy ; Disease Models, Animal
Chemical Substances	Esomeprazole (N3PA6559FT) ; pirfenidone (D7NLD2JX7U) ; Transforming Growth Factor beta ; Proton Pump Inhibitors
Language	English
Publishing date	2022-11-30
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-24985-x
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Article ; Online: Post-Transcriptional Regulation of Alpha One Antitrypsin by a Proteasome Inhibitor.

Rao, Lang / Xu, Yi / Reineke, Lucas Charles / Bhattacharya, Abhisek / Tyryshkin, Alexey / Shin, Jin Na / Eissa, N Tony

International journal of molecular sciences

2020 Volume 21, Issue 12

Abstract: Alpha one antitrypsin (α1AT), a serine proteinase inhibitor primarily produced by the liver, protects pulmonary tissue from neutrophil elastase digestion. Mutations of ... ...

Abstract	Alpha one antitrypsin (α1AT), a serine proteinase inhibitor primarily produced by the liver, protects pulmonary tissue from neutrophil elastase digestion. Mutations of the
MeSH term(s)	Gene Expression Regulation/drug effects ; Hepatocytes/drug effects ; Hepatocytes/metabolism ; Humans ; Induced Pluripotent Stem Cells/cytology ; Induced Pluripotent Stem Cells/metabolism ; Proteasome Inhibitors/pharmacology ; Protein Biosynthesis/drug effects ; RNA Processing, Post-Transcriptional/drug effects ; Stress, Physiological ; alpha 1-Antitrypsin/biosynthesis ; alpha 1-Antitrypsin/genetics
Chemical Substances	Proteasome Inhibitors ; SERPINA1 protein, human ; alpha 1-Antitrypsin
Language	English
Publishing date	2020-06-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms21124318
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