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110 records – page 1 of 11.

Adapting to environmental stresses: the role of the microbiota in controlling innate immunity and behavioral responses.

https://arctichealth.org/en/permalink/ahliterature128781
Source
Immunol Rev. 2012 Jan;245(1):250-64
Publication Type
Article
Date
Jan-2012
Author
Caio T Fagundes
Flávio A Amaral
Antônio L Teixeira
Danielle G Souza
Mauro M Teixeira
Author Affiliation
Immunopharmacology, Departamento de Bioquímica e Imunologia, Instituto de Ciências Biológicas, Universidade Federal de Minas Gerais, Belo Horizonte, MG, Brazil.
Source
Immunol Rev. 2012 Jan;245(1):250-64
Date
Jan-2012
Language
English
Publication Type
Article
Keywords
Adaptation, Biological
Animals
Bacterial Infections - immunology - microbiology - psychology
Behavior
Host-Pathogen Interactions
Humans
Immunity, Innate
Inflammation - immunology
Nociceptors - immunology
Stress, Physiological - immunology
Abstract
Mammals are subject to colonization by an astronomical number of mutualistic and commensal microorganisms on their environmental exposed surfaces. These mutualistic species build up a complex community, called the indigenous microbiota, which aid their hosts in several physiological activities. In this review, we show that the transition between a non-colonized and a colonized state is associated with modification on the pattern of host inflammatory and behavioral responsiveness. There is a shift from innate anti-inflammatory cytokine production to efficient release of proinflammatory mediators and rapid mobilization of leukocytes upon infection or other stimuli. In addition, host responses to hypernociceptive and stressful stimuli are modulated by indigenous microbiota, partly due to the altered pattern of innate and acquired immune responsiveness of the non-colonized host. These altered responses ultimately lead to significant alteration in host behavior to environmental threats. Therefore, host colonization by indigenous microbiota modifies the way the host perceives and reacts to environmental stimuli, improving resilience of the entire host-microorganism consortium to environmental stresses.
Notes
Erratum In: Immunol Rev. 2014 Jul;260(1):261
PubMed ID
22168425 View in PubMed
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Allelic distribution of the CCR5, CCR2, and SDF1 gene polymorphisms associated with HIV-1/AIDS resistance in Russian populations.

https://arctichealth.org/en/permalink/ahliterature160875
Source
Dokl Biol Sci. 2007 Jul-Aug;415:320-3
Publication Type
Article

Animal models of gastrointestinal and liver diseases. Animal models of necrotizing enterocolitis: pathophysiology, translational relevance, and challenges.

https://arctichealth.org/en/permalink/ahliterature104414
Source
Am J Physiol Gastrointest Liver Physiol. 2014 Jun 1;306(11):G917-28
Publication Type
Article
Date
Jun-1-2014
Author
Peng Lu
Chhinder P Sodhi
Hongpeng Jia
Shahab Shaffiey
Misty Good
Maria F Branca
David J Hackam
Author Affiliation
Department of Surgery, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania;
Source
Am J Physiol Gastrointest Liver Physiol. 2014 Jun 1;306(11):G917-28
Date
Jun-1-2014
Language
English
Publication Type
Article
Keywords
Animals
Disease Models, Animal
Enterocolitis, Necrotizing - physiopathology
Humans
Immunity, Innate
Infant, Newborn
Infant, Premature
Intestinal Mucosa - immunology
Reproducibility of Results
Research Design
Abstract
Necrotizing enterocolitis is the leading cause of morbidity and mortality from gastrointestinal disease in premature infants and is characterized by initial feeding intolerance and abdominal distention followed by the rapid progression to coagulation necrosis of the intestine and death in many cases. Although the risk factors for NEC development remain well accepted, namely premature birth and formula feeding, the underlying mechanisms remain incompletely understood. Current thinking indicates that NEC develops in response to an abnormal interaction between the mucosal immune system of the premature host and an abnormal indigenous microflora, leading to an exaggerated mucosal inflammatory response and impaired mesenteric perfusion. In seeking to understand the molecular and cellular events leading to NEC, various animal models have been developed. However, the large number and variability between the available animal models and the unique characteristics of each has raised important questions regarding the validity of particular models for NEC research. In an attempt to provide some guidance to the growing community of NEC researchers, we now seek to review the key features of the major NEC models that have been developed in mammalian and nonmammalian species and to assess the advantages, disadvantage, challenges and major scientific discoveries yielded by each. A strategy for model validation is proposed, the principal models are compared, and future directions and challenges within the field of NEC research are explored.
PubMed ID
24763555 View in PubMed
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[Antimycotic chemotherapy in weakened resistance].

https://arctichealth.org/en/permalink/ahliterature240271
Source
Immun Infekt. 1984 Aug;12(4):181-5
Publication Type
Article
Date
Aug-1984
Author
T. Wegmann
Source
Immun Infekt. 1984 Aug;12(4):181-5
Date
Aug-1984
Language
German
Publication Type
Article
Keywords
Amphotericin B - therapeutic use
Antifungal Agents - therapeutic use
Azo Compounds - therapeutic use
Disease Susceptibility
Flucytosine - therapeutic use
Humans
Immunity, Innate
Mycoses - drug therapy
Abstract
Antifungal chemotherapy in weakened resistance is restricted to the following three substances: amphotericin B, 5-fluorocytosine and the azo dyes. The paper only discusses the therapy of indigenous iatrogenic fungal infections due to mycelial fungi (molds) and yeasts. The pathogenesis must be investigated in every case, since a healthy individual does not contract such a fungal infection. Prophylaxis would be more important than treatment of such complications. At the end of the paper, the therapy is summarized in a table. It is clearly seen from the table that the optimal modern therapy of systemic mycoses is a combination of 5-fluorocytosine in a normal dosage and amphotericin B at reduced dosage.
PubMed ID
6480026 View in PubMed
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Aroclor 1254 exposure reduces disease resistance and innate immune responses in fasted Arctic charr.

https://arctichealth.org/en/permalink/ahliterature302920
Source
Environ Toxicol Chem. 2005 Jan;24(1):117-24.
Publication Type
Article
Date
2005
Author
Maule AG
Jørgensen EH
Vijayan MM
Killie JE
Source
Environ Toxicol Chem. 2005 Jan;24(1):117-24.
Date
2005
Language
English
Publication Type
Article
Keywords
Aeromonas salmonicida
Metabolism
toxicity
Immunology
Physiology
Chemistry
Drug effects
Animals
Chlorodiphenyl (54% Chlorine)
Food Deprivation
Gram-Negative Bacterial Infections
Immunity, Innate
Kidney
Lectins
Muramidase
Muscle, Skeletal
Salmonidae
Water Pollutants, Chemical
Abstract
To examine the immunological impacts of polychlorinated biphenyls (PCBs) in an environmentally relevant way, we orally contaminated Arctic charr (Salvelinus alpinus) with Aroclor 1254. After contamination, fish were either fed (0 and 100 mg Aroclor 1254 kg(-1) fish wt) or fasted (0, 1, 10, and 100 mg kg(-1)) to mimic cycles of feeding-fasting experienced by Arctic animals. After four months, PCB concentrations in muscle were the same in fasted and fed fish; however, PCBs in kidneys of fed fish were 33 to 50% of those in fasted fish. Arctic charr were exposed to Aeromonas salmonicida, the bacteria responsible for furunculosis, by cohabitation with infected conspecifics. Fasted fish had a significant trend toward lower survival with higher dose of PCBs--from 68% in controls to 48% in treatment involving 100 mg kg(-1). Independent of PCB contamination, fed fish had the lowest survival; we attribute this to stress associated with establishing and maintaining feeding hierarchies. A significant decrease in the activity of lysozyme was observed in skin mucus, as was hemagglutination ability of a putative rhamnose lectin in fasted, but not in fed, PCB-treated fish. These results demonstrate the immunosuppressive effects of PCBs on Arctic charr, and they illustrate the importance of considering environmentally relevant nutritional status in ecotoxicological studies.
PubMed ID
15683174 View in PubMed
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Can single nucleotide polymorphisms in innate immune receptors predict development of septic complications in intensive care unit patients?

https://arctichealth.org/en/permalink/ahliterature175842
Source
Crit Care Med. 2005 Mar;33(3):695-6
Publication Type
Article
Date
Mar-2005

CARD8 gene encoding a protein of innate immunity is expressed in human atherosclerosis and associated with markers of inflammation.

https://arctichealth.org/en/permalink/ahliterature114521
Source
Clin Sci (Lond). 2013 Oct;125(8):401-7
Publication Type
Article
Date
Oct-2013
Author
Geena Varghese Paramel
Lasse Folkersen
Rona J Strawbridge
Ali Ateia Elmabsout
Eva Särndahl
Pia Lundman
Jan-Håkan Jansson
Göran K Hansson
Allan Sirsjö
Karin Fransén
Author Affiliation
Department of Clinical Medicine, School of Health and Medical Sciences, Örebro University, Örebro, Sweden.
Source
Clin Sci (Lond). 2013 Oct;125(8):401-7
Date
Oct-2013
Language
English
Publication Type
Article
Keywords
Atherosclerosis - blood - genetics
Biological Markers - blood
C-Reactive Protein - metabolism
CARD Signaling Adaptor Proteins - genetics
Chemokine CCL2 - blood
Cohort Studies
Cytokines - blood
Gene Expression Profiling
Gene Frequency
Genotype
Humans
Immunity, Innate - genetics
Inflammation - blood - genetics
Inflammation Mediators - blood
Myocardial Infarction - blood - genetics
Neoplasm Proteins - genetics
Oligonucleotide Array Sequence Analysis
Plaque, Atherosclerotic - blood - genetics
Polymorphism, Single Nucleotide
Risk factors
Sweden
Abstract
Inflammation is a key factor in the development of atherosclerotic coronary artery disease. It is promoted through the inflammasome, a molecular machine that produces IL (interleukin)-1? in response to cholesterol crystal accumulation in macrophages. The CARD8 (caspase recruitment domain 8) protein modulates this process by suppressing caspase 1 and the transcription factor NF-?B (nuclear factor ?B). The expression of CARD8 mRNA was examined in atherosclerotic vascular tissue and the impact on MI (myocardial infarction) of a polymorphism in the CARD8 gene determined. CARD8 mRNA was analysed by microarray of human atherosclerotic tissue and compared with transplant donor arterial tissue. Microarray analysis was performed for proximal genes associated with the rs2043211 locus in plaque. The CARD8 rs2043211 polymorphism was analysed by genotyping of two Swedish MI cohorts, FIA (First Myocardial Infarction in Northern Sweden) and SCARF (Stockholm Coronary Atherosclerosis Risk Factor). The CRP (C-reactive protein) level was measured in both cohorts, but the levels of the pro-inflammatory cytokines IL-1?, IL-18, TNF (tumour necrosis factor) and MCP-1 (monocyte chemoattractant protein) were measured in sera available from the SCARF cohort. CARD8 mRNA was highly expressed in atherosclerotic plaques compared with the expression in transplant donor vessel (P
PubMed ID
23611467 View in PubMed
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110 records – page 1 of 11.