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Acute local reactions after intraarticular hylan for osteoarthritis of the knee.

https://arctichealth.org/en/permalink/ahliterature212049
Source
J Rheumatol. 1996 May;23(5):945-6
Publication Type
Article
Date
May-1996

Basophil mediated pro-allergic inflammation in vehicle-emitted particles exposure.

https://arctichealth.org/en/permalink/ahliterature282459
Source
Environ Res. 2017 Jan;152:308-314
Publication Type
Article
Date
Jan-2017
Author
Alexander M Zakharenko
Ayse Basak Engin
Valery V Chernyshev
Vladimir V Chaika
Sergey M Ugay
Ramin Rezaee
Gholamreza Karimi
Vladimir A Drozd
Anna V Nikitina
Sergey F Solomennik
Olga R Kudryavkina
Liu Xin
Yuan Wenpeng
Manolis Tzatzarakis
Aristidis M Tsatsakis
Kirill S Golokhvast
Source
Environ Res. 2017 Jan;152:308-314
Date
Jan-2017
Language
English
Publication Type
Article
Keywords
Air Pollutants - toxicity
Animals
Automobiles
Basophils - drug effects - immunology
Inflammation - chemically induced - immunology
Male
Mice
Particulate Matter - toxicity
Polycyclic Aromatic Hydrocarbons - toxicity
Russia
Specific Pathogen-Free Organisms
Vehicle Emissions - toxicity
Abstract
Despite of the fact that engine manufacturers develop a new technology to reduce exhaust emissions, insufficient attention given to particulate emissions. However, diesel exhaust particles are a major source of air-borne pollution, contain vast amount of polycyclic aromatic hydrocarbons (PAHs) and may have deleterious effects on the immune system, resulting in the induction and enhancement of pro-allergic processes. In the current study, vehicle emitted particles (VEP) from 2 different types of cars (diesel - D and gasoline - G) and locomotive (L) were collected. Overall, 129 four-week-old, male SPF-class Kunming mice were subcutaneously instilled with either low dose 100, 250 or high dose, 500mg/kg VEP and 15 mice were assigned as control group. The systemic toxicity was evaluated and alterations in the percentages of the CD3, CD4, CD8, CD16, CD25 expressing cells, basophils, eosinophils and neutrophils were determined. Basophil percentages were inversely associated with the PAH content of the VEPs, however basophil sensitization was more important than cell count in VEP exposure. Thus, the effects of VEP-PAHs emerge with the activation of basophils in an allergen independent fashion. Despite the increased percentage of CD4+ T cells, a sharp decrease in basophil counts at 500mg/kg of VEP indicates a decreased inhibitory effect of CD16+ monocytes on the proliferation of CD4+ T cell and suppressed polarization into a Th2 phenotype. Therefore, although the restrictions for vehicles emissions differ between countries, follow up studies and strict regulations are needed.
PubMed ID
27833058 View in PubMed
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Cadmium exposure is associated with soluble urokinase plasminogen activator receptor, a circulating marker of inflammation and future cardiovascular disease.

https://arctichealth.org/en/permalink/ahliterature282462
Source
Environ Res. 2017 Jan;152:185-191
Publication Type
Article
Date
Jan-2017
Author
Björn Fagerberg
Yan Borné
Lars Barregard
Gerd Sallsten
Niklas Forsgard
Bo Hedblad
Margaretha Persson
Gunnar Engström
Source
Environ Res. 2017 Jan;152:185-191
Date
Jan-2017
Language
English
Publication Type
Article
Keywords
1-Alkyl-2-acetylglycerophosphocholine Esterase - blood
Biomarkers - blood
C-Reactive Protein - metabolism
Cadmium - blood
Cardiovascular Diseases - chemically induced - epidemiology
Cross-Sectional Studies
Environmental Exposure
Environmental pollutants - blood
Female
Humans
Inflammation - chemically induced - epidemiology
Leukocyte Count
Lymphocytes - metabolism
Male
Middle Aged
Neutrophils - metabolism
Receptors, Urokinase Plasminogen Activator - blood
Sweden - epidemiology
Abstract
Diet and smoking are the main sources of cadmium exposure in the general population. Cadmium increases the risk of cardiovascular diseases, and experimental studies show that it induces inflammation. Blood cadmium levels are associated with macrophages in human atherosclerotic plaques. Soluble urokinase-type plasminogen activator receptor (suPAR) is an emerging biomarker for cardiovascular events related to inflammation and atherosclerotic plaques. The aim was to examine whether blood cadmium levels are associated with circulating suPAR and other markers of inflammation.
A population sample of 4648 Swedish middle-aged women and men was examined cross-sectionally in 1991-1994. Plasma suPAR was assessed by ELISA, leukocytes were measured by standard methods, and blood cadmium was analysed by inductively coupled plasma mass spectrometry. Prevalent cardiovascular disease, ultrasound-assessed carotid plaque occurrence, and several possible confounding factors were recorded.
After full adjustment for risk factors and confounding variables, a 3-fold increase in blood cadmium was associated with an 10.9% increase in suPAR concentration (p
PubMed ID
27792942 View in PubMed
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Change in airway inflammatory markers in Danish energy plant workers during a working week.

https://arctichealth.org/en/permalink/ahliterature264032
Source
Ann Agric Environ Med. 2014;21(3):534-40
Publication Type
Article
Date
2014
Author
Yuduo Zheng
Vivi Schlünssen
Jakob Bønløkke
Anne M Madsen
Simon Skov
Torben Sigsgaard
Source
Ann Agric Environ Med. 2014;21(3):534-40
Date
2014
Language
English
Publication Type
Article
Keywords
Air Pollutants, Occupational - toxicity
Biological Markers - metabolism
Denmark
Dust - analysis
Endotoxins - toxicity
Environmental monitoring
Humans
Hydrogen-Ion Concentration
Inflammation - chemically induced
Inhalation Exposure
Interleukin-1beta - metabolism
Interleukin-8 - metabolism
Male
Occupational Exposure
Power Plants
Respiratory System - drug effects - immunology
Time Factors
Abstract
It is well known that exposure to organic dust can cause adverse respiratory effect. The pathogen-associated molecular patterns (PAMPS) in the organic dust, such as endotoxin from Gram-negative bacteria cell wall and fungal components, can trigger the release of cytokine (e.g. Interleukin 1ß (IL-1ß)) and chemokine (e.g. Interleukin 8 (IL-8)) from the immune cells in the airways.
To evaluate the potential inflammatory effects of organic dust exposure in energy plants in Denmark.
Nasal lavage (NAL) and exhaled breath condensate (EBC) were sampled at Monday morning (referred to as before work) and again at Thursday afternoon (referred to as after work). NAL IL-8, EBC pH, IL-1ß concentration were measured. Personal exposure to endotoxin and dust was calculated from time spent on different tasks and measured average work area exposures.
Before work, workers from biofuel plants had a higher IL-1ß and IL-8 concentration compared to conventional fuel plants (control group). Specifically, the IL-1ß level of moderately and most exposed group, and IL-8 level of the least exposed group were higher compared to the control group. The changes of IL-1ß, pH and IL-8 during a work week were not significant. Workers with rhinitis had a lower percentage change of IL-8 compared to healthy workers.
An increased level of EBC IL-1ß in biofuel energy plant workers before work indicated a chronic or sub-chronic inflammation. The percentage change of IL-8 was lower in workers with rhinitis compared to healthy workers.
PubMed ID
25292124 View in PubMed
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Combined oral contraception and obesity are strong predictors of low-grade inflammation in healthy individuals: results from the Danish Blood Donor Study (DBDS).

https://arctichealth.org/en/permalink/ahliterature259714
Source
PLoS One. 2014;9(2):e88196
Publication Type
Article
Date
2014
Author
Cecilie J Sørensen
Ole B Pedersen
Mikkel S Petersen
Erik Sørensen
Sebastian Kotzé
Lise W Thørner
Henrik Hjalgrim
Andreas S Rigas
Bjarne Møller
Klaus Rostgaard
Mads Riiskjær
Henrik Ullum
Christian Erikstrup
Source
PLoS One. 2014;9(2):e88196
Date
2014
Language
English
Publication Type
Article
Keywords
Adult
Blood Donors
C-Reactive Protein - metabolism
Cohort Studies
Contraceptives, Oral, Combined - adverse effects
Denmark
Female
Health
Humans
Inflammation - chemically induced - complications
Logistic Models
Male
Menopause
Multivariate Analysis
Obesity - complications
Smoking
Abstract
C-reactive protein (CRP) is a well-established marker of inflammation. The level of CRP is affected by several lifestyle factors. A slightly increased CRP level, also known as low-grade inflammation (LGI), is associated with increased risk of several diseases, especially cardiovascular disease. The aim of this study was to identify predictors of increased CRP levels in healthy individuals. We therefore assessed CRP in a large cohort of blood donors.
We measured plasma CRP levels in 15,684 participants from the Danish Blood Donor Study. CRP was measured by a commercial assay. Furthermore, all participants completed a standard questionnaire on smoking status, alcohol consumption, physical activity, diet, and various body measurements. Female participants also reported the use of contraception, childbirth, and menopausal status. The relationship between LGI (defined here as a plasma CRP level between 3 mg/L and 10 mg/L) and predictors was explored by multivariable logistic regression analysis. Results were presented as odds ratios (OR) with 95% confidence intervals (CI).
We found LGI in a total of 1,561 (10.0%) participants. LGI was more frequent in women using combined oral contraception (OC) (29.9%) than in men (6.1%) and women not using OC (7.9%). Among premenopausal women, OC was the strongest predictor of LGI (odds ratio?=?8.98, p
Notes
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PubMed ID
24516611 View in PubMed
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Fish consumption, omega-3 fatty acids, and environmental contaminants in relation to low-grade inflammation and early atherosclerosis.

https://arctichealth.org/en/permalink/ahliterature119561
Source
Environ Res. 2013 Jan;120:43-54
Publication Type
Article
Date
Jan-2013
Author
A W Turunen
A. Jula
A L Suominen
S. Männistö
J. Marniemi
H. Kiviranta
P. Tiittanen
H. Karanko
L. Moilanen
M S Nieminen
Y A Kesäniemi
M. Kähönen
P K Verkasalo
Author Affiliation
Department of Environmental Health, National Institute for Health and Welfare, Neulaniementie 4, P.O. Box 95, FI-70210 Kuopio, Finland. anu.turunen@thl.fi
Source
Environ Res. 2013 Jan;120:43-54
Date
Jan-2013
Language
English
Publication Type
Article
Keywords
Adult
Aged
Atherosclerosis - chemically induced
Diet - statistics & numerical data
Environmental Pollutants - adverse effects
Fatty Acids, Omega-3 - blood
Female
Finland
Humans
Inflammation - chemically induced
Male
Middle Aged
Seafood - statistics & numerical data
Young Adult
Abstract
Fish consumption and omega-3 polyunsaturated fatty acid (PUFA) intake are shown to protect from cardiovascular diseases (CVD). However, most fish contain environmental contaminants such as dibenzo-p-dioxins and dibenzofurans (PCDD/Fs), polychlorinated biphenyls (PCBs), and methylmercury (MeHg) that may have adverse effects on cardiovascular health.
Our aim was to elucidate the associations of fish consumption, omega-3 PUFAs, environmental contaminants with low-grade inflammation, early atherosclerosis, and traditional CVD risk factors.
The Health 2000 survey participants (n=1173) represented the general Finnish population and the Fishermen study participants (n=255) represented a population with high fish consumption and high exposure to environmental contaminants. Model-adjusted geometric means and tests for linear trend were calculated for CVD risk factors by tertiles of fish consumption and serum omega-3 PUFAs, and additionally in the Fishermen study only, by tertiles of serum PCDD/F+PCB, and blood MeHg.
Serum triglyceride decreased across omega-3 PUFA tertiles in both sexes and studies. Insulin resistance, C-reactive protein, tumour necrosis factor a, and interleukin 6 decreased across omega-3 PUFA tertiles among the Health 2000 survey participants. Among the Fishermen study men, insulin resistance and arterial stiffness indicated by ß-stiffness index tended to increase and the RR estimate for carotid artery plaque tended to decrease across tertiles of PCDD/F+PCB and MeHg.
Previously established hypotriglyceridemic and anti-inflammatory effects of omega-3 PUFAs were seen also in this study. The hypothesised favourable effect on insulin sensitivity and arterial elasticity was suggested to be counteracted by high exposure to environmental contaminants but the effect on plaque prevalence appeared not to be harmful.
PubMed ID
23089109 View in PubMed
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Increased immune and inflammatory responses to dust mite antigen in rats exposed to 5 ppm NO2.

https://arctichealth.org/en/permalink/ahliterature57643
Source
Fundam Appl Toxicol. 1996 May;31(1):65-70
Publication Type
Article
Date
May-1996
Author
M I Gilmour
P. Park
M J Selgrade
Author Affiliation
Center for Environmental Medicine, University of North Carolina at Chapel Hill, North Carolina 27514, USA.
Source
Fundam Appl Toxicol. 1996 May;31(1):65-70
Date
May-1996
Language
English
Publication Type
Article
Keywords
Air Pollutants, Environmental - administration & dosage - toxicity
Allergens - administration & dosage - toxicity
Animals
Bronchoalveolar Lavage Fluid - cytology
Dust - adverse effects
Enzyme-Linked Immunosorbent Assay
Female
Immunity - drug effects
Immunoglobulin G - immunology
Immunoglobulins - biosynthesis
Inflammation - chemically induced - pathology
Intubation, Intratracheal
Lung Diseases - chemically induced - immunology - pathology
Lymphocyte Activation - drug effects
Mites
Nitrogen Dioxide - administration & dosage - toxicity
Rats
Rats, Inbred BN
Research Support, U.S. Gov't, Non-P.H.S.
Abstract
Immune hypersensitivity to house dust mite antigen (HDM) is a frequent cause of respiratory allergy. The objective of this study was to determine whether exposure to NO2, a common indoor air pollutant, modulates immune responses to HDM and influences immune-mediated lung disease. Brown Norway rats were immunized ip with 100 micrograms semipurified antigen and Bordetella pertussis adjuvant and challenged 2 weeks later with an intratracheal injection of 50 micrograms of a crude antigen preparation. Exposure to 5 ppm NO2 for 3 hr after both immunization and challenge procedures resulted in significantly higher levels of antigen-specific serum IgE, local IgA, IgG, and IgE antibody than air controls, and increased numbers of inflammatory cells in the lungs. Lymphocyte responsiveness to antigen in the spleen and MLN was also significantly higher in NO2-exposed animals. These data show that exposure to a common air pollutant can upregulate specific immune responses and subsequent immune-mediated pulmonary inflammation.
PubMed ID
8998954 View in PubMed
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Influence of the new angiotensin converting enzyme inhibitor ramipril on several models of acute inflammation and the adjuvant arthritis in the rat.

https://arctichealth.org/en/permalink/ahliterature14599
Source
Arzneimittelforschung. 1986 Nov;36(11):1605-8
Publication Type
Article
Date
Nov-1986
Author
G. Caspritz
H G Alpermann
R. Schleyerbach
Source
Arzneimittelforschung. 1986 Nov;36(11):1605-8
Date
Nov-1986
Language
English
Publication Type
Article
Keywords
Acute Disease
Angiotensin-Converting Enzyme Inhibitors
Animals
Arthritis - drug therapy
Arthritis, Experimental - drug therapy
Bicyclo Compounds - pharmacology - therapeutic use
Bridged Compounds - pharmacology
Disease Models, Animal
Inflammation - chemically induced - drug therapy
Male
Ramipril
Rats
Rats, Inbred Strains
Abstract
Paw oedema in the rat by carrageenin and kaolin partially caused by Hageman factor activation was potentiated by the new angiotensin converting enzyme (ACE) inhibitor 2-[N-[(S)-1-ethoxycarbonyl-3-phenylpropyl-L-alanyl]-(lS,3S,5S)-2- azabicyclo[3.3.0]octane-3-carboxylic acid] (ramipril, Hoe 498) due to its inhibition of kininase II which results in increased bradykinin levels. A dose of 1 microgram ramipril injected into the hind paw of Sprague-Dawley rats concomitantly with, or 1 mg/kg given orally 30 min before administration of the irritants, led to significantly increased inflammatory reactions. The same effects were observed when ramipril was administered 3 h after carrageenin. In the kallikrein-kinin-deficient Brown-Norway rat strain Mai Pfd/f, ramipril did not significantly alter the paw oedema induced as described above. In addition, pretreatment of Sprague-Dawley rats with 10 mg/kg i.v. bromelains completely prevented the potentiation of inflammation by ramipril. Paw oedema provoked by the Hageman factor non-activators serotonin, dextran, ovalbumin and anti-rat IgG was not potentiated by ramipril. The chronic adjuvant arthritis in Lewis rats was not influenced by daily oral treatment with 0.1-3 mg/kg ramipril. Thus, in the rat only those inflammatory reactions involving kinins, presumably generated by Hageman factor activators, are potentiated by ramipril and presumably by other ACE-inhibitors.
PubMed ID
3028436 View in PubMed
Less detail

In vitro analysis of inflammatory responses following environmental exposure to pharmaceuticals and inland waters.

https://arctichealth.org/en/permalink/ahliterature154023
Source
Sci Total Environ. 2009 Feb 1;407(4):1452-60
Publication Type
Article
Date
Feb-1-2009
Author
Hazem Khalaf
Lotta Salste
Patrik Karlsson
Per Ivarsson
Jana Jass
Per-Erik Olsson
Author Affiliation
Biology, Orebro Life Science Center, School of Science and Technology, Orebro University, SE-701 82 Orebro, Sweden.
Source
Sci Total Environ. 2009 Feb 1;407(4):1452-60
Date
Feb-1-2009
Language
English
Publication Type
Article
Keywords
Cell Line, Tumor
Gas Chromatography-Mass Spectrometry
Humans
Inflammation - chemically induced - metabolism
Jurkat Cells
NF-kappa B - analysis
Pharmaceutical Preparations - analysis
Rivers
Solid Phase Extraction
Sweden
Transcription Factor AP-1 - analysis
Water Pollutants, Chemical - analysis - pharmacology
Xenobiotics - analysis - pharmacology
Abstract
Pharmaceuticals are regularly released into the environment; in particular non-steroidal anti-inflammatory drugs (NSAIDs) and antibiotics. Erythromycin, naproxen, furosemide and atenolol are reported to be stable for up to 1 year in the environment, which increases the risk for accumulation. In the present study we have measured the occurrence and concentration of pharmaceuticals in river Viskan (Jössabron) downstream of a sewage treatment plant in Borås, Sweden. Pharmaceuticals and water samples were tested for potential human risk by evaluating inflammatory responses (NF-kappaB and AP-1) using human T24 bladder epithelial cells and Jurkat T-cells. NF-kappaB activity in T24 cells was significantly reduced by all NSAIDs analysed (diclofenac, ketoprofen, naproxen, ibuprophen and dextropropoxyphene), but also by trimethoprim, using environmentally relevant concentrations. NF-kappaB and AP-1 activation was further analysed in response to water samples collected from different locations in Sweden. Dose-dependent down-regulation of AP-1 activity in Jurkat cells was observed at all locations. At two locations (Jössabron and Almenäs) down-regulation of NF-kappaB was observed. In contrast, the NF-kappaB response was potentiated by exposure to water from both locations following activation of NF-kappaB by treatment with heat-killed Escherichia coli. To determine the involvement of pharmaceuticals in the responses, T24 cells were exposed to the pharmaceutical mixture, based on the determined levels at Jössabron. This resulted in reduction of the NF-kappaB response following exposure to the pharmaceutical mixture alone while no potentiation was observed when cells were co-exposed to heat killed E. coli and pharmaceuticals. The obtained results demonstrate that the identified pharmaceuticals affect the inflammatory responses and furthermore indicate the presence of unknown substance(s) with the ability to potentiate inflammatory responses.
PubMed ID
19038416 View in PubMed
Less detail

Maternal endotoxin-induced preterm birth in mice: fetal responses in toll-like receptors, collectins, and cytokines.

https://arctichealth.org/en/permalink/ahliterature87345
Source
Pediatr Res. 2008 Mar;63(3):280-6
Publication Type
Article
Date
Mar-2008
Author
Salminen Annamari
Paananen Reija
Vuolteenaho Reetta
Metsola Juhani
Ojaniemi Marja
Autio-Harmainen Helena
Hallman Mikko
Author Affiliation
Department of Pediatrics, University of Oulu, Oulu, FIN-90014, Finland. annamari.salminen@oulu.fi
Source
Pediatr Res. 2008 Mar;63(3):280-6
Date
Mar-2008
Language
English
Publication Type
Article
Keywords
Amniotic Fluid - immunology
Animals
Chemokine CCL2 - metabolism
Collectins - blood - metabolism
Cytokines - blood - metabolism
Extraembryonic Membranes - immunology
Female
Fetal Blood - immunology
Fetal Death
Fetus - immunology
Gestational Age
Immunohistochemistry
Inflammation - chemically induced - immunology - physiopathology
Interleukin-10 - metabolism
Interleukin-6 - metabolism
Lipopolysaccharides
Lung - embryology - immunology
Maternal-Fetal Exchange
Mice
Mice, Inbred C57BL
Placenta - immunology
Pregnancy
Premature Birth - etiology - immunology - physiopathology
Pulmonary Surfactant-Associated Protein A - metabolism
Pulmonary Surfactant-Associated Protein D - metabolism
Time Factors
Toll-Like Receptor 2 - metabolism
Toll-Like Receptor 4 - metabolism
Toll-Like Receptors - blood - metabolism
Tumor Necrosis Factor-alpha - metabolism
Uterine Diseases - chemically induced - immunology - physiopathology
Uterus - immunology
Abstract
Major cause of prematurity is spontaneous preterm birth (PTB) associated with intrauterine inflammation. Our aim was to establish a model of endotoxin Lipopolysaccharide-induced PTB of live-born pups and to study early immune activation in fetal and maternal compartments. Expression of several proteins that bind microbes (Toll-like receptors TLR4, TLR2; surfactant proteins SP-A, SP-D) was analyzed. At 16 or 17 d of gestation, C57BL/6 dams received a single dose of intraperitoneal LPS, leading to PTB within 17 h. Cytokine levels increased in maternal serum, followed by a modest increase in fetal serum and in amniotic fluid. In uterus, placenta, and fetal membranes, LPS mostly increased the expressions of TLR, SPs, and cytokines. The number of TLR2-positive macrophages increased in labyrinthine placenta. In fetal lung, intestine, liver, and brain there were modest changes in cytokine expressions. In fetal lung, SP and TLR mRNAs decreased and TLR2-positive macrophages redistributed around vessels. LPS-induced fetal deaths associated with early age (16 d gestation) rather than with proinflammatory activation. Here we propose that maternal LPS response leads to PTB and acute decrease of immune proteins in epithelial lining of fetal lung. Instead, acceleration of lung maturity has been previously observed in intraamniotic inflammation.
PubMed ID
18287966 View in PubMed
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19 records – page 1 of 2.