Comparative analysis of topical and systemic respiratory tract inflammation markers in COPD patients exposed to industrial chemical aerosol

2018 ◽  
pp. 128-138
Author(s):  
Л.В. Артемова ◽  
◽  
О.И. Румянцева ◽  
С.Г. Комарова ◽  
А.Н. Николайчук
Keyword(s):  
Comparative Analysis ◽  
Respiratory Tract ◽  
Inflammation Markers ◽  
Industrial Chemical ◽  
Copd Patients ◽  
Respiratory Tract Inflammation

Clinical and functional peculiarities at patients with bronchial asthma, chronic obstructive pulmonary disease and overlap of asthma-chronic obstructive pulmonary disease

2020 ◽  
Vol 24 (4) ◽  
pp. 80-86
Author(s):  
V. I. Trofimov ◽  
D. Z. Baranov
Keyword(s):  
Chronic Obstructive Pulmonary Disease ◽  
Pulmonary Disease ◽  
Bronchial Asthma ◽  
Blood Test ◽  
Chronic Obstructive ◽  
Inflammation Markers ◽  
Obstructive Pulmonary Disease ◽  
Copd Patients ◽  
Functional Features ◽  
Lower Airways

BACKGROUND: a comparative analysis of laboratory and instrumental tests at patients with bronchial obstructive diseases seems very actual due to the wide prevalence of these diseases. THE AIM: to evaluate characteristics of spirometry as well as allergic (total IgE, sputum eosinophils) and infectious (blood and sputum leucocytes, ESR, CRP, fibrinogen) inflammation markers at patients with bronchial obstructive diseases. PATIENTS AND METHODS: 104 case histories of patients with bronchial asthma, chronic obstructive pulmonary disease and overlap were analyzed including age, duration of smoking (pack-years), laboratory (clinical blood test, biochemical blood test, general sputum analysis, sputum culture) and instrumental (spirometry, body plethysmography, echocardiography) tests. Data were processed statistically with non-parametric methods. RESULTS: COPD patients were older than other groups’ patients, had the highest pack-years index. ACO patients were marked with maximal TLC and Raw, minimal FEV1, FEF25-75, FEV1/FVC. Patients with COPD had the highest inflammation markers (leucocyte count, CRP, fibrinogen). CONCLUSION: high active inflammation may cause severe lower airways possibility disorders at patients with COPD. Data related to a possible role of K. pneumoniaе in the pathogenesis of eosinophilic inflammation in lower airways are of significant interest. Patients with ACO occupy an intermediate position between asthma and COPD patients based on clinical and functional features.

scholarly journals Molecular Analysis of Tetracycline Resistance inPasteurella aerogenes

2001 ◽  
Vol 45 (10) ◽  
pp. 2885-2890 ◽  
Author(s):  
Corinna Kehrenberg ◽  
Stefan Schwarz
Keyword(s):  
Comparative Analysis ◽  
Respiratory Tract ◽  
Molecular Analysis ◽  
Intestinal Tract ◽  
Tetracycline Resistance ◽  
Illegitimate Recombination ◽  
Pcr Analysis ◽  
Chromosomal Dna ◽  
Gene Copies

ABSTRACT Tetracycline-resistant Pasteurella aerogenes isolates obtained from the intestinal tract of swine were investigated for theirtet genes by PCR analysis and hybridization experiments. In contrast to Pasteurella isolates from the respiratory tract, tet(H) genes were detected in the chromosomal DNA of only 2 of the 24 isolates, one of which also carried two copies of atet(B) gene. All other P. aerogenes isolates carried tet(B) genes, which are the predominanttet genes among Enterobacteriaceae. A single isolate harbored a tet(B) gene as part of a truncated Tn10 element on the 4.8-kb plasmid pPAT2. Comparative analysis of the pPAT2 sequence suggested that the Tn10relic on plasmid pPAT2 is the result of several illegitimate recombination events. The remaining 21 P. aerogenesisolates carried one or two copies of the tet(B) gene in their chromosomal DNA. In the majority of the cases, thesetet(B) genes were associated with copies of Tn10 as confirmed by their SfuI andBamHI hybridization patterns. No correlation between the number of tet gene copies and the MICs of tetracycline, doxycyline and minocycline was observed.

scholarly journals DNA Damage in Nasal and Brain Tissues of Canines Exposed to Air Pollutants Is Associated with Evidence of Chronic Brain Inflammation and Neurodegeneration

2003 ◽  
Vol 31 (5) ◽  
pp. 524-538 ◽  
Author(s):  
Lilian Calderon-Garciduenas ◽  
Robert R. Maronpot ◽  
Ricardo Torres-Jardon ◽  
Carlos Henriquez-Roldan ◽  
Robert Schoonhoven ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Dna Damage ◽  
Olfactory Bulb ◽  
Respiratory Tract ◽  
Mexico City ◽  
Air Pollutants ◽  
Urban Pollution ◽  
Ap Sites ◽  
The Brain ◽  
Respiratory Tract Inflammation

Acute, subchronic, or chronic exposures to particulate matter (PM) and pollutant gases affect people in urban areas and those exposed to fires, disasters, and wars. Respiratory tract inflammation, production of mediators of inflammation capable of reaching the brain, systemic circulation of PM, and disruption of the nasal respiratory and olfactory barriers are likely in these populations. DNA damage is crucial in aging and in age-associated diseases such as Alzheimer's disease. We evaluated apurinic/apyrimidinic (AP) sites in nasal and brain genomic DNA, and explored by immunohistochemistry the expression of nuclear factor NF κB p65, inducible nitric oxide synthase (iNOS), cyclo-oxygenase 2 (COX2), metallothionein I and II, apolipoprotein E, amyloid precursor protein (APP), and beta-amyloid1-42 in healthy dogs naturally exposed to urban pollution in Mexico City. Nickel (Ni) and vanadium (V) were measured by inductively coupled plasma mass spectrometry (ICP-MS). Forty mongrel dogs, ages 7 days—10 years were studied (14 controls from Tlaxcala and 26 exposed to urban pollution in South West Metropolitan Mexico City (SWMMC)). Nasal respiratory and olfactory epithelium were found to be early pollutant targets. Olfactory bulb and hippocampal AP sites were significantly higher in exposed than in control age matched animals. Ni and V were present in a gradient from olfactory mucosa > olfactory bulb > frontal cortex. Exposed dogs had (a) nuclear neuronal NF κB p65, (b) endothelial, glial and neuronal iNOS, (c) endothelial and glial COX2, (d) ApoE in neuronal, glial and vascular cells, and (e) APP and β amyloid1-42 in neurons, diffuse plaques (the earliest at age 11 months), and in subarachnoid blood vessels. Increased AP sites and the inflammatory and stress protein brain responses were early and significant in dogs exposed to urban pollution. Oil combustion PM-associated metals Ni and V were detected in the brain. There was an acceleration of Alzheimer's-type pathology in dogs chronically exposed to air pollutants. Respiratory tract inflammation and deteriorating olfactory and respiratory barriers may play a role in the observed neuropathology. These data suggest that Alzheimer's disease may be the sequela of air pollutant exposures and the resulting systemic inflammation.

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