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Airway inflammation among compost workers exposed to actinomycetes spores.

https://arctichealth.org/en/permalink/ahliterature271518
Source
Ann Agric Environ Med. 2015;22(2):253-8
Publication Type
Article
Date
2015
Author
Kari Kulvik Heldal
Lene Madsø
Wijnand Eduard
Source
Ann Agric Environ Med. 2015;22(2):253-8
Date
2015
Language
English
Publication Type
Article
Keywords
Actinobacteria - chemistry
Adult
Aerosols - toxicity
Air Pollutants, Occupational - toxicity
Biomarkers - blood
Female
Humans
Male
Middle Aged
Norway - epidemiology
Occupational Exposure
Pulmonary Surfactant-Associated Protein A - blood
Pulmonary Surfactant-Associated Protein D - blood
Respiratory Hypersensitivity - epidemiology - microbiology
Sewage
Spores, Bacterial - chemistry
Uteroglobin - blood
Abstract
To study the associations between exposure to bioaerosols and work-related symptoms, lung function and biomarkers of airway inflammation in compost workers.
Personal full-shift exposure measurements were performed on 47 workers employed at five windrow plants (n=20) and five reactor plants (n=27). Samples were analyzed for endotoxins, bacteria, fungal and actinomycetes spores. Health examinations were performed on workers and 37 controls before and after work on the day exposure was measured. The examinations included symptoms recorded by questionnaire, lung function by spirometry and nasal dimensions by acoustic rhinometry (AR). The pneumoproteins CC16, SP-D and SP-A were measured in a blood sample drawn at the end of the day.
The levels of endotoxins (median 3 EU/m(3), range 0-730 EU/m(3)) and actinomycetes spores (median 0.2 ? 10(6) spores/m(3), range 0-590 ? 10(6) spores/m(3)) were significantly higher in reactor plants compared to windrow plants. However, windrow composting workers reported more symptoms than reactor composting workers, probably due to use of respiratory protection. Exposure-response relationships between actinomycetes spores exposure and respiratory effects, found as cough and nose irritation during a shift, was significantly increased (OR 4.3, 95% CI 1.1-16, OR 6.1, 95% CI 1.5-25, respectively, p
PubMed ID
26094519 View in PubMed
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Association between the surfactant protein D (SFTPD) gene and subclinical carotid artery atherosclerosis.

https://arctichealth.org/en/permalink/ahliterature278404
Source
Atherosclerosis. 2016 Mar;246:7-12
Publication Type
Article
Date
Mar-2016
Author
Grith L Sorensen
Else Marie Bladbjerg
Rudi Steffensen
Qihua Tan
Jens Madsen
Thomas Drivsholm
Uffe Holmskov
Source
Atherosclerosis. 2016 Mar;246:7-12
Date
Mar-2016
Language
English
Publication Type
Article
Keywords
Asymptomatic Diseases
Carotid Arteries - diagnostic imaging
Carotid Artery Diseases - blood - diagnostic imaging - genetics
Carotid Intima-Media Thickness
Chi-Square Distribution
Denmark
Female
Genetic Association Studies
Genetic Predisposition to Disease
Humans
Linear Models
Logistic Models
Male
Middle Aged
Multivariate Analysis
Phenotype
Plaque, Atherosclerotic
Polymorphism, Single Nucleotide
Pulmonary Surfactant-Associated Protein D - blood - genetics
Risk assessment
Risk factors
Smoking - adverse effects
Abstract
Surfactant protein D (SP-D) is a defense collectin with inflammation-modulating properties. SP-D deficiency inhibits atherosclerosis in vivo, and the circulatory SP-D levels have been previously associated with cardiovascular disease mortality. We hypothesized that plasma SP-D (pSP-D) and SP-D gene (SFTPD) single nucleotide polymorphisms (SNPs) are risk factors for atherosclerosis.
We evaluated individuals who were all 60 years old and participated in The Glostrup Population Study. Subclinical atherosclerosis was diagnosed based on the ultrasonographic measurement of intima-media thickness (IMT) and protruding plaques in the right carotid artery. Associations between cardiovascular traits and the levels of pSP-D (n = 687) or two coding SFTPD SNPs rs3088308 and rs721917 (n = 396) were investigated using multiple linear regressions and logistic regressions.
There was no significant association between pSP-D and the presence of plaques or IMT. The SFTPD SNP rs3088308 was nominally associated with the presence of plaques, and rs721917 was nominally associated with IMT. The directions of effects of associations were markedly dependent on current smoking status.
The results do not support that pSP-D levels influence the development of subclinical atherosclerosis. However, the SFTPD SNP data support previous observations from animal studies that SP-D plays a role in the etiology of atherosclerotic disease development. The nominal significant effects are likely to be mediated by structural variant SP-D modulation of effects of tobacco smoking and are independent of pSP-D levels. The data warrant confirmation in larger cohorts.
PubMed ID
26748346 View in PubMed
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Circulating surfactant protein D is associated to mortality in elderly women: a twin study.

https://arctichealth.org/en/permalink/ahliterature120460
Source
Immunobiology. 2013 May;218(5):712-7
Publication Type
Article
Date
May-2013
Author
Helle Wulf-Johansson
Mikael Thinggaard
Qihua Tan
Sofie Lock Johansson
Anders Schlosser
Kaare Christensen
Uffe Holmskov
Grith Lykke Sorensen
Author Affiliation
Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark, J.B. Winsløws Vej 25, 5000 Odense, Denmark. hwulf@health.sdu.dk
Source
Immunobiology. 2013 May;218(5):712-7
Date
May-2013
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Biological Markers - blood
Body mass index
Denmark - epidemiology
Female
Health status
Humans
Incidence
Longitudinal Studies
Male
Mortality
Probability
Pulmonary Surfactant-Associated Protein D - blood
Risk factors
Smoking - mortality
Survival Analysis
Abstract
Surfactant protein D (SP-D) is produced in the lungs and additional mucosal surfaces. Systemic SP-D levels are previously associated to aging-related- and lifestyle-related disorders and predicts mortality in cardiovascular and lung diseases. However, the association between higher serum SP-D levels and mortality in the general population is unknown. We hypothesized that increased systemic levels of SP-D may be used as prognostic factor for assessing the mortality in the elderly.
SP-D serum levels were measured in 689 elderly subjects and mortality ratios were investigated after a 13-year follow-up period. Survival analysis showed that increasing quartiles of serum SP-D levels were associated to mortality in 70+ year old women (hazard ratio [HR], 1.29; 95% confidence interval [CI], 0.93-1.78; p = 0.032) adjusted for age, smoking and BMI. Women with SP-D levels above 2100 ng/ml had significantly increased mortality when compared to elderly women with SP-D levels equal to or below 2100 ng/ml (HR, 1.45; 95% CI, 1.12-1.88; p = 0.005). The likelihood that the female twin with the highest SP-D level died first increased with increasing SP-D levels (p = 0.031) - that is, the bigger intra-pair difference in SP-D level, the higher the probability that the twin with the highest measure died first (odds ratio [OR], 1.66; p = 0.047).
The study demonstrates that higher circulating SP-D levels are associated with increased mortality rate in elderly women in this population-based cohort study. SP-D may serve as a biomarker to track the cardio-pulmonary health status in elderly women.
PubMed ID
22999473 View in PubMed
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The effects of fluticasone with or without salmeterol on systemic biomarkers of inflammation in chronic obstructive pulmonary disease.

https://arctichealth.org/en/permalink/ahliterature158537
Source
Am J Respir Crit Care Med. 2008 Jun 1;177(11):1207-14
Publication Type
Article
Date
Jun-1-2008
Author
Don D Sin
S F Paul Man
Darcy D Marciniuk
Gordon Ford
Mark FitzGerald
Eric Wong
Ernest York
Rajesh R Mainra
Warren Ramesh
Lyle S Melenka
Eric Wilde
Robert L Cowie
Dave Williams
Wen Q Gan
Roxanne Rousseau
Author Affiliation
Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, Canada.
Source
Am J Respir Crit Care Med. 2008 Jun 1;177(11):1207-14
Date
Jun-1-2008
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Adrenergic beta-Agonists - administration & dosage
Aged
Albuterol - administration & dosage - analogs & derivatives
Androstadienes - administration & dosage
Anti-Inflammatory Agents - administration & dosage
Biological Markers - metabolism
C-Reactive Protein - metabolism
Canada
Double-Blind Method
Drug Combinations
Female
Humans
Interleukin-6 - metabolism
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive - drug therapy - metabolism - pathology
Pulmonary Surfactant-Associated Protein D - metabolism
Respiratory Function Tests
Treatment Outcome
Abstract
Small studies have suggested that inhaled corticosteroids can suppress systemic inflammation in chronic obstructive pulmonary disease (COPD).
To determine the effect of inhaled corticosteroids with or without long-acting beta(2)-adrenergic agonist on systemic biomarkers of inflammation.
We conducted a double-blind randomized placebo-controlled trial across 11 centers (n = 289 patients with FEV(1) of 47.8 +/- 16.2% of predicted) to compare the effects of inhaled fluticasone alone or in combination with salmeterol against placebo on circulating biomarkers of systemic inflammation over 4 weeks. The primary endpoint was C-reactive protein (CRP) level. Secondary molecules of interest were IL-6 and surfactant protein D (SP-D).
Neither fluticasone nor the combination of fluticasone/salmeterol had a significant effect on CRP or IL-6 levels. There was, however, a significant reduction in SP-D levels with fluticasone and fluticasone/salmeterol compared with placebo (P = 0.002). Health status also improved significantly in both the fluticasone and fluticasone/salmeterol groups compared with placebo, driven mostly by improvements in the symptom scores. Changes in the circulating SP-D levels were related to changes in health status scores. FEV(1) improved significantly only in the fluticasone/salmeterol group compared with placebo.
ICS in conjunction with long-acting beta(2)-adrenergic agonist do not reduce CRP or IL-6 levels in serum of patients with COPD over 4 weeks. They do, however, significantly reduce serum SP-D levels. These data suggest that these drugs reduce lung-specific but not generalized biomarkers of systemic inflammation in COPD.
Notes
Comment In: Am J Respir Crit Care Med. 2008 Jun 1;177(11):1177-818487618
Comment In: Am J Respir Crit Care Med. 2009 Jan 15;179(2):170; author reply 170-119119152
Comment In: Expert Opin Pharmacother. 2008 Dec;9(18):3271-319040347
PubMed ID
18310480 View in PubMed
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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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The PROTECCT-M study: a cohort study investigating associations between novel specific biomarkers, patient-related, healthcare system markers and the trajectory of COPD patients treated in primary care.

https://arctichealth.org/en/permalink/ahliterature260468
Source
BMC Pulm Med. 2014;14:88
Publication Type
Article
Date
2014
Author
Jens Søndergaard
Anders Halling
Source
BMC Pulm Med. 2014;14:88
Date
2014
Language
English
Publication Type
Article
Keywords
Adult
Biological Markers - blood
Carrier Proteins - blood
Cohort Studies
Denmark
Disease Progression
Early Diagnosis
Electronic Health Records
Extracellular Matrix Proteins - blood
Female
Glycoproteins - blood
Humans
Male
Middle Aged
Physician's Practice Patterns
Primary Health Care - methods
Prognosis
Pulmonary Disease, Chronic Obstructive - blood - diagnosis - therapy
Pulmonary Surfactant-Associated Protein D - blood
Registries
Research Design
Treatment Outcome
Abstract
Chronic Obstructive Pulmonary Disease (COPD) is the most common severe chronic disease in primary care. It is typically diagnosed at a late stage, and it is also difficult to predict its trajectory and hence to tailor treatment and rehabilitation. The overall aim is to study determinants of exacerbations of COPD treated in primary care and to study, if the prognosis is related to patient-related, healthcare system markers or levels of the potential biomarkers such as microfibrillar-associated protein 4 (MFAP4) and surfactant protein D (SP-D). Furthermore, we aim to establish a cohort of COPD patients treated in Danish primary care comprising register data, data captured from the GPs' electronic patient record system (EPR) and a biobank in order to make analyses on factors associated with different tractories of COPD treated in primary care.
A cohort study of incident and prevalent COPD patients treated and followed by their GPs using data capture, which is a computer system collecting data from the GPs' own EPR and transferring them to the Danish General Practice Research Database. The participating COPD patients were investigated at a baseline consultation by their own GP, and the results were registered using a pop-up menu by the GP. During the consultation blood samples were taken and the patients were given a questionnaire. The patients will then be followed prospectively at yearly consultations and in between these consultations by means of the data capture system. The collected data will also be combined with register data from other sources. The data collection started in December 2012, and so far 30 practices with 77 GPs have included about 350 patients. The study aims to include 2000 patients till the end of 2016, and after that to continue to collect data on these patients using the data capture system.
The GP currently lacks tools to predict trajectory of their COPD patients. The measurement of lung function only reflects loss of lung capacity and not disease activity. Use of biomarkers for detection of early COPD could be a possible way of predicting trajectory to aid both the GP and his/her patients. This study aims to provide evidence of determinants of a COPD trajectory, including novel specific biomarkers and other patient- and healthcare system-related markers.
ClinicalTrials.gov Protocol Registration System, Identifier: NCT01698151.
Notes
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PubMed ID
24886233 View in PubMed
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Sputum neutrophils are elevated in smelter workers, and systemic neutrophils are associated with rapid decline in FEV1.

https://arctichealth.org/en/permalink/ahliterature283070
Source
Occup Environ Med. 2016 Jul;73(7):459-66
Publication Type
Article
Date
Jul-2016
Author
Liv Ingunn Bjoner Sikkeland
Helle Laier Johnsen
Tonje Bøyum Riste
Neil E Alexis
Bente Halvorsen
Vidar Søyseth
Johny Kongerud
Source
Occup Environ Med. 2016 Jul;73(7):459-66
Date
Jul-2016
Language
English
Publication Type
Article
Keywords
Adult
Case-Control Studies
Female
Forced expiratory volume
Humans
Industry
Linear Models
Male
Matrix Metalloproteinases, Secreted - analysis
Metals - adverse effects
Middle Aged
Neutrophils - drug effects
Nitric Oxide - analysis
Norway - epidemiology
Occupational Exposure - adverse effects
Pulmonary Surfactant-Associated Protein D - analysis
Smoking - epidemiology
Spirometry
Sputum - chemistry - immunology
Surveys and Questionnaires
Transforming Growth Factor beta - analysis
Abstract
In a previous study on smelter workers we, found significant relationship between exposure to dust and accelerated annual decline in forced expiratory volume in 1 s (FEV1). In this cross-sectional study at the end of a follow-up, we aimed to investigate the possible association between annual decline in FEV1 and markers of airways, and systemic inflammation in smelter workers.
Employees (n=76 (27 current smokers)) who had been part of a longitudinal study (9-13 years) that included spirometry (>6 measurements) and respiratory questionnaires, performed induced sputum, exhaled NO and had blood drawn. Participants with annual decline in FEV1=45 mL were compared with participants with annual decline
PubMed ID
27052769 View in PubMed
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Surfactant protein D gene polymorphism associated with severe respiratory syncytial virus infection.

https://arctichealth.org/en/permalink/ahliterature31549
Source
Pediatr Res. 2002 Jun;51(6):696-9
Publication Type
Article
Date
Jun-2002
Author
Meri Lahti
Johan Lofgren
Riita Marttila
Marjo Renko
Tuula Klaavuniemi
Ritva Haataja
Mika Ramet
Mikko Hallman
Author Affiliation
Department of Pediatrics and Biocenter Oulu, University of Oulu, PO Box 5000, FIN-90014 Oulu, Finland.
Source
Pediatr Res. 2002 Jun;51(6):696-9
Date
Jun-2002
Language
English
Publication Type
Article
Keywords
Female
Gene Frequency
Genetic Predisposition to Disease
Genotype
Glycoproteins - genetics
Humans
Infant, Newborn
Logistic Models
Male
Polymorphism, Genetic
Pulmonary Surfactant-Associated Protein D
Pulmonary Surfactants
Research Support, Non-U.S. Gov't
Respiratory Syncytial Virus Infections - genetics
Respiratory Tract Infections - genetics - virology
Abstract
Respiratory syncytial virus (RSV) is the major respiratory tract pathogen in infancy. Host-related differences in susceptibility to severe RSV infection suggest that genetic factors may play a role. In this study, a candidate-gene approach was used to study whether the surfactant protein D (SP-D) gene polymorphism associates with severe RSV infection. DNA samples from 84 infants hospitalized for the treatment of RSV bronchiolitis and 93 healthy controls were analyzed. The controls were matched with the cases on the basis of sex, hospital district, date of birth (+/-2 wk) and gestational age at birth (+/-2 wk). Three biallelic SP-D gene polymorphisms were genotyped. Significant differences were observed in the SP-D allele frequencies for amino acid 11 between the RSV infants and their matched controls. The frequency of the allele coding for Met 11 (p = 0.033) was increased in the severe RSV group. The frequency of the homozygous genotype Met/Met for amino acid 11 was increased in the RSV group relative to the controls, whereas the heterozygous genotype tended to be less frequent among the RSV cases than in the matched controls. Conditional logistic regression analysis was used to study whether the confounders, i.e. smoking and number of children in the family, influence the association between the homozygous SP-D genotype for methionine 11 and the risk of RSV bronchiolitis. The results further confirmed this association (p = 0.028). To our knowledge, the present report provides the first evidence of a specific gene associated with susceptibility to severe RSV infection.
PubMed ID
12032263 View in PubMed
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Surfactant protein D is a candidate biomarker for subclinical tobacco smoke-induced lung damage.

https://arctichealth.org/en/permalink/ahliterature104792
Source
Am J Physiol Lung Cell Mol Physiol. 2014 May 1;306(9):L887-95
Publication Type
Article
Date
May-1-2014
Author
Sofie L Johansson
Qihua Tan
René Holst
Lene Christiansen
Niels C G Hansen
Allan T Hojland
Helle Wulf-Johansson
Anders Schlosser
Ingrid L Titlestad
Jørgen Vestbo
Uffe Holmskov
Kirsten O Kyvik
Grith L Sorensen
Author Affiliation
Cardiovascular and Renal Research, Institute of Molecular Medicine, Univ. of Southern Denmark, Odense, Denmark. glsorensen@health.sdu.dk.
Source
Am J Physiol Lung Cell Mol Physiol. 2014 May 1;306(9):L887-95
Date
May-1-2014
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Aged
Biological Markers - analysis
Cross-Sectional Studies
Denmark
Female
Forced expiratory volume
Genetic Association Studies
Haplotypes - genetics
Humans
Lung Diseases - chemically induced - diagnosis - genetics
Male
Middle Aged
Polymorphism, Single Nucleotide - genetics
Prognosis
Pulmonary Surfactant-Associated Protein D - genetics
Pulmonary Surfactants - metabolism
Smoking - adverse effects
Vital Capacity
Young Adult
Abstract
Variation in surfactant protein D (SP-D) is associated with lung function in tobacco smoke-induced chronic respiratory disease. We hypothesized that the same association exists in the general population and could be used to identify individuals sensitive to smoke-induced lung damage. The association between serum SP-D (sSP-D) and expiratory lung function was assessed in a cross-sectional design in a Danish twin population (n = 1,512, 18-72 yr old). The adjusted heritability estimates for expiratory lung function, associations between SP-D gene (SFTPD) single-nucleotide polymorphisms or haplotypes, and expiratory lung function were assessed using twin study methodology and mixed-effects models. Significant inverse associations were evident between sSP-D and the forced expiratory volume in 1 s and forced vital capacity in the presence of current tobacco smoking but not in nonsmokers. The two SFTPD single-nucleotide polymorphisms, rs1923536 and rs721917, and haplotypes, including these single-nucleotide polymorphisms or rs2243539, were inversely associated with expiratory lung function in interaction with smoking. In conclusion, SP-D is phenotypically and genetically associated with lung function measures in interaction with tobacco smoking. The obtained data suggest sSP-D as a candidate biomarker in risk assessments for subclinical tobacco smoke-induced lung damage. The data and derived conclusion warrant confirmation in a longitudinal population following chronic obstructive pulmonary disease initiation and development.
PubMed ID
24610936 View in PubMed
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Surfactant proteins A and D in Eustachian tube epithelium.

https://arctichealth.org/en/permalink/ahliterature58617
Source
Am J Physiol Lung Cell Mol Physiol. 2001 Sep;281(3):L660-7
Publication Type
Article
Date
Sep-2001
Author
R. Paananen
R. Sormunen
V. Glumoff
M. van Eijk
M. Hallman
Author Affiliation
Biocenter Oulu, University of Oulu, FIN-90014 Oulu, Finland. rpaanane@cc.oulu.fi
Source
Am J Physiol Lung Cell Mol Physiol. 2001 Sep;281(3):L660-7
Date
Sep-2001
Language
English
Publication Type
Article
Keywords
Animals
Blotting, Western
Bronchoalveolar Lavage Fluid - chemistry
Epithelial Cells - cytology - metabolism
Eustachian Tube - anatomy & histology - cytology - metabolism
Glycoproteins - metabolism
In Situ Hybridization
Irrigation
Microscopy, Electron
Microscopy, Immunoelectron
Proteolipids - metabolism
Pulmonary Surfactant-Associated Protein A
Pulmonary Surfactant-Associated Protein D
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants - metabolism
Research Support, Non-U.S. Gov't
Swine
Tissue Distribution
Abstract
Surfactant protein (SP) A and SP-D are collectins that have roles in host defense. The Eustachian tube (ET) maintains the patency between the upper airways and the middle ear. Dysfunction of local mucosal immunity in ET may predispose infants to recurrent otitis media. We recently described preliminary evidence of the expression of SP-A and SP-D in the ET. Our present aim was to establish the sites of SP-A and SP-D expression within the epithelium of the ET in vivo. With in situ hybridization, electron microscopy, and immunoelectron microscopy, the cells responsible for SP-A and SP-D expression and storage were identified. SP-A expression was localized within the ET epithelium, and the protein was found in the electron-dense granules of microvillar epithelial cells. Being concentrated in the epithelial lining, only a few cells revealed intracellular SP-D, and it was not associated with granules. The SP-A and SP-D immunoreactivities in ET lavage fluid, as shown by Western blot analyses, were similar to those in bronchoalveolar lavage fluid. We propose that there are specialized cells in the ET epithelium expressing and secreting SP-A and SP-D. SP-A and SP-D may be important for antibody-independent protection of the middle ear against infections.
PubMed ID
11504694 View in PubMed
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10 records – page 1 of 1.