Cockroach extract antigen increases bronchial airway epithelial permeability

Background: The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of asthma has been reported in inner-city children. The increased incidence of asthma in inner-city children is thought to be caused, i...

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Published inJournal of allergy and clinical immunology Vol. 110; no. 4; pp. 589 - 595
Main Authors Antony, Ajay B., Tepper, Robert S., Mohammed, Kamal A.
Format Journal Article
LanguageEnglish
Published New York, NY Mosby, Inc 01.10.2002
Elsevier
Elsevier Limited
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ISSN0091-6749
1097-6825
DOI10.1067/mai.2002.127798

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Abstract Background: The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of asthma has been reported in inner-city children. The increased incidence of asthma in inner-city children is thought to be caused, in part, by frequent exposure to allergens of the common household pest the cockroach. Objective: We sought to investigate whether cockroach extract antigen (CrAg) induces vascular permeability factor, also known as vascular endothelial growth factor (VEGF), and whether it increases permeability in bronchial airway epithelial cells (BAECs). Methods: We estimated CrAg-induced VEGF release in BAECs by using an ELISA and VEGF mRNA expression by using an RT-PCR reaction. The influence of CrAg on BAEC barrier function was estimated by measuring electrical resistance with an electric cell substrate impedance-sensing system. Results: Our results demonstrate that CrAg induces VEGF release in BAECs in a time-dependent manner. The VEGF induction was also confirmed by means of VEGF mRNA expression in CrAg-stimulated BAECs. CrAg decreased electrical resistance across BAEC monolayers. The maximum decrease in electrical resistance was noticed 6 hours after activation and reached a plateau thereafter. Neutralizing antibodies to VEGF significantly inhibited the decrease in BAEC electrical resistance caused by CrAg. Conclusions: These data suggest that CrAg induces VEGF release in BAECs and alters bronchial airway permeability. (J Allergy Clin Immunol 2002;110:589-95.)
AbstractList Background:The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of asthma has been reported in inner-city children. The increased incidence of asthma in inner-city children is thought to be caused, in part, by frequent exposure to allergens of the common household pest the cockroach.Objective:We sought to investigate whether cockroach extract antigen (CrAg) induces vascular permeability factor, also known as vascular endothelial growth factor (VEGF), and whether it increases permeability in bronchial airway epithelial cells (BAECs).Methods:We estimated CrAg-induced VEGF release in BAECs by using an ELISA and VEGF mRNA expression by using an RT-PCR reaction. The influence of CrAg on BAEC barrier function was estimated by measuring electrical resistance with an electric cell substrate impedance-sensing system.Results:Our results demonstrate that CrAg induces VEGF release in BAECs in a time-dependent manner. The VEGF induction was also confirmed by means of VEGF mRNA expression in CrAg-stimulated BAECs. CrAg decreased electrical resistance across BAEC monolayers. The maximum decrease in electrical resistance was noticed 6 hours after activation and reached a plateau thereafter. Neutralizing antibodies to VEGF significantly inhibited the decrease in BAEC electrical resistance caused by CrAg.Conclusions:These data suggest that CrAg induces VEGF release in BAECs and alters bronchial airway permeability. (J Allergy Clin Immunol 2002;110:589-95.)
The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of asthma has been reported in inner-city children. The increased incidence of asthma in inner-city children is thought to be caused, in part, by frequent exposure to allergens of the common household pest the cockroach. We sought to investigate whether cockroach extract antigen (CrAg) induces vascular permeability factor, also known as vascular endothelial growth factor (VEGF), and whether it increases permeability in bronchial airway epithelial cells (BAECs). We estimated CrAg-induced VEGF release in BAECs by using an ELISA and VEGF mRNA expression by using an RT-PCR reaction. The influence of CrAg on BAEC barrier function was estimated by measuring electrical resistance with an electric cell substrate impedance-sensing system. Our results demonstrate that CrAg induces VEGF release in BAECs in a time-dependent manner. The VEGF induction was also confirmed by means of VEGF mRNA expression in CrAg-stimulated BAECs. CrAg decreased electrical resistance across BAEC monolayers. The maximum decrease in electrical resistance was noticed 6 hours after activation and reached a plateau thereafter. Neutralizing antibodies to VEGF significantly inhibited the decrease in BAEC electrical resistance caused by CrAg. These data suggest that CrAg induces VEGF release in BAECs and alters bronchial airway permeability.
The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of asthma has been reported in inner-city children. The increased incidence of asthma in inner-city children is thought to be caused, in part, by frequent exposure to allergens of the common household pest the cockroach. Objective: We sought to investigate whether cockroach extract antigen (CrAg) induces vascular permeability factor, also known as vascular endothelial growth factor (VEGF), and whether it increases permeability in bronchial airway epithelial cells (BAECs). Methods: We estimated CrAg-induced VEGF release in BAECs by using an ELISA and VEGF mRNA expression by using an RT-PCR reaction. The influence of CrAg on BAEC barrier function was estimated by measuring electrical resistance with an electric cell substrate impedance-sensing system. Results: Our results demonstrate that CrAg induces VEGF release in BAECs in a time-dependent manner. The VEGF induction was also confirmed by means of VEGF mRNA expression in CrAg-stimulated BAECs. CrAg decreased electrical resistance across BAEC monolayers. The maximum decrease in electrical resistance was noticed 6 hours after activation and reached a plateau thereafter. Neutralizing antibodies to VEGF significantly inhibited the decrease in BAEC electrical resistance caused by CrAg. Conclusions: These data suggest that CrAg induces VEGF release in BAECs and alters bronchial airway permeability.
The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of asthma has been reported in inner-city children. The increased incidence of asthma in inner-city children is thought to be caused, in part, by frequent exposure to allergens of the common household pest the cockroach.BACKGROUNDThe bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of asthma has been reported in inner-city children. The increased incidence of asthma in inner-city children is thought to be caused, in part, by frequent exposure to allergens of the common household pest the cockroach.We sought to investigate whether cockroach extract antigen (CrAg) induces vascular permeability factor, also known as vascular endothelial growth factor (VEGF), and whether it increases permeability in bronchial airway epithelial cells (BAECs).OBJECTIVEWe sought to investigate whether cockroach extract antigen (CrAg) induces vascular permeability factor, also known as vascular endothelial growth factor (VEGF), and whether it increases permeability in bronchial airway epithelial cells (BAECs).We estimated CrAg-induced VEGF release in BAECs by using an ELISA and VEGF mRNA expression by using an RT-PCR reaction. The influence of CrAg on BAEC barrier function was estimated by measuring electrical resistance with an electric cell substrate impedance-sensing system.METHODSWe estimated CrAg-induced VEGF release in BAECs by using an ELISA and VEGF mRNA expression by using an RT-PCR reaction. The influence of CrAg on BAEC barrier function was estimated by measuring electrical resistance with an electric cell substrate impedance-sensing system.Our results demonstrate that CrAg induces VEGF release in BAECs in a time-dependent manner. The VEGF induction was also confirmed by means of VEGF mRNA expression in CrAg-stimulated BAECs. CrAg decreased electrical resistance across BAEC monolayers. The maximum decrease in electrical resistance was noticed 6 hours after activation and reached a plateau thereafter. Neutralizing antibodies to VEGF significantly inhibited the decrease in BAEC electrical resistance caused by CrAg.RESULTSOur results demonstrate that CrAg induces VEGF release in BAECs in a time-dependent manner. The VEGF induction was also confirmed by means of VEGF mRNA expression in CrAg-stimulated BAECs. CrAg decreased electrical resistance across BAEC monolayers. The maximum decrease in electrical resistance was noticed 6 hours after activation and reached a plateau thereafter. Neutralizing antibodies to VEGF significantly inhibited the decrease in BAEC electrical resistance caused by CrAg.These data suggest that CrAg induces VEGF release in BAECs and alters bronchial airway permeability.CONCLUSIONSThese data suggest that CrAg induces VEGF release in BAECs and alters bronchial airway permeability.
Author Mohammed, Kamal A.
Antony, Ajay B.
Tepper, Robert S.
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Issue 4
Keywords Bronchial airway epithelial cells
BAEC
bronchial epithelial permeability
CrAg
vascular endothelial growth factor
VEGF
cockroach extract antigen
ECIS
SFM
GAPDH
Human
Immunopathology
Allergy
Urban environment
Respiratory disease
Pathogenesis
Insecta
Blattellidae
Extract
Permeability
Asthma
Antigen
Respiratory tract
Vascular endothelium growth factor
Arthropoda
Epithelial cell
Obstructive pulmonary disease
Molecular biology
Invertebrata
Child
Reverse transcription polymerase chain reaction
ELISA assay
Dictyoptera
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Snippet Background: The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high...
The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high incidence of...
Background:The bronchial epithelial cells of airways are subject to recurrent environmental injury throughout the life of an individual. Recently, a high...
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SubjectTerms Allergic diseases
Allergies
Animals
Antigens - chemistry
Antigens - pharmacology
Aspartic Acid Endopeptidases - analysis
Biological and medical sciences
Bronchi - metabolism
Bronchi - physiology
Bronchial airway epithelial cells
bronchial epithelial permeability
Cell culture
Cells, Cultured
cockroach extract antigen
Cockroaches - chemistry
Electric Impedance
Endothelial Growth Factors - genetics
Endothelial Growth Factors - metabolism
Enzymes
Epithelium - metabolism
Epithelium - physiology
Gene expression
Humans
Immunopathology
Inner city
Lymphokines - genetics
Lymphokines - metabolism
Medical sciences
Milk
Permeability
Permeability - drug effects
Proteins
Respiratory and ent allergic diseases
RNA, Messenger - metabolism
Serine Endopeptidases - analysis
Studies
Tissue Extracts - chemistry
Tissue Extracts - pharmacology
Vascular endothelial growth factor
Vascular Endothelial Growth Factor A
Vascular Endothelial Growth Factors
Title Cockroach extract antigen increases bronchial airway epithelial permeability
URI https://www.clinicalkey.com/#!/content/1-s2.0-S0091674902001550
https://dx.doi.org/10.1067/mai.2002.127798
https://www.ncbi.nlm.nih.gov/pubmed/12373266
https://www.proquest.com/docview/1504836981
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https://www.proquest.com/docview/72169153
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