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 in | Journal of allergy and clinical immunology Vol. 110; no. 4; pp. 589 - 595 |
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Main Authors | , , |
Format | Journal Article |
Language | English |
Published |
New York, NY
Mosby, Inc
01.10.2002
Elsevier Elsevier Limited |
Subjects | |
Online Access | Get full text |
ISSN | 0091-6749 1097-6825 |
DOI | 10.1067/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.) |
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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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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 |
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