Upregulation of αGM-CSF-receptor in nonatopic asthma but not in atopic asthma
Background: Intrinsic asthma is characterized by an increased number of activated eosinophils and macrophages and an increased expression of the hematopoietic growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF) in the bronchial mucosa. Objective: This study was carried out to inv...
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| Veröffentlicht in: | Journal of allergy and clinical immunology 1997-05, Vol.99 (5), p.666-672 |
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| creator | Kotsimbos, A.Thomas C. Humbert, Marc Minshall, Eleanor Durham, Stephen Pfister, Rudi Menz, Gunter Tavernier, Jan Kay, A.Barry Hamid, Qutayba |
| description | Background: Intrinsic asthma is characterized by an increased number of activated eosinophils and macrophages and an increased expression of the hematopoietic growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF) in the bronchial mucosa.
Objective: This study was carried out to investigate the expression of αGM-CSF receptor (αGM-CSFr) messenger RNA and protein in the bronchial mucosa of patients with intrinsic or atopic asthma and of control subjects and to correlate the expression of αGM-CSFr to the number of EG2
+ cells (eosinophils) and CD68
+ cells (macrophages) and pulmonary function.
Methods: Nineteen patients with stable asthma (9 with atopic and 10 with intrinsic asthma) and 22 normal control subjects (12 atopic and 10 nonatopic subjects) were recruited, and FEV
1 (percent predicted) and PC
20 were measured before bronchoscopy. Endobronchial biopsy specimens were obtained and examined for membrane-bound αGM-CSFr by using in situ hybridization and immunocytochemistry.
Results: αGM-CSFr mRNA- and protein-positive cells were identified in biopsy specimens from all four groups studied. There was no significant difference in the number of cells expressing αGM-CSFr mRNA and protein in patients with atopic asthma compared with atopic and nonatopic control subjects. However, the numbers of αGM-CSFr mRNA- and protein-positive cells were significantly higher in nonatopic patients with asthma compared with atopic patients with asthma and atopic and nonatopic control subjects (
p < 0.001). In the patients with intrinsic asthma, the number of αGM-CSFr mRNA-positive cells per millimeter of basement membrane correlated with numbers of CD68
+ cells (
r
2
= 0.87,
p < 0.001) but not with EG2
+ cells, and colocalization studies demonstrated that 80% of the cells expressing αGMCSFr mRNA were CD68
+. The expression of GM-CSF was also significantly increased in patients with intrinsic asthma compared with those with atopic asthma and control subjects (
p < 0.05). In addition, in intrinsic asthma, there was a correlation between αGM-CSFr mRNA and FEV
1 (
r
2
= 0.61,
p < 0.05).
Conclusion: These results demonstrate that elevated numbers of cells expressing αGM-CSFr can be detected in nonatopic asthma but not in atopic asthma and suggest that this increased expression is predominantly macrophage-associated and may play an important pathophysiologic role in intrinsic asthma. (J Allergy Clin Immunol 1997;99:666-72.) |
| doi_str_mv | 10.1016/S0091-6749(97)70029-0 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_79011999</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0091674997700290</els_id><sourcerecordid>79011999</sourcerecordid><originalsourceid>FETCH-LOGICAL-c420t-76fdb05f9cead874cde64b221eafa5f362fdc790340b89ec79c75eb0a905ee163</originalsourceid><addsrcrecordid>eNqFkc9u1DAQhy0EKtuWR6iUQ4XoITB2Yjs-IbSiLVKhh9Kz5ThjcJWNg-0g8Vi8CM9Ub3e1Eqee_Of3zXj0mZAzCu8pUPHhDkDRWshWvVPyQgIwVcMLsqKgZC06xl-S1QF5TY5TeoBybjp1RI4U5bxr2hX5dj9H_LGMJvswVcFV__5efa3Xd5d1RItzDrHyUzWFyeQwe1uZlH9uTNUvuVzmbfZfcEpeOTMmfLNfT8j95efv6-v65vbqy_rTTW1bBrmWwg09cKcsmqGTrR1QtD1jFI0z3DWCucFKBU0LfaewbK3k2INRwBGpaE7I213fOYZfC6asNz5ZHEczYViSLrWUKqWeBalgjDW8LSDfgTaGlCI6PUe_MfGPpqC3wvWTcL21qZXUT8I1lLqz_QNLv8HhULU3XPLzfW6SNaOLZrI-HTAmhOTtds6POwyLtd8eo07W42Rx8OUjsh6Cf2aQR91fnWY</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>16222354</pqid></control><display><type>article</type><title>Upregulation of αGM-CSF-receptor in nonatopic asthma but not in atopic asthma</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><creator>Kotsimbos, A.Thomas C. ; Humbert, Marc ; Minshall, Eleanor ; Durham, Stephen ; Pfister, Rudi ; Menz, Gunter ; Tavernier, Jan ; Kay, A.Barry ; Hamid, Qutayba</creator><creatorcontrib>Kotsimbos, A.Thomas C. ; Humbert, Marc ; Minshall, Eleanor ; Durham, Stephen ; Pfister, Rudi ; Menz, Gunter ; Tavernier, Jan ; Kay, A.Barry ; Hamid, Qutayba</creatorcontrib><description>Background: Intrinsic asthma is characterized by an increased number of activated eosinophils and macrophages and an increased expression of the hematopoietic growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF) in the bronchial mucosa.
Objective: This study was carried out to investigate the expression of αGM-CSF receptor (αGM-CSFr) messenger RNA and protein in the bronchial mucosa of patients with intrinsic or atopic asthma and of control subjects and to correlate the expression of αGM-CSFr to the number of EG2
+ cells (eosinophils) and CD68
+ cells (macrophages) and pulmonary function.
Methods: Nineteen patients with stable asthma (9 with atopic and 10 with intrinsic asthma) and 22 normal control subjects (12 atopic and 10 nonatopic subjects) were recruited, and FEV
1 (percent predicted) and PC
20 were measured before bronchoscopy. Endobronchial biopsy specimens were obtained and examined for membrane-bound αGM-CSFr by using in situ hybridization and immunocytochemistry.
Results: αGM-CSFr mRNA- and protein-positive cells were identified in biopsy specimens from all four groups studied. There was no significant difference in the number of cells expressing αGM-CSFr mRNA and protein in patients with atopic asthma compared with atopic and nonatopic control subjects. However, the numbers of αGM-CSFr mRNA- and protein-positive cells were significantly higher in nonatopic patients with asthma compared with atopic patients with asthma and atopic and nonatopic control subjects (
p < 0.001). In the patients with intrinsic asthma, the number of αGM-CSFr mRNA-positive cells per millimeter of basement membrane correlated with numbers of CD68
+ cells (
r
2
= 0.87,
p < 0.001) but not with EG2
+ cells, and colocalization studies demonstrated that 80% of the cells expressing αGMCSFr mRNA were CD68
+. The expression of GM-CSF was also significantly increased in patients with intrinsic asthma compared with those with atopic asthma and control subjects (
p < 0.05). In addition, in intrinsic asthma, there was a correlation between αGM-CSFr mRNA and FEV
1 (
r
2
= 0.61,
p < 0.05).
Conclusion: These results demonstrate that elevated numbers of cells expressing αGM-CSFr can be detected in nonatopic asthma but not in atopic asthma and suggest that this increased expression is predominantly macrophage-associated and may play an important pathophysiologic role in intrinsic asthma. (J Allergy Clin Immunol 1997;99:666-72.)</description><identifier>ISSN: 0091-6749</identifier><identifier>EISSN: 1097-6825</identifier><identifier>DOI: 10.1016/S0091-6749(97)70029-0</identifier><identifier>PMID: 9155834</identifier><identifier>CODEN: JACIBY</identifier><language>eng</language><publisher>New York, NY: Mosby, Inc</publisher><subject>Adult ; Antigens, CD ; Antigens, Differentiation, Myelomonocytic ; Asthma - metabolism ; Basement Membrane - cytology ; Biological and medical sciences ; Biopsy ; Bronchi - cytology ; Bronchi - metabolism ; Chronic obstructive pulmonary disease, asthma ; Forced Expiratory Volume ; GM-CSF receptor ; Humans ; Hypersensitivity, Immediate - metabolism ; In Situ Hybridization ; Intrinsic asthma ; macrophages ; Macrophages - classification ; Macrophages - cytology ; Medical sciences ; Middle Aged ; Pneumology ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - genetics ; RNA, Messenger - biosynthesis ; Up-Regulation</subject><ispartof>Journal of allergy and clinical immunology, 1997-05, Vol.99 (5), p.666-672</ispartof><rights>1997 Mosby, Inc.</rights><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-76fdb05f9cead874cde64b221eafa5f362fdc790340b89ec79c75eb0a905ee163</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0091674997700290$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2667549$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9155834$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kotsimbos, A.Thomas C.</creatorcontrib><creatorcontrib>Humbert, Marc</creatorcontrib><creatorcontrib>Minshall, Eleanor</creatorcontrib><creatorcontrib>Durham, Stephen</creatorcontrib><creatorcontrib>Pfister, Rudi</creatorcontrib><creatorcontrib>Menz, Gunter</creatorcontrib><creatorcontrib>Tavernier, Jan</creatorcontrib><creatorcontrib>Kay, A.Barry</creatorcontrib><creatorcontrib>Hamid, Qutayba</creatorcontrib><title>Upregulation of αGM-CSF-receptor in nonatopic asthma but not in atopic asthma</title><title>Journal of allergy and clinical immunology</title><addtitle>J Allergy Clin Immunol</addtitle><description>Background: Intrinsic asthma is characterized by an increased number of activated eosinophils and macrophages and an increased expression of the hematopoietic growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF) in the bronchial mucosa.
Objective: This study was carried out to investigate the expression of αGM-CSF receptor (αGM-CSFr) messenger RNA and protein in the bronchial mucosa of patients with intrinsic or atopic asthma and of control subjects and to correlate the expression of αGM-CSFr to the number of EG2
+ cells (eosinophils) and CD68
+ cells (macrophages) and pulmonary function.
Methods: Nineteen patients with stable asthma (9 with atopic and 10 with intrinsic asthma) and 22 normal control subjects (12 atopic and 10 nonatopic subjects) were recruited, and FEV
1 (percent predicted) and PC
20 were measured before bronchoscopy. Endobronchial biopsy specimens were obtained and examined for membrane-bound αGM-CSFr by using in situ hybridization and immunocytochemistry.
Results: αGM-CSFr mRNA- and protein-positive cells were identified in biopsy specimens from all four groups studied. There was no significant difference in the number of cells expressing αGM-CSFr mRNA and protein in patients with atopic asthma compared with atopic and nonatopic control subjects. However, the numbers of αGM-CSFr mRNA- and protein-positive cells were significantly higher in nonatopic patients with asthma compared with atopic patients with asthma and atopic and nonatopic control subjects (
p < 0.001). In the patients with intrinsic asthma, the number of αGM-CSFr mRNA-positive cells per millimeter of basement membrane correlated with numbers of CD68
+ cells (
r
2
= 0.87,
p < 0.001) but not with EG2
+ cells, and colocalization studies demonstrated that 80% of the cells expressing αGMCSFr mRNA were CD68
+. The expression of GM-CSF was also significantly increased in patients with intrinsic asthma compared with those with atopic asthma and control subjects (
p < 0.05). In addition, in intrinsic asthma, there was a correlation between αGM-CSFr mRNA and FEV
1 (
r
2
= 0.61,
p < 0.05).
Conclusion: These results demonstrate that elevated numbers of cells expressing αGM-CSFr can be detected in nonatopic asthma but not in atopic asthma and suggest that this increased expression is predominantly macrophage-associated and may play an important pathophysiologic role in intrinsic asthma. (J Allergy Clin Immunol 1997;99:666-72.)</description><subject>Adult</subject><subject>Antigens, CD</subject><subject>Antigens, Differentiation, Myelomonocytic</subject><subject>Asthma - metabolism</subject><subject>Basement Membrane - cytology</subject><subject>Biological and medical sciences</subject><subject>Biopsy</subject><subject>Bronchi - cytology</subject><subject>Bronchi - metabolism</subject><subject>Chronic obstructive pulmonary disease, asthma</subject><subject>Forced Expiratory Volume</subject><subject>GM-CSF receptor</subject><subject>Humans</subject><subject>Hypersensitivity, Immediate - metabolism</subject><subject>In Situ Hybridization</subject><subject>Intrinsic asthma</subject><subject>macrophages</subject><subject>Macrophages - classification</subject><subject>Macrophages - cytology</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Pneumology</subject><subject>Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis</subject><subject>Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - genetics</subject><subject>RNA, Messenger - biosynthesis</subject><subject>Up-Regulation</subject><issn>0091-6749</issn><issn>1097-6825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQhy0EKtuWR6iUQ4XoITB2Yjs-IbSiLVKhh9Kz5ThjcJWNg-0g8Vi8CM9Ub3e1Eqee_Of3zXj0mZAzCu8pUPHhDkDRWshWvVPyQgIwVcMLsqKgZC06xl-S1QF5TY5TeoBybjp1RI4U5bxr2hX5dj9H_LGMJvswVcFV__5efa3Xd5d1RItzDrHyUzWFyeQwe1uZlH9uTNUvuVzmbfZfcEpeOTMmfLNfT8j95efv6-v65vbqy_rTTW1bBrmWwg09cKcsmqGTrR1QtD1jFI0z3DWCucFKBU0LfaewbK3k2INRwBGpaE7I213fOYZfC6asNz5ZHEczYViSLrWUKqWeBalgjDW8LSDfgTaGlCI6PUe_MfGPpqC3wvWTcL21qZXUT8I1lLqz_QNLv8HhULU3XPLzfW6SNaOLZrI-HTAmhOTtds6POwyLtd8eo07W42Rx8OUjsh6Cf2aQR91fnWY</recordid><startdate>19970501</startdate><enddate>19970501</enddate><creator>Kotsimbos, A.Thomas C.</creator><creator>Humbert, Marc</creator><creator>Minshall, Eleanor</creator><creator>Durham, Stephen</creator><creator>Pfister, Rudi</creator><creator>Menz, Gunter</creator><creator>Tavernier, Jan</creator><creator>Kay, A.Barry</creator><creator>Hamid, Qutayba</creator><general>Mosby, Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19970501</creationdate><title>Upregulation of αGM-CSF-receptor in nonatopic asthma but not in atopic asthma</title><author>Kotsimbos, A.Thomas C. ; Humbert, Marc ; Minshall, Eleanor ; Durham, Stephen ; Pfister, Rudi ; Menz, Gunter ; Tavernier, Jan ; Kay, A.Barry ; Hamid, Qutayba</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-76fdb05f9cead874cde64b221eafa5f362fdc790340b89ec79c75eb0a905ee163</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adult</topic><topic>Antigens, CD</topic><topic>Antigens, Differentiation, Myelomonocytic</topic><topic>Asthma - metabolism</topic><topic>Basement Membrane - cytology</topic><topic>Biological and medical sciences</topic><topic>Biopsy</topic><topic>Bronchi - cytology</topic><topic>Bronchi - metabolism</topic><topic>Chronic obstructive pulmonary disease, asthma</topic><topic>Forced Expiratory Volume</topic><topic>GM-CSF receptor</topic><topic>Humans</topic><topic>Hypersensitivity, Immediate - metabolism</topic><topic>In Situ Hybridization</topic><topic>Intrinsic asthma</topic><topic>macrophages</topic><topic>Macrophages - classification</topic><topic>Macrophages - cytology</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Pneumology</topic><topic>Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis</topic><topic>Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - genetics</topic><topic>RNA, Messenger - biosynthesis</topic><topic>Up-Regulation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kotsimbos, A.Thomas C.</creatorcontrib><creatorcontrib>Humbert, Marc</creatorcontrib><creatorcontrib>Minshall, Eleanor</creatorcontrib><creatorcontrib>Durham, Stephen</creatorcontrib><creatorcontrib>Pfister, Rudi</creatorcontrib><creatorcontrib>Menz, Gunter</creatorcontrib><creatorcontrib>Tavernier, Jan</creatorcontrib><creatorcontrib>Kay, A.Barry</creatorcontrib><creatorcontrib>Hamid, Qutayba</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of allergy and clinical immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kotsimbos, A.Thomas C.</au><au>Humbert, Marc</au><au>Minshall, Eleanor</au><au>Durham, Stephen</au><au>Pfister, Rudi</au><au>Menz, Gunter</au><au>Tavernier, Jan</au><au>Kay, A.Barry</au><au>Hamid, Qutayba</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of αGM-CSF-receptor in nonatopic asthma but not in atopic asthma</atitle><jtitle>Journal of allergy and clinical immunology</jtitle><addtitle>J Allergy Clin Immunol</addtitle><date>1997-05-01</date><risdate>1997</risdate><volume>99</volume><issue>5</issue><spage>666</spage><epage>672</epage><pages>666-672</pages><issn>0091-6749</issn><eissn>1097-6825</eissn><coden>JACIBY</coden><abstract>Background: Intrinsic asthma is characterized by an increased number of activated eosinophils and macrophages and an increased expression of the hematopoietic growth factor granulocyte-macrophage colony-stimulating factor (GM-CSF) in the bronchial mucosa.
Objective: This study was carried out to investigate the expression of αGM-CSF receptor (αGM-CSFr) messenger RNA and protein in the bronchial mucosa of patients with intrinsic or atopic asthma and of control subjects and to correlate the expression of αGM-CSFr to the number of EG2
+ cells (eosinophils) and CD68
+ cells (macrophages) and pulmonary function.
Methods: Nineteen patients with stable asthma (9 with atopic and 10 with intrinsic asthma) and 22 normal control subjects (12 atopic and 10 nonatopic subjects) were recruited, and FEV
1 (percent predicted) and PC
20 were measured before bronchoscopy. Endobronchial biopsy specimens were obtained and examined for membrane-bound αGM-CSFr by using in situ hybridization and immunocytochemistry.
Results: αGM-CSFr mRNA- and protein-positive cells were identified in biopsy specimens from all four groups studied. There was no significant difference in the number of cells expressing αGM-CSFr mRNA and protein in patients with atopic asthma compared with atopic and nonatopic control subjects. However, the numbers of αGM-CSFr mRNA- and protein-positive cells were significantly higher in nonatopic patients with asthma compared with atopic patients with asthma and atopic and nonatopic control subjects (
p < 0.001). In the patients with intrinsic asthma, the number of αGM-CSFr mRNA-positive cells per millimeter of basement membrane correlated with numbers of CD68
+ cells (
r
2
= 0.87,
p < 0.001) but not with EG2
+ cells, and colocalization studies demonstrated that 80% of the cells expressing αGMCSFr mRNA were CD68
+. The expression of GM-CSF was also significantly increased in patients with intrinsic asthma compared with those with atopic asthma and control subjects (
p < 0.05). In addition, in intrinsic asthma, there was a correlation between αGM-CSFr mRNA and FEV
1 (
r
2
= 0.61,
p < 0.05).
Conclusion: These results demonstrate that elevated numbers of cells expressing αGM-CSFr can be detected in nonatopic asthma but not in atopic asthma and suggest that this increased expression is predominantly macrophage-associated and may play an important pathophysiologic role in intrinsic asthma. (J Allergy Clin Immunol 1997;99:666-72.)</abstract><cop>New York, NY</cop><pub>Mosby, Inc</pub><pmid>9155834</pmid><doi>10.1016/S0091-6749(97)70029-0</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of allergy and clinical immunology, 1997-05, Vol.99 (5), p.666-672 |
| issn | 0091-6749 1097-6825 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_79011999 |
| source | MEDLINE; Elsevier ScienceDirect Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals |
| subjects | Adult Antigens, CD Antigens, Differentiation, Myelomonocytic Asthma - metabolism Basement Membrane - cytology Biological and medical sciences Biopsy Bronchi - cytology Bronchi - metabolism Chronic obstructive pulmonary disease, asthma Forced Expiratory Volume GM-CSF receptor Humans Hypersensitivity, Immediate - metabolism In Situ Hybridization Intrinsic asthma macrophages Macrophages - classification Macrophages - cytology Medical sciences Middle Aged Pneumology Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - biosynthesis Receptors, Granulocyte-Macrophage Colony-Stimulating Factor - genetics RNA, Messenger - biosynthesis Up-Regulation |
| title | Upregulation of αGM-CSF-receptor in nonatopic asthma but not in atopic asthma |
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