AustralieFrV1, PascalFrancis, Curation, bibRecord, 004832

Expression and regulation of CCL15 by human airway smooth muscle cells

Identifieur interne : 004832 ( PascalFrancis/Curation ); précédent : 004831; suivant : 004833

Expression and regulation of CCL15 by human airway smooth muscle cells

Auteurs : P. Joubert [Canada] ; S. Lajoie-Kadoch [Canada] ; V. Wellemans [Canada] ; S. Letuve [France] ; M. K. Tulic [Australie] ; A. J. Halayko [Canada] ; Q. Hamid [Canada]

Source :

Clinical and experimental allergy : (Print) [ 0954-7894 ] ; 2012.

RBID : Pascal:12-0042283

Descripteurs français

Pascal (Inist)
- Asthme, Régulation, Homme, Voie respiratoire, Muscle lisse, Myocyte, Chimiokine, Cytokine, Immunologie.
Wicri :
- topic : Homme, Immunologie.

English descriptors

KwdEn :
- Asthma, Chemokine, Cytokine, Human, Immunology, Myocyte, Regulation(control), Respiratory tract, Smooth muscle.

Abstract

Background Structural cells are an important reservoir of chemokines that coordinate the influx of various immune cells to the lungs of asthmatics. Airway smooth muscle cells (ASMC) are an important source of these chemokines. CCL 15 is a recently described chemo-attractant for neutrophils, eosinophils, monocytes and lymphocytes. Objective To determine the production and the regulation of CCL15 by ASMC and to investigate its production in asthmatic airways. Methods Human ASMC were obtained from main bronchial airway segments of patients with mild, moderate and severe asthma. To induce chemokine production, cells were incubated with IL-4, IL-13, TNF-α or IFN-γ in presence or absence of dexamethasone, mithramycin A (SP-1 inhibitor) or the IKK-2 inhibitor, AS602868. CCL15 mRNA expression was evaluated by real-time PCR. Immunoreactive CCL15 was detected by immuno-fluorescence and CCL15 protein concentration in the supernatant was measured using ELISA. Results CCL15 is constitutively expressed in human ASMC and is strongly up-regulated by TNF-α. This up-regulation is inhibited by dexamethasone, mithramycin A and AS602868. TNF-α-induced CCL 15 levels can be synergistically enhanced by the presence of IFN-γ, at both the transcriptional and translation level. This synergism is NF-κB-dependent. Asthmatic biopsies demonstrated higher expression of CCL15 compared with non-asthmatic controls. Conclusion and Clinical Relevance Our results show that ASMC are a potent source of CCL15 in the airways and may directly participate in the recruitment of inflammatory cells to asthmatic airways. Targeting the production of CCL15 by ASMC might reduce the inflammatory response within the airways of asthmatic patients.

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A03		`1`		`@0 Clin. exp. allergy : (Print)`
A05				`@2 42`
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A08	`01`	`1`	`ENG`	`@1 Expression and regulation of CCL15 by human airway smooth muscle cells`
A11	`01`	`1`		`@1 JOUBERT (P.)`
A11	`02`	`1`		`@1 LAJOIE-KADOCH (S.)`
A11	`03`	`1`		`@1 WELLEMANS (V.)`
A11	`04`	`1`		`@1 LETUVE (S.)`
A11	`05`	`1`		`@1 TULIC (M. K.)`
A11	`06`	`1`		`@1 HALAYKO (A. J.)`
A11	`07`	`1`		`@1 HAMID (Q.)`
A14	`01`			`@1 Meakins-Christie Laboratories, McGill University @2 Montréal, Québec @3 CAN @Z 1 aut. @Z 2 aut. @Z 7 aut.`
A14	`02`			`@1 UMF CSSS Baie-des-Chaleurs, Université de Montréal @2 Maria, Québec @3 CAN @Z 3 aut.`
A14	`03`			`@1 Faculté de médecine, Inserm U700, Universite Paris Diderot @2 Paris @3 FRA @Z 4 aut.`
A14	`04`			`@1 School of Paediatrics & Child Health, University of Western Australia @2 Perth @3 AUS @Z 5 aut.`
A14	`05`			`@1 Faculty of Medicine, Departments of Internal Medicine & Physiology, University of Manitoba @2 Winnipeg, Manitoba @3 CAN @Z 6 aut.`
A20				`@1 85-94`
A21				`@1 2012`
A23	`01`			`@0 ENG`
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A44				`@0 0000 @1 © 2012 INIST-CNRS. All rights reserved.`
A45				`@0 39 ref.`
A47	`01`	`1`		`@0 12-0042283`
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A64	`01`	`1`		`@0 Clinical and experimental allergy : (Print)`
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C01	`01`		`ENG`	@0 Background Structural cells are an important reservoir of chemokines that coordinate the influx of various immune cells to the lungs of asthmatics. Airway smooth muscle cells (ASMC) are an important source of these chemokines. CCL 15 is a recently described chemo-attractant for neutrophils, eosinophils, monocytes and lymphocytes. Objective To determine the production and the regulation of CCL15 by ASMC and to investigate its production in asthmatic airways. Methods Human ASMC were obtained from main bronchial airway segments of patients with mild, moderate and severe asthma. To induce chemokine production, cells were incubated with IL-4, IL-13, TNF-α or IFN-γ in presence or absence of dexamethasone, mithramycin A (SP-1 inhibitor) or the IKK-2 inhibitor, AS602868. CCL15 mRNA expression was evaluated by real-time PCR. Immunoreactive CCL15 was detected by immuno-fluorescence and CCL15 protein concentration in the supernatant was measured using ELISA. Results CCL15 is constitutively expressed in human ASMC and is strongly up-regulated by TNF-α. This up-regulation is inhibited by dexamethasone, mithramycin A and AS602868. TNF-α-induced CCL 15 levels can be synergistically enhanced by the presence of IFN-γ, at both the transcriptional and translation level. This synergism is NF-κB-dependent. Asthmatic biopsies demonstrated higher expression of CCL15 compared with non-asthmatic controls. Conclusion and Clinical Relevance Our results show that ASMC are a potent source of CCL15 in the airways and may directly participate in the recruitment of inflammatory cells to asthmatic airways. Targeting the production of CCL15 by ASMC might reduce the inflammatory response within the airways of asthmatic patients.
C02	`01`	`X`		`@0 002A06`
C02	`02`	`X`		`@0 002B11B`
C03	`01`	`X`	`FRE`	`@0 Asthme @5 01`
C03	`01`	`X`	`ENG`	`@0 Asthma @5 01`
C03	`01`	`X`	`SPA`	`@0 Asma @5 01`
C03	`02`	`X`	`FRE`	`@0 Régulation @5 09`
C03	`02`	`X`	`ENG`	`@0 Regulation(control) @5 09`
C03	`02`	`X`	`SPA`	`@0 Regulación @5 09`
C03	`03`	`X`	`FRE`	`@0 Homme @5 10`
C03	`03`	`X`	`ENG`	`@0 Human @5 10`
C03	`03`	`X`	`SPA`	`@0 Hombre @5 10`
C03	`04`	`X`	`FRE`	`@0 Voie respiratoire @5 11`
C03	`04`	`X`	`ENG`	`@0 Respiratory tract @5 11`
C03	`04`	`X`	`SPA`	`@0 Vía respiratoria @5 11`
C03	`05`	`X`	`FRE`	`@0 Muscle lisse @5 12`
C03	`05`	`X`	`ENG`	`@0 Smooth muscle @5 12`
C03	`05`	`X`	`SPA`	`@0 Músculo liso @5 12`
C03	`06`	`X`	`FRE`	`@0 Myocyte @5 13`
C03	`06`	`X`	`ENG`	`@0 Myocyte @5 13`
C03	`06`	`X`	`SPA`	`@0 Miocito @5 13`
C03	`07`	`X`	`FRE`	`@0 Chimiokine @5 14`
C03	`07`	`X`	`ENG`	`@0 Chemokine @5 14`
C03	`07`	`X`	`SPA`	`@0 Quimioquina @5 14`
C03	`08`	`X`	`FRE`	`@0 Cytokine @5 15`
C03	`08`	`X`	`ENG`	`@0 Cytokine @5 15`
C03	`08`	`X`	`SPA`	`@0 Citoquina @5 15`
C03	`09`	`X`	`FRE`	`@0 Immunologie @5 16`
C03	`09`	`X`	`ENG`	`@0 Immunology @5 16`
C03	`09`	`X`	`SPA`	`@0 Inmunología @5 16`
C07	`01`	`X`	`FRE`	`@0 Appareil respiratoire @5 37`
C07	`01`	`X`	`ENG`	`@0 Respiratory system @5 37`
C07	`01`	`X`	`SPA`	`@0 Aparato respiratorio @5 37`
C07	`02`	`X`	`FRE`	`@0 Pathologie de l'appareil respiratoire @5 38`
C07	`02`	`X`	`ENG`	`@0 Respiratory disease @5 38`
C07	`02`	`X`	`SPA`	`@0 Aparato respiratorio patología @5 38`
C07	`03`	`X`	`FRE`	`@0 Bronchopneumopathie obstructive @5 39`
C07	`03`	`X`	`ENG`	`@0 Obstructive pulmonary disease @5 39`
C07	`03`	`X`	`SPA`	`@0 Enfermedad pulmonar obstructiva @5 39`
C07	`04`	`X`	`FRE`	`@0 Pathologie des bronches @5 40`
C07	`04`	`X`	`ENG`	`@0 Bronchus disease @5 40`
C07	`04`	`X`	`SPA`	`@0 Bronquio patología @5 40`
C07	`05`	`X`	`FRE`	`@0 Pathologie des poumons @5 41`
C07	`05`	`X`	`ENG`	`@0 Lung disease @5 41`
C07	`05`	`X`	`SPA`	`@0 Pulmón patología @5 41`
N21				`@1 023`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

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Pascal:12-0042283

Le document en format XML

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<front><div type="abstract" xml:lang="en">Background Structural cells are an important reservoir of chemokines that coordinate the influx of various immune cells to the lungs of asthmatics. Airway smooth muscle cells (ASMC) are an important source of these chemokines. CCL 15 is a recently described chemo-attractant for neutrophils, eosinophils, monocytes and lymphocytes. Objective To determine the production and the regulation of CCL15 by ASMC and to investigate its production in asthmatic airways. Methods Human ASMC were obtained from main bronchial airway segments of patients with mild, moderate and severe asthma. To induce chemokine production, cells were incubated with IL-4, IL-13, TNF-α or IFN-γ in presence or absence of dexamethasone, mithramycin A (SP-1 inhibitor) or the IKK-2 inhibitor, AS602868. CCL15 mRNA expression was evaluated by real-time PCR. Immunoreactive CCL15 was detected by immuno-fluorescence and CCL15 protein concentration in the supernatant was measured using ELISA. Results CCL15 is constitutively expressed in human ASMC and is strongly up-regulated by TNF-α. This up-regulation is inhibited by dexamethasone, mithramycin A and AS602868. TNF-α-induced CCL 15 levels can be synergistically enhanced by the presence of IFN-γ, at both the transcriptional and translation level. This synergism is NF-κB-dependent. Asthmatic biopsies demonstrated higher expression of CCL15 compared with non-asthmatic controls. Conclusion and Clinical Relevance Our results show that ASMC are a potent source of CCL15 in the airways and may directly participate in the recruitment of inflammatory cells to asthmatic airways. Targeting the production of CCL15 by ASMC might reduce the inflammatory response within the airways of asthmatic patients.</div>
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<sZ>2 aut.</sZ>
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<s2>Maria, Québec</s2>
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<sZ>3 aut.</sZ>
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<fA14 i1="03"><s1>Faculté de médecine, Inserm U700, Universite Paris Diderot</s1>
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<s3>FRA</s3>
<sZ>4 aut.</sZ>
</fA14>
<fA14 i1="04"><s1>School of Paediatrics & Child Health, University of Western Australia</s1>
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<s3>AUS</s3>
<sZ>5 aut.</sZ>
</fA14>
<fA14 i1="05"><s1>Faculty of Medicine, Departments of Internal Medicine & Physiology, University of Manitoba</s1>
<s2>Winnipeg, Manitoba</s2>
<s3>CAN</s3>
<sZ>6 aut.</sZ>
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<fC01 i1="01" l="ENG"><s0>Background Structural cells are an important reservoir of chemokines that coordinate the influx of various immune cells to the lungs of asthmatics. Airway smooth muscle cells (ASMC) are an important source of these chemokines. CCL 15 is a recently described chemo-attractant for neutrophils, eosinophils, monocytes and lymphocytes. Objective To determine the production and the regulation of CCL15 by ASMC and to investigate its production in asthmatic airways. Methods Human ASMC were obtained from main bronchial airway segments of patients with mild, moderate and severe asthma. To induce chemokine production, cells were incubated with IL-4, IL-13, TNF-α or IFN-γ in presence or absence of dexamethasone, mithramycin A (SP-1 inhibitor) or the IKK-2 inhibitor, AS602868. CCL15 mRNA expression was evaluated by real-time PCR. Immunoreactive CCL15 was detected by immuno-fluorescence and CCL15 protein concentration in the supernatant was measured using ELISA. Results CCL15 is constitutively expressed in human ASMC and is strongly up-regulated by TNF-α. This up-regulation is inhibited by dexamethasone, mithramycin A and AS602868. TNF-α-induced CCL 15 levels can be synergistically enhanced by the presence of IFN-γ, at both the transcriptional and translation level. This synergism is NF-κB-dependent. Asthmatic biopsies demonstrated higher expression of CCL15 compared with non-asthmatic controls. Conclusion and Clinical Relevance Our results show that ASMC are a potent source of CCL15 in the airways and may directly participate in the recruitment of inflammatory cells to asthmatic airways. Targeting the production of CCL15 by ASMC might reduce the inflammatory response within the airways of asthmatic patients.</s0>
</fC01>
<fC02 i1="01" i2="X"><s0>002A06</s0>
</fC02>
<fC02 i1="02" i2="X"><s0>002B11B</s0>
</fC02>
<fC03 i1="01" i2="X" l="FRE"><s0>Asthme</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="ENG"><s0>Asthma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="01" i2="X" l="SPA"><s0>Asma</s0>
<s5>01</s5>
</fC03>
<fC03 i1="02" i2="X" l="FRE"><s0>Régulation</s0>
<s5>09</s5>
</fC03>
<fC03 i1="02" i2="X" l="ENG"><s0>Regulation(control)</s0>
<s5>09</s5>
</fC03>
<fC03 i1="02" i2="X" l="SPA"><s0>Regulación</s0>
<s5>09</s5>
</fC03>
<fC03 i1="03" i2="X" l="FRE"><s0>Homme</s0>
<s5>10</s5>
</fC03>
<fC03 i1="03" i2="X" l="ENG"><s0>Human</s0>
<s5>10</s5>
</fC03>
<fC03 i1="03" i2="X" l="SPA"><s0>Hombre</s0>
<s5>10</s5>
</fC03>
<fC03 i1="04" i2="X" l="FRE"><s0>Voie respiratoire</s0>
<s5>11</s5>
</fC03>
<fC03 i1="04" i2="X" l="ENG"><s0>Respiratory tract</s0>
<s5>11</s5>
</fC03>
<fC03 i1="04" i2="X" l="SPA"><s0>Vía respiratoria</s0>
<s5>11</s5>
</fC03>
<fC03 i1="05" i2="X" l="FRE"><s0>Muscle lisse</s0>
<s5>12</s5>
</fC03>
<fC03 i1="05" i2="X" l="ENG"><s0>Smooth muscle</s0>
<s5>12</s5>
</fC03>
<fC03 i1="05" i2="X" l="SPA"><s0>Músculo liso</s0>
<s5>12</s5>
</fC03>
<fC03 i1="06" i2="X" l="FRE"><s0>Myocyte</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="ENG"><s0>Myocyte</s0>
<s5>13</s5>
</fC03>
<fC03 i1="06" i2="X" l="SPA"><s0>Miocito</s0>
<s5>13</s5>
</fC03>
<fC03 i1="07" i2="X" l="FRE"><s0>Chimiokine</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="ENG"><s0>Chemokine</s0>
<s5>14</s5>
</fC03>
<fC03 i1="07" i2="X" l="SPA"><s0>Quimioquina</s0>
<s5>14</s5>
</fC03>
<fC03 i1="08" i2="X" l="FRE"><s0>Cytokine</s0>
<s5>15</s5>
</fC03>
<fC03 i1="08" i2="X" l="ENG"><s0>Cytokine</s0>
<s5>15</s5>
</fC03>
<fC03 i1="08" i2="X" l="SPA"><s0>Citoquina</s0>
<s5>15</s5>
</fC03>
<fC03 i1="09" i2="X" l="FRE"><s0>Immunologie</s0>
<s5>16</s5>
</fC03>
<fC03 i1="09" i2="X" l="ENG"><s0>Immunology</s0>
<s5>16</s5>
</fC03>
<fC03 i1="09" i2="X" l="SPA"><s0>Inmunología</s0>
<s5>16</s5>
</fC03>
<fC07 i1="01" i2="X" l="FRE"><s0>Appareil respiratoire</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="ENG"><s0>Respiratory system</s0>
<s5>37</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Aparato respiratorio</s0>
<s5>37</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Pathologie de l'appareil respiratoire</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Respiratory disease</s0>
<s5>38</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Aparato respiratorio patología</s0>
<s5>38</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Bronchopneumopathie obstructive</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Obstructive pulmonary disease</s0>
<s5>39</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Enfermedad pulmonar obstructiva</s0>
<s5>39</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Pathologie des bronches</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Bronchus disease</s0>
<s5>40</s5>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Bronquio patología</s0>
<s5>40</s5>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Pathologie des poumons</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Lung disease</s0>
<s5>41</s5>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Pulmón patología</s0>
<s5>41</s5>
</fC07>
<fN21><s1>023</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
</inist>
</record>

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Expression and regulation of CCL15 by human airway smooth muscle cells

Expression and regulation of CCL15 by human airway smooth muscle cells

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