Home
|
Inbox
|
Search
|
View Abstract
Direct Effects of Interleukins on Airway Smooth Muscle Cell Functions
Description
.abstract img { width:300px !important; height:auto; display:block; text-align:center; margin-top:10px } .abstract { overflow-x:scroll } .abstract table { width:100%; display:block; border:hidden; border-collapse: collapse; margin-top:10px } .abstract td, th { border-top: 1px solid #ddd; padding: 4px 8px; } .abstract tbody tr:nth-child(even) td { background-color: #efefef; } .abstract a { overflow-wrap: break-word; word-wrap: break-word; }
A1212 - Direct Effects of Interleukins on Airway Smooth Muscle Cell Functions
Author Block: N. M. Bexiga1, H. Lam2, A. M. Alencar3, M. A. Stephano1, S. S. An2; 1Pharmaceutical Biochemistry Technology Department, University of Sao Paulo, Sao Paulo, Brazil, 2Environmental Health and Engineering, Johns Hopkins University, Baltimore, MD, United States, 3Department of General Physics, University of Sao Paulo, Sao Paulo, Brazil.
OBJECTIVE
Asthma is a complex respiratory disorder driven by T helper-2 mediated inflammation and characterized by bronchial obstruction due to airway smooth muscle (ASM) contraction. Recently, we have identified an inflammation-independent contraction mechanophenotype of ASM in asthma (J. Allergy Clin. Immunol. 138, 294-297, 2016). Here we explored the contribution of pro-inflammatory and anti-inflammatory cytokines associated with asthma diathesis in isolated human ASM cells.
METHODS
Human ASM cells were treated for 72h with vehicle, IL-9, IL-10, IL-13, IL-17 or IL-22 (0.1, 1, 10, and 50 ng/ml) and contracted with histamine (1 μM). Dynamic changes in ASM stiffness were measured with magnetic twisting cytometry (MTC) as an index of single-cell contractility. For these studies, we applied primary human ASM cells isolated from non-asthmatic (n=3) and asthmatic (n=3) lung donors.
RESULTS
Th2 and Th17 cytokines (IL-13, IL-17, and IL-22) augmented cell stiffness responses to histamine in non-asthmatic ASM cells, but had no effects in asthmatic ASM cells. In contrast, IL-9 and IL-10 markedly attenuated histamine-induced cell stiffening in non-asthmatic ASM cells. In asthmatic ASM cells, IL-10, but not IL-9, decreased cell stiffening responses to histamine.
CONCLUSIONS
These results demonstrate both inflammation-dependent and independent mechanisms for bronchial obstruction in asthma. While further investigation is underway to determine the precise mechanisms involved in IL-10-induced cell stiffening responses, our findings suggest that IL-10 may potentially be used to provide local inhibitory effects of inflammatory signals that fashion mechanophenotype of asthma in ASM cells.
Author Block: N. M. Bexiga1, H. Lam2, A. M. Alencar3, M. A. Stephano1, S. S. An2; 1Pharmaceutical Biochemistry Technology Department, University of Sao Paulo, Sao Paulo, Brazil, 2Environmental Health and Engineering, Johns Hopkins University, Baltimore, MD, United States, 3Department of General Physics, University of Sao Paulo, Sao Paulo, Brazil.
OBJECTIVE
Asthma is a complex respiratory disorder driven by T helper-2 mediated inflammation and characterized by bronchial obstruction due to airway smooth muscle (ASM) contraction. Recently, we have identified an inflammation-independent contraction mechanophenotype of ASM in asthma (J. Allergy Clin. Immunol. 138, 294-297, 2016). Here we explored the contribution of pro-inflammatory and anti-inflammatory cytokines associated with asthma diathesis in isolated human ASM cells.
METHODS
Human ASM cells were treated for 72h with vehicle, IL-9, IL-10, IL-13, IL-17 or IL-22 (0.1, 1, 10, and 50 ng/ml) and contracted with histamine (1 μM). Dynamic changes in ASM stiffness were measured with magnetic twisting cytometry (MTC) as an index of single-cell contractility. For these studies, we applied primary human ASM cells isolated from non-asthmatic (n=3) and asthmatic (n=3) lung donors.
RESULTS
Th2 and Th17 cytokines (IL-13, IL-17, and IL-22) augmented cell stiffness responses to histamine in non-asthmatic ASM cells, but had no effects in asthmatic ASM cells. In contrast, IL-9 and IL-10 markedly attenuated histamine-induced cell stiffening in non-asthmatic ASM cells. In asthmatic ASM cells, IL-10, but not IL-9, decreased cell stiffening responses to histamine.
CONCLUSIONS
These results demonstrate both inflammation-dependent and independent mechanisms for bronchial obstruction in asthma. While further investigation is underway to determine the precise mechanisms involved in IL-10-induced cell stiffening responses, our findings suggest that IL-10 may potentially be used to provide local inhibitory effects of inflammatory signals that fashion mechanophenotype of asthma in ASM cells.
|
Home
|
Inbox
|
Search
|