Dubai Final-v20.indd - World Allergy Organization

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1320
il-17 DriVES THE rECrUiTmEnT oF B CEllS To THE BronCHial TiSSUE oF SEVErE aSTHmaTiC PaTiEnTS
Halwani, r. 1 , Al-muhsen, s. 2 and Hamid, Q. 3
1Asthma research Chair and Prince naif Center for immunological research, College of medicine, King saud University., riyadh,
saudi Arabia. 2Department of Pediatrics, College of medicine, King saud University. 3mcgill University, meakins-Christie laboratories,
montreal, Canada.
Background: B-cells play an important role in asthma development mostly via the production of igE. A number of reports have
shown local production of igE in B cells present in lung tissues of mild allergic asthmatics. However, it is not clear whether there
is an increase in the number of B cells in severe asthma and how do B cell migrates to the mucosal site. Our objective in this
study was to determine the number and pattern of infiltrated B cells into lung tissues in severe compared to mild asthma and to
investigate the mechanism behind this infiltration.
methods: Bronchial biopsies from severe versus mild asthmatics were stained for B cells marker (CD20) using
immunohistochemistry. moreover, migration towards il-17 gradient was determined using Boyden chamber.
results: the number of CD20 positive cells in severe asthmatic biopsies was significantly higher than those in mild asthmatics.
interestingly, we have also observed lymph follicles in 40% of severe compared to 15% of mild asthmatic airways. most of
the cells in the lymph follicles were CD20 positive cells. these lymph follicles were very close to the epithelial surface. We
have recently reported high expression of il-17 in severe asthma. We tested the hypothesis that il-17 is involved in migration
of B cells to the mucosal surface of the airways. Although B cells were shown to migrate towards both il-17A and il-17F,
much lower concentrations of il-17F, compared to il-17A, were sufficient to induce migration. moreover, B cells within airway
mucosa of severe asthmatics were shown to express higher level of il-17r compared to those of mild asthmatic patients using
immunohistochemistry as well as qPCr.
Conclusion:il-17 might drive the migration of B cells in the lung tissues and could play a critical role in the formation of lymphoid
follicles in severe asthmatic airways.
1321
EoSinoPHilS EnHanCE airWaY SmooTH mUSClE CEll ProliFEraTion
Halwani, r. 1 , Al-muhsen, s. 2 and Hamid, Q. 3
1Asthma research Chair and Prince naif Center for immunological research, College of medicine, King saud University.,
riyadh, saudi Arabia. 2Department of Pediatrics, College of medicine, King saud University. 3mcgill University, 2meakins-Christie laboratories, montreal, Canada.
Background: Asthma is a chronic inflammatory disorder of the lung airways that is associated with airway remodeling and
hyperresponsiveness. its is well documented that the smooth muscle mass in asthmatic airways is increased due to hypertrophy
and hyperplasia of the Asm cells. moreover, eosinophils have been proposed in different studies to play a major role in airway
remodeling. Here, we hypothesized that eosinophils modulate the airways through enhancing Asm cell proliferation. the aim of this
study is to examine the effect of eosinophils on Asm cell proliferation using eosinophils isolated from asthmatic and normal control
subjects.
methods: Eosinophils were isolated from peripheral blood of 6 mild asthmatics and 6 normal control subjects. Asm cells were
incubated with eosinophils or eosinophil membranes and Asm proliferation was estimated using thymidine incorporation. the
mrnA expression of extracellular matrix (ECm) in Asm cells was measured using quantitative real-time PCr. the effect of
eosinophil-derived proliferative cytokines on Asm cells was determined using neutralizing antibodies.
results: Co-culture with eosinophils significantly increased Asm cell proliferation. However, there was no significant difference in
Asm proliferation following incubation with eosinophils from asthmatic versus normal control subjects. Co-culture with eosinophil
membranes had no effect on Asm proliferation. moreover, there was no significant change in the mrnA expression of ECm proteins
in Asm cells following co-culture with eosinophils when compared with medium alone.
Conclusion: Eosinophils induces Asm cell proliferation independent of direct cell to cell contact or ECm synthesis. Eosinophils may
induce Asm proliferation via the secretion of proliferative cytokines.
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