Page 86 - Livre électronique du Congrès National de Pneumologie 2018

P7 IL-26 IS OVEREXPRESSED IN SEVERE ASTHMA AND INDUCES IL-9 AND IL-17 CYTOKINE

PRODUCTION

R. Belhajab – S. Louhaichi a,b,c – B. Hamdi a,b,c – I. Khalfallah a,b,c – J. Ammar a,b,c - K. Hamzaoui a,b,c - A.
Hamzaoui a,b,c
(A) UNIT RESEARCH 12SP15 “EXPRESSION MOLECULAIRE DES INTERACTIONS CELLULAIRES ET LEUR MODE DE
COMMUNICATION DANS LE POUMON PROFOND”, A. MAMI HOSPITAL, ARIANA, TUNISIA.
(B) UNIVERSITÉ DE TUNIS EL MANAR, FACULTY OF MEDICINE OF TUNIS, DEPARTMENT OF BASIC SCIENCES, TUNIS, TUNISIA.
(C) DIVISION OF PULMONOLOGY, DEPARTMENT OF PAEDIATRIC AND RESPIRATORY DISEASES, ABDERRAHMAN MAMI HOSPITAL,
PAVILLON B; ARIANA, TUNISIA.

Interleukin (IL)-26 is abundant in human airways. Several pro-inflammatory cytokines interacted with IL-26 in the lung
and were involved in different pathogenic pathways leading to the development of asthma severity.

To investigate IL-26 expression in the induced sputum of severe asthmatic patients and to investigate its eventual
correlation with TNF-α IFN-γ, IL-17 and IL-9. Stimuled PBMCs by IL-37 or IL-26 were tested for cytokines generation
or suppression.

A total of 50 patients with severe asthma were recruited. ELISA and real-time polymerase chain reaction (RT-PCR)
analyzed the expression of IL-26. The mRNA and protein expression of IL-26 was significantly enhanced in the sputum
and in the serum of patients with severe asthma. A significant correlation was observed between FEV1% and IL-26
level in severe asthmatics. Sputum and serum cytokines (TNF-α, IFN-γ, IL-17, and IL-9) were found highly expressed
and correlated with IL-26 in severe asthmatics. PBMCs stimulated with recombinant IL-37 and LPS suppressed
significantly IL-26, IL-17 and IL-9.

Our data suggested that IL-26 plays a role in the pathophysiology of severe asthma inducing the secretion of
inflammatory mediators, where as IL-37 alleviates airway inflammation. This evidence could improve the knowledge
regarding the role of IL-26 in asthma.

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