Page 45 - Livre électronique du Congrès CNP 2021
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     ASSESSMENT OF TSLP AND IL 32 IN PATIENTS WITH
                                    SEVERE ASTHMA
                 P10                H. Neffati  , S. Louhaichi  , I. Khalfallah  , B. Hamdi  , K. Hamzaoui  , A. Hamzaoui
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                                    1 RESEARCH LABORATORY 19SP02 "CHRONIC PULMONARY PATHOLOGIES : FROM GENOME TO
                                    MANAGEMENT", ABDERRAHMAN MAMI HOSPITAL, ARIANA, TUNISIA.
                                    2 MEDICINE FACULTY OF TUNIS, DEPARTMENT OF BASIC SCIENCES, TUNIS EL MANAR UNIVERSITY, TUNIS,
                                    TUNISIA.
                                    3 DEPARTMENT OF PAEDIATRIC AND RESPIRATORY DISEASES, ABDERRAHMAN MAMI HOSPITAL, PAVILLON B,
                                    ARIANA, TUNISIA.
               Interleukin (IL)-32, a novel cytokine, participates in a variety of inflammatory disorders. Thymic
               stromal lymphopoietin (TSLP) was initially demonstrated to be critical in regulating inflammatory
               responses among various allergic disorders (such as atopic dermatitis and asthma). However, the
               association of IL-32 with TSLP in severe asthma surface remains unclear.
               The present work aimed to assess the expression of IL-32 and TSLP in the induced sputum and
               serum of patients with severe asthma.
               Twenty patients with severe asthma and 20 age-matched healthy control (HC) were included in
               the study. TSLP and IL-32 protein levels were quantiated by ELISA in serum and induced sputum
               of severe asthmatic patients compared to HC. Asthmatic isolated induced sputum mononuclear
               cells (ISMNCs) were cultured with administered different concentrations of recombinant (r)IL-32
               to assess TSLP levels as well as the molecular pathways that control pro-inflammatory cytokine
               production (TNF- and IL-6).
               TSLP and IL-32 proteins were highly expressed in sputum  and serum  of  asthmatic patients
               compared to  healthy controls. TSLP and IL-32 were more  expressed in asthmatic sputum
               compared to their own serum. Addition of rIL-32 to ISMNCs increased significantly the protein
               levels of TSLP and inflammatory cytokines. In contrast, administration of anti-IL-32 to sputum cells
               reduced significantly TSLP and pro-inflammatory cytokines (TNF and IL-6) in severe asthmatics
               at the protein and  mARN levels.
               These findings demonstrate that IL-32 and TSLP are  critical cytokines that  participate
               simultaneously in the inflammatory process in severe asthmatic patients. Our data suggested new
               molecular targets for severe asthma. IL-32 and TSLP have a potential inflammatory process in
               sputum cells from patients with severe asthma.
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