PT  - JOURNAL ARTICLE
AU  - Erica Bazzan
AU  - Mariaenrica Tinè
AU  - Graziella Turato
AU  - Umberto Semenzato
AU  - Micaela Romagnoli
AU  - Manuel Cosio
AU  - Marina Saetta
TI  - Upregulation of Suppressors of Cytokine Signalling (SOCS)3 in COPD alveolar macrophages
AID  - 10.1183/13993003.congress-2020.2284
DP  - 2020 Sep 07
TA  - European Respiratory Journal
PG  - 2284
VI  - 56
IP  - suppl 64
4099  - http://erj.ersjournals.com/content/56/suppl_64/2284.short
4100  - http://erj.ersjournals.com/content/56/suppl_64/2284.full
SO  - Eur Respir J2020 Sep 07; 56
AB  - Background: The Suppressor of Cytokine Signalling (SOCS) proteins, particularly SOCS3, and its regulation by TNF-α, have been originally described in animal and in vitro studies as inhibitors of cytokine-signalling in response to a chronic inflammation. However, more recently, the suppressive role of SOCS3 has been questioned by other animal studies, which suggested an important proinflammatory role for this protein.Aim: To investigate in a human inflammatory disease, COPD, the expression of SOCS3 and its inducer TNF-α in alveolar macrophages (AM).Methods: SOCS3 and TNF-α expression was quantified in alveolar macrophages (SOCS3+AM%, TNF-α+AM%) in lungs from 19 smokers with COPD (COPD) [FEV1: 60±31(%)], 16 smokers without COPD (noCOPD) and 9 nonsmokers (NS) using immunochemistry.Results: The percentage of SOCS3+AM was higher in COPD [68(31-95)%] than in noCOPD [48(22-78)% p=0.04] and NS [10(4-56)% p=0.005]. This pattern was paralleled by the expression of TNF-α in AM, that was higher in COPD [90(52-97)%] than in noCOPD [32(17-60)%] and in NS [1(0-15)% p<0.001]. In alveolar macrophages, TNF-α expression was correlated with that of SOCS3+ (r=0.5; p=0.02).Conclusions: The increased expression of SOCS3 and its modulator TNF-α in alveolar macrophages of COPD, a chronic inflammatory disease, casts some doubts about SOCS3 suppressor function and rather favours a role for SOCS3 as a proinflammatory mediator.FootnotesCite this article as: European Respiratory Journal 2020; 56: Suppl. 64, 2284.This abstract was presented at the 2020 ERS International Congress, in session “Respiratory viruses in the "pre COVID-19" era”.This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).