Almeida-Oliveira, A. R.
Aquino, Jr., J. C. J.
Oliveira, Jr., M. C.
Alberca-Custodio, R. W.
Rigonato-Oliveira, N. C.
Salley-Dias, L. P.
Damaceno-Rodrigues, N. R.
Caldini, E. G.
Arantes-Costa, F. M.
Ligeiro-Oliveira, A. P.
Belvisi, M. G.
Vieira, R. P.
[2, 4, 8, 9]
Total Authors: 14
 Nove de Julho Univ, Rua Vergueiro 235-249, BR-01504001 Sao Paulo, SP - Brazil
 Brazilian Inst Teaching & Res Pulm & Exercise Imm, Rua Pedro Ernesto 240, BR-12245520 Sao Jose Dos Campos, SP - Brazil
 UCLA Med Ctr, Los Angeles Biomed Res Inst Harbor, Dept Med, Div Resp & Crit Care Physiol & Med, Torrance, CA 90502 - USA
 Univ Brasil, Postgrad Program Bioengn & Biomed Engn, Campus Itaquera, Rua Carolina Fonseca 235, BR-08230030 Sao Paulo, SP - Brazil
 Univ Sao Paulo, Sch Med, Dept Pathol, Lab Cell Biol LIM 59, Ave Doutor Arnaldo 455, BR-01246903 Sao Paulo, SP - Brazil
 Univ Sao Paulo, Sch Med, Dept Clin Med, Lab Expt Therapeut LIM 20, Ave Doutor Arnaldo 455, BR-01246903 Sao Paulo, SP - Brazil
 Imperial Coll London, Natl Heart & Lung Inst, Airway Dis, Resp Pharmacol Grp, London - England
 Fed Univ Sao Paulo UNIFESP, Postgrad Program Sci Human Movement & Rehabil, Campus Baixada Santista, Av Ana Costa, BR-11060001 Santos, SP - Brazil
 Anhembi Morumbi Univ, Sch Med, Ave Deputado Benedito Matarazzo, 4050 Jardim, BR-12230002 Sao Jose Dos Campos, SP - Brazil
Total Affiliations: 9
EXERCISE IMMUNOLOGY REVIEW;
Web of Science Citations:
Background: Aerobic training (AT) decreases airway inflammation in asthma, but the underlying cellular and molecular mechanisms are not completely understood. Thus, this study evaluated the participation of SOCS-JAK-STAT signaling in the effects of AT on airway inflammation, remodeling and hyperresponsiveness in a model of allergic airway inflammation. Methods: C57Bl/6 mice were divided into Control (Co), Exercise (Ex), HDM (HDM), and HDM+ Exercise (HDM+ Ex). Dermatophagoides pteronyssinus (100ug/mouse) were administered oro-tracheally on days 0, 7, 14, 21, 28, 35, 42 and 49. AT was performed in a treadmill during 4 weeks in moderate intensity, from day 24 until day 52. Results: AT inhibited HDM-induced total cells (p<0.001), eosinophils (p<0.01), neutrophils (p<0.01) and lymphocytes (p<0.01) in BAL, and eosinophils (p<0.01), neutrophils (p<0.01) and lymphocytes (p<0.01) in peribronchial space. AT also reduced BAL levels of IL-4 (p<0.001), IL-5 (p<0.001), IL-13 (p<0.001), CXCL1 (p<0.01), IL-17 (p<0.01), IL-23 (p<0.05), IL-33 (p<0.05), while increased IL-10 (p<0.05). Airway collagen fibers (p<0.01), elastic fibers p<0.01) and mucin (p<0.01) were also reduced by AT. AT also inhibited HDM-induced airway hyperresponsiveness (AHR) to methacholine 6,25mg/ml (p<0.01), 12,5mg/mL (p<0.01), 25mg/mL (p<0.01) and 50mg/mL (p<0.01). Mechanistically, AT reduced the expression of STAT6 (p<0.05), STAT3 (p<0.001), STAT5 (p<0.01) and JAK2 (p<0.001), similarly by peribronchial leukocytes and by airway epithelial cells. SOCS1 expression (p<0.001) was upregulated in leukocytes and in epithelial cells, SOCS2 (p<0.01) was upregulated in leukocytes and SOCS3 down-regulated in leukocytes (p<0.05) and in epithelial cells (p<0.001). Conclusions: AT reduces asthma phenotype involving SOCS-JAK-STAT signaling. (AU)