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Elevated levels of eosinophil extracellular traps (EETs) in bronchoalveolar lavage fluid (BALF) correlate with asthma severity. Sj16 is a protein from\n                      <jats:italic>Schistosoma japonicum<\/jats:italic>\n                      with known immunoregulatory properties. Exosomes, with their protective phospholipid bilayer, serve as efficient drug carriers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We extracted exosomes secreted by\n                      <jats:italic>Escherichia coli<\/jats:italic>\n                      Nissle 1917 engineered to express Sj16 (EcN-Sj16-Exo), and sought to investigate the role of EcN-Sj16-Exo in asthma. In an ovalbumin-induced experimental asthma model in mice, EET levels were elevated. The experimental asthma model was treated with EcN-Sj16-Exo. EET formation was assessed using immunofluorescence and scanning electron microscopy. Lung function, airway remodelling and inflammation were evaluated. Wiskott\u2013Aldrich syndrome-like (\n                      <jats:italic>WASL<\/jats:italic>\n                      ) knockout mice and recombinant adeno-associated virus (rAAV)-expressing neural Wiskott\u2013Aldrich syndrome protein (N-WASP) were used to investigate the potential mechanisms of EcN-Sj16-Exo.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      EET formation is increased in sputum and BALF from patients with asthma. We demonstrate that Sj16 inhibits EET formation\n                      <jats:italic>in vitro<\/jats:italic>\n                      and localises primarily in exosomes when secreted by EcN-Sj16. In the experimental asthma model, EcN-Sj16-Exo significantly reduced EET formation. Moreover, EcN-Sj16-Exo significantly attenuated airway hyperreactivity and airway remodelling, as evidenced by reduced lung resistance, improved dynamic compliance and diminished inflammatory cell infiltration, fibrosis and mucus hypersecretion. Furthermore, EcN-Sj16-Exo decreased eosinophil and neutrophil counts, IgE levels and type 2 cytokine levels in BALF while increasing T-regulatory cells in the spleen. Mechanistically, EcN-Sj16-Exo inhibited EET formation by upregulating N-WASP.\n                      <jats:italic>WASL-<\/jats:italic>\n                      knockout mice and AAV6-WASL-mediated N-WASP expression confirmed that EcN-Sj16-Exo alleviates experimental asthma by upregulating N-WASP to inhibit EET formation.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings suggest that EcN-Sj16-Exo represents a promising therapeutic approach in asthma, highlighting the potential of targeting EETs and N-WASP in asthma therapy.<\/jats:p>\n                  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