Our findings of enhanced shedding of sIL-6R from neutrophils of Asp358Ala homozygotes and an increase in the MCP-1 release from lung endothelial cells using serum from these individuals provides evidence of a mechanism through which IL-6 trans-signaling may contribute to disease severity in severe, neutrophil-driven, asthma phenotypes. Here, IL6R is linked to asthma.