However, this inhibitory effect on neutrophil infiltration was not associated with significant suppression of the levels of the Th2 (IL-4 and IL-13)- or Th17 (IL-17A, -E, F or IL-22)-associated cytokines, chemokines (eotaxin-1, -2 or MCP-1) or the inflammatory mediator, periostin (results not shown) implicated in the recruitment of pro-inflammatory cells to the airways during asthma pathogenesis. The gene discussed is CCL2; the disease is asthma.