Prolonged and elevated levels of IL-6 in the lungs of C57BL/6 mice may initially serve to recruit and protect neutrophils and minimize their depletion from the site of infection [64], after which apoptosis induced shedding of IL-6R from neutrophil surface and the formation of IL-6/sIL-6R complex leads to IL-6 trans-signaling. This evidence concerns the gene IL6R and infection.