Therefore, the increase in neutrophil surface CD11b, CD44 and L-selectin on ECRG4 KO neutrophils can directly restrain neutrophil recruitment through increased adhesion, as well as decrease neutrophil response to PAMPs/DAMPs via reduced TLR signaling, thus providing a mechanism for the delayed neutrophil recruitment with more severe infection seen in the ECRG4 KO mouse. Here, ITGAM is linked to infection.