While their results suggested infection-induced neutrophil recruitment induces mucosal C3 levels and is associated with alternative pathway-mediated phagocytosis, our data directly demonstrates C3 as being critical for initial recruitment of phagocytic cells to the infection site and thereby suggests a broader role for C3 in defense of the gastrointestinal tract in the context of Kpn infection. The gene discussed is C3; the disease is infection.