These results suggest that LGG may increase sensitivity to IL-10, and implicate IL-10 signaling as a key pathway mediating the anti-inflammatory effects of LGG. Of interest, IL-10 is increased in models of NEC and in patients with severe or surgical NEC [54] we found that IL-10 was in fact increased after intestinal injury in both LGG- and vehicle-treated mice. The gene discussed is IL10; the disease is necrotizing enterocolitis.