“…For example, three species of Bifidobacterium decrease incidence and severity of NEC in animal models 39-41 but appear to utilize different mechanisms: B. longum subsp infantis attenuates induction of IL6, IL8, TNFα and IL23 in the rat NEC model 39 , decreases IL1β induced IL8 and IL6 expression in immature human gut xenografts 42 , and has a competitive advantage over other gut microbes in the presence of human milk oligosaccharides 43 ; B. bifidum improves barrier function 44 , decreases apoptosis 45 and attenuates IL6 induction in the rat NEC model 40 and alters short chain fatty acid production in vitro in feces from premature infants 46 ; and B. breve decreases inflammation in the rat NEC model 41 and alters butyrate production 46 and increases serum levels of TGFβ expression in premature infants 47 . Lactobacilli also show diversity of function with 3 species that decrease NEC in animal models 48-50 with different mechanisms: L. acidophilus secretes one or more molecules that inhibit induction of inflammation by platelet activating factor 51 and alters expression of hundreds of genes important in apoptosis, angiogenesis, and immune response 52 ; L. reuteri decreases expression of IL6 and TNFα and increases ileal regulatory T cells in the rat NEC model 53 and increases intestinal motility 54 ; L. rhamnosus (strain GG, ATCC 53103) decreases expression of TNFα and MIP2 through upregulation of the IL10 receptor 55 and decreases intestinal permeability 56 through both increased expression of tight junction proteins 57 and decreased apoptosis 58 , while a different strain (HN001) decreases incidence and severity of NEC in both a mouse and a piglet model, through alterations in TLR9 signaling 49 .…”