Bacterial invasion, and/or local inflammatory cytokines,
may cause progression of the gut injury to necrosis
following the loss of intestinal barrier integrity with intestinal
bacteria translocation. Studies have reported their
inability to induce severe NEC in animal models without the
pathologic flora. Oppositely, commensal bacteria can
regulate the expression of genes important for barrier
function, digestion, and angiogenesis.In vitro studies
have demonstrated that many species of the commensal
bacteria have the ability to dampen the inflammatory
response, through inhibition of the transcription nuclear
factor kB (NF-kB). It is likely that the balance of
proinflammatory and antiinflammatory signaling is critical
in maintaining normal intestinal functions.