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Bifidobacterium bifidum reduces apoptosis in the intestinal epithelium in necrotizing enterocolitis

Ludmila Khailova1, Sarah K Mount Patrick, Kelly M Arganbright

  • 1Department of Pediatrics and Steele Children's Research Center, University of Arizona, Tucson, Arizona 85724-5073, USA.

American Journal of Physiology. Gastrointestinal and Liver Physiology
|August 14, 2010
PubMed

Insights

Bifidobacterium bifidum administration protects against necrotizing enterocolitis (NEC) by reducing intestinal apoptosis. This probiotic activates cyclooxygenase-2 (COX-2) and prostaglandin E(2) (PGE(2)) signaling, preserving intestinal integrity in a rat model.

Area of Science:

  • Neonatal Medicine
  • Gastroenterology
  • Microbiology

Background:

  • Necrotizing enterocolitis (NEC) is a severe intestinal disease in neonates.
  • Probiotics, including Bifidobacterium bifidum, show promise in NEC prevention.
  • Cyclooxygenase-2 (COX-2) and prostaglandin E(2) (PGE(2)) may suppress intestinal apoptosis.

Purpose of the Study:

  • To investigate the protective effect of Bifidobacterium bifidum against NEC.
  • To elucidate the role of B. bifidum in regulating intestinal apoptosis.
  • To examine the involvement of COX-2 and PGE(2) in B. bifidum's protective mechanism.

Main Methods:

  • A rat model of NEC was established, with groups receiving dam feeding, formula feeding (NEC), or formula with B. bifidum (NEC + B. bifidum).
  • Intestinal expression of Toll-like receptor-2 (TLR-2), COX-2, PGE(2), and apoptotic markers were measured.
  • The effects were validated in an in vitro model using the intestinal epithelial cell line IEC-6.

Main Results:

  • B. bifidum administration increased TLR-2, COX-2, and PGE(2) expression in the intestinal epithelium.
  • Apoptosis was significantly reduced in B. bifidum-treated rats and IEC-6 cells.
  • The Bax-to-Bcl-w ratio shifted towards survival, and cleaved caspase-3 positive cells decreased.
  • Inhibition of COX-2 signaling abrogated the protective effects of B. bifidum.

Conclusions:

  • Oral B. bifidum activates TLR-2 and upregulates COX-2, leading to increased PGE(2) production.
  • This COX-2-dependent pathway protects against intestinal apoptosis in NEC.
  • B. bifidum demonstrates potential for reducing mucosal injury and preserving intestinal integrity in NEC.

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