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Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine.
Am J Physiol Gastrointest Liver Physiol. 2014 Oct 01; 307(7):G689-99.AJ

Abstract

A balance between pro- and anti-inflammatory signals from milk and microbiota controls intestinal homeostasis just after birth, and an optimal balance is particularly important for preterm neonates that are sensitive to necrotizing enterocolitis (NEC). We suggest that the intestinal cytokine IL-8 plays an important role and hypothesize that transforming growth factor-β2 (TGF-β2) acts in synergy with bacterial lipopolysaccharide (LPS) to control IL-8 levels, thereby supporting intestinal homeostasis. Preterm pigs were fed colostrum (containing TGF-β2) or infant formula (IF) with or without antibiotics (COLOS, n = 27; ANTI, n = 11; IF, n = 40). Intestinal IL-8 levels and NEC incidence were much higher in IF than in COLOS and ANTI pigs (P < 0.001), but IL-8 levels did not correlate with NEC severity. Intestinal TGF-β2 levels were high in COLOS but low in IF and ANTI pigs. Based on these observations, the interplay among IL-8, TGF-β2, and LPS was investigated in a porcine intestinal epithelial cell line. TGF-β2 attenuated LPS-induced IL-6, IL-1β, and TNF-α release by reducing early ERK activation, whereas IL-8 secretion was synergistically induced by LPS and TGF-β2 via NF-κB. The TGF-β2/LPS-induced IL-8 levels stimulated cell proliferation and migration following epithelial injury, without continuous NF-κB activation and cyclooxygenase-2 expression. We suggest that a combined TGF-β2-LPS induction of IL-8 stimulates epithelial repair just after birth when the intestine is first exposed to colonizing bacteria and TGF-β2-containing milk. Moderate IL-8 levels may act to control intestinal inflammation, whereas excessive IL-8 production may enhance the damaging proinflammatory cascade leading to NEC.

Authors+Show Affiliations

Faculty of Science, Department of Food Science, University of Copenhagen, Copenhagen, Denmark; and.Faculty of Science, Department of Nutrition, Exercise, and Sports, University of Copenhagen, Copenhagen, Denmark.Faculty of Science, Department of Nutrition, Exercise, and Sports, University of Copenhagen, Copenhagen, Denmark.Faculty of Science, Department of Nutrition, Exercise, and Sports, University of Copenhagen, Copenhagen, Denmark.Faculty of Science, Department of Food Science, University of Copenhagen, Copenhagen, Denmark; and Faculty of Science, Department of Nutrition, Exercise, and Sports, University of Copenhagen, Copenhagen, Denmark dcha@food.ku.dk.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25147235

Citation

Nguyen, Duc Ninh, et al. "Transforming Growth Factor-β2 and Endotoxin Interact to Regulate Homeostasis Via Interleukin-8 Levels in the Immature Intestine." American Journal of Physiology. Gastrointestinal and Liver Physiology, vol. 307, no. 7, 2014, pp. G689-99.
Nguyen DN, Sangild PT, Ostergaard MV, et al. Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine. Am J Physiol Gastrointest Liver Physiol. 2014;307(7):G689-99.
Nguyen, D. N., Sangild, P. T., Ostergaard, M. V., Bering, S. B., & Chatterton, D. E. (2014). Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine. American Journal of Physiology. Gastrointestinal and Liver Physiology, 307(7), G689-99. https://doi.org/10.1152/ajpgi.00193.2014
Nguyen DN, et al. Transforming Growth Factor-β2 and Endotoxin Interact to Regulate Homeostasis Via Interleukin-8 Levels in the Immature Intestine. Am J Physiol Gastrointest Liver Physiol. 2014 Oct 1;307(7):G689-99. PubMed PMID: 25147235.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Transforming growth factor-β2 and endotoxin interact to regulate homeostasis via interleukin-8 levels in the immature intestine. AU - Nguyen,Duc Ninh, AU - Sangild,Per T, AU - Ostergaard,Mette V, AU - Bering,Stine B, AU - Chatterton,Dereck E W, Y1 - 2014/08/21/ PY - 2014/8/23/entrez PY - 2014/8/26/pubmed PY - 2014/12/15/medline KW - lipopolysaccharide KW - necrotizing enterocolitis KW - nuclear factor-κB KW - preterm infants SP - G689 EP - 99 JF - American journal of physiology. Gastrointestinal and liver physiology JO - Am J Physiol Gastrointest Liver Physiol VL - 307 IS - 7 N2 - A balance between pro- and anti-inflammatory signals from milk and microbiota controls intestinal homeostasis just after birth, and an optimal balance is particularly important for preterm neonates that are sensitive to necrotizing enterocolitis (NEC). We suggest that the intestinal cytokine IL-8 plays an important role and hypothesize that transforming growth factor-β2 (TGF-β2) acts in synergy with bacterial lipopolysaccharide (LPS) to control IL-8 levels, thereby supporting intestinal homeostasis. Preterm pigs were fed colostrum (containing TGF-β2) or infant formula (IF) with or without antibiotics (COLOS, n = 27; ANTI, n = 11; IF, n = 40). Intestinal IL-8 levels and NEC incidence were much higher in IF than in COLOS and ANTI pigs (P < 0.001), but IL-8 levels did not correlate with NEC severity. Intestinal TGF-β2 levels were high in COLOS but low in IF and ANTI pigs. Based on these observations, the interplay among IL-8, TGF-β2, and LPS was investigated in a porcine intestinal epithelial cell line. TGF-β2 attenuated LPS-induced IL-6, IL-1β, and TNF-α release by reducing early ERK activation, whereas IL-8 secretion was synergistically induced by LPS and TGF-β2 via NF-κB. The TGF-β2/LPS-induced IL-8 levels stimulated cell proliferation and migration following epithelial injury, without continuous NF-κB activation and cyclooxygenase-2 expression. We suggest that a combined TGF-β2-LPS induction of IL-8 stimulates epithelial repair just after birth when the intestine is first exposed to colonizing bacteria and TGF-β2-containing milk. Moderate IL-8 levels may act to control intestinal inflammation, whereas excessive IL-8 production may enhance the damaging proinflammatory cascade leading to NEC. SN - 1522-1547 UR - https://www.unboundmedicine.com/medline/citation/25147235/Transforming_growth_factor_β2_and_endotoxin_interact_to_regulate_homeostasis_via_interleukin_8_levels_in_the_immature_intestine_ L2 - https://journals.physiology.org/doi/10.1152/ajpgi.00193.2014?url_ver=Z39.88-2003&amp;rfr_id=ori:rid:crossref.org&amp;rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -