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Trophic Effect of Multiple Growth Factors in Amniotic Fluid or Human Milk on Cultured Human Fetal Small Intestinal Cells

Hirai, Chie*; Ichiba, Hiroyuki*; Saito, Mika*; Shintaku, Haruo*; Yamano, Tsunekazu*; Kusuda, Satoshi†

Journal of Pediatric Gastroenterology & Nutrition: May 2002 - Volume 34 - Issue 5 - pp 524-528
Original Articles

Objectives: To evaluate the role of growth factors in amniotic fluid and in human milk on gastrointestinal adaptation of the fetus and very low-birth-weight infants, the effects of these fluids and multiple growth factors were investigated in a human fetal small intestinal cell line (FHs 74 Int).

Methods: After FHs 74 Int cells were incubated with amniotic fluid, human milk, or recombinant growth factors, growth-promoting activity was measured by [3H]-thymidine incorporation into cells.

Results: Incubating cells with amniotic fluid or human milk promoted growth dose dependently. Genistein almost completely inhibited growth-promoting activity in amniotic fluid P = 0.002), and growth was partially inhibited by antibodies against epidermal growth factor (EGF) (P = 0.047), insulin-like growth factor-1 (IGF-1, P = 0.047), or fibroblast growth factor (FGF, P = 0.014). This activity in human milk was inhibited almost completely by genistein (P h 0.0001) and partially inhibited by antibodies against EGF (P = 0.036), IGF-1 (P = 0.009), FGF (P = 0.004), hepatocyte growth factor (HGF, P = 0.001), or transforming growth factor-α (TGF-α, P = 0.001). Although recombinant EGF, IGF-1, FGF, HGF, and TGF-α elicited a synergistic trophic response on cultured cells, the response was much less than with amniotic fluid or with human milk.

Conclusion: In aminiotic fluid and in human milk, EGF, IGF-1, FGF, HGF, and TGF-α have a strong trophic effect on immature intestinal cells and may be involved in perinatal gastrointestinal adaptation.

*Department of Pediatrics, Osaka City University Graduate School of Medicine, and †Department of Neonatology, Osaka City General Hospital, Osaka, Japan

Received June 19, 2001; accepted November 9, 2001.

This work was supported by the Morinaga Houshi-Kai, Japan.

Address correspondence and reprint requests to Dr. Hiroyuki Ichiba, Department of Pediatrics, Osaka City University Graduate School of Medicine, 1–4-3 Asahimachi, Abenoku, Osaka 545–8586, Japan (e-mail: h-ichiba@med.osaka-cu.ac.jp).

This article is accompanied by an editorial. Please see J Pediatr Gastroenterol Nutr 2002;34:513–514.

© 2002 Lippincott Williams & Wilkins, Inc.