Effect of maternal sialoadenectomy on ontogenic response of rat gastric mucosa to luminal H+

Abstract

Epidermal growth factor (EGF) originating from salivary glands has been shown to affect the development and integrity of rodent gastrointestinal mucosa. Because newborn rats receive EGF from maternal milk, we have examined the effect of sialoadenectomy as a method of depleting EGF in milk on the resistance of neonatal rat mucosa to luminal H+. Rat dams were sialoadenectomized (SALX) or sham operated 5 days after parturition. Experiments were performed on newborns 10-22 days old. Mucosal permeability responses to intraluminal HCl (300 mM) were examined in terms of luminal appearances of Na+, K+, and protein and H+ loss. EGF levels in maternal milk were determined by immunoassay. In rat pups from control litters, luminal HCl resulted in an age-associated increase in cation and protein flux across the gastric mucosa. Luminal cation and protein fluxes observed in 10- to 18-day-old rat pups from SALX dams were not significantly different from similarly aged rats from control dams. However, in 19- to 22-day-old rats from SALX dams, the permeability responses to luminal HCl were exacerbated compared with similarly aged neonates from control dams. These responses were reduced by treatment with EGF. EGF levels in milk from sham-operated and SALX dams were not significantly different in the 10- to 16-day lactational period. However, in SALX dams EGF was significantly reduced at 19 and 22 days. Chromatographic elution pattern of milk EGF was dissimilar to the pattern exhibited by submandibular gland EGF.(ABSTRACT TRUNCATED AT 250 WORDS)

Epidermal Growth Factor Prevents Acetaldehyde‐Induced Paracellular Permeability in Caco‐2 Cell Monolayer

“…EGF has been shown to protect gastrointestinal mucosa from injury by a variety of factors (Brzozowski et al, 1991;Ishikawa et al, 1994;Konturek et al, 1991a,b;Rao and Porreca, 1996;Rao et al, 1997Rao et al, , 1999Tepperman et al 1993;Uribe and Barrett, 1997). The present study shows that EGF protects the epithelial barrier function by preventing acetaldehyde-induced disruption of tight junctions and paracellular permeability in Caco-2 cell monolayer, an intestinal epithelial cell line.…”

“…Mucosal protection from luminal irritants is an important acute effect of EGF (Konturek et al, 1990). EGF prevents gastric ulceration induced by aspirin, stress, ethanol, and acid (Brzozowski et al, 1991;Konturek et al, 1990Konturek et al, , 1991aTepperman et al, 1993) and duodenal ulceration by cysteamine (Tepperman et al, 1993). EGF also protects the intestinal mucosa from injury induced by a variety of insults (Ishikawa et al, 1994;Lawrence et al, 1997;Rao and Porreca, 1996;Rao et al, 1999).…”

MAPK interacts with occludin and mediates EGF-induced prevention of tight junction disruption by hydrogen peroxide

“…It is secreted in saliva and other gastrointestinal secretions at high concentrations [33] and is considered an important mucosal protective factor. In addition to its growth promoting effect, it prevents gastric ulceration induced by aspirin, stress, ethanol and acid [34][35][36][37], and attenuates the intestinal mucosal damage induced by a variety of insults [38][39][40]. EGF receptor activation turns on the Ras/MAPK (mitogenactivated protein kinase) pathway and mediates the promotion of cell proliferation, growth and differentiation [41].…”

Regulation of leukocyte adhesion to heart by the tripeptides feG and feG(NH2)

“…Submandibular glands are rich in anti-inflammatory factors that play a well-recognized role in the regulation of inflammation and tissue repair in the mouth (Dolce et al 1994;Hutson et al 1979) and the digestive tract (Konturek et al 1995;Tepperman et al 1993). These immunomodulatory influences extend beyond the digestive tract with healing of peripheral (Aloe et al 1986) and internal wounds (Konturek et al 1995) and modulation of systemic inflammatory reactions (Mathison et al 1994;Mathison 1998).…”