The effect of acute in vivo epidermal growth factor (EGF) exposure on intestinal absorptive surface area was examined in blind jejunal loops in New Zealand White rabbits (500-900 g). Brush-border surface area was assessed by electron microscopy at 30 and 120 min, and total surface area was assessed by the fluorophore 1-[4-(trimethylamino)phenyl)]-6-phenylhexatriene (TMA-DPH) at 10 and 60 min after EGF exposure. Mucosa obtained at 120 min was also used for morphometrics and analysis of membrane composition and fluidity. Brush-border surface area was significantly increased in EGF-treated tissue after 30 (42%) and 120 min (60%). Total absorptive surface area measured by TMA-DPH was increased more than twofold after 10 and 60 min EGF exposure. The increase in absorptive surface area was abolished by pretreatment with intravenous verapamil. Mucosal morphometrics and membrane sucrase activity, total phospholipids, cholesterol content, cholesterol-to-phospholipid ratio, phospholipid species (wt%), phospholipid fatty acid composition, and fluidity did not differ between control and EGF-treated tissue. These findings indicate that EGF can rapidly increase brush-border surface area by a mechanism that appears to be due to a redistribution of existing performed microvillus plasma membrane.

Giardiasis has been associated with an increase in allergic disease following infection suggesting an alteration in mucosal immune function. Jejunal in vivo and in vitro macromolecular transport, epithelial permeability, and mucosal and connective tissue mast cell counts were examined in Mongolian gerbils (35-45 g) orogastrically inoculated (I) with a pathogenic strain of Giardia lamblia and compared to age- and weight-matched, sham-treated controls (C) 6 and 21 days postinoculation. Macromolecular uptake was significantly increased in infected tissue at 6 days both in vivo (I 134 +/- 19 vs. C 74 +/- 17 ng/hr; n = 8; P < 0.05) and in vitro (I 125 +/- 17 vs. C 67 +/- 8 ng/hr/cm; n = 12; P < 0.05). Macromolecular uptake did not differ between groups at 21 days. Infection had no effect on mucosal permeability of [51Cr]EDTA. Mucosal mast cell counts did not differ at 6 days but were significantly elevated in infected tissue at 21 days (I 33.3 +/- 6.8 vs. C 2.7 +/- 0.4 per high magnification field; n = 5; P < 0.01) as were connective tissue mast cell counts (I 1.7 +/- 0.2 vs. C 1.0 +/- 0.1 per high magnification field; n = 13; P < 0.005). The findings indicate that during the peak phase of giardiasis, jejunal active antigen uptake is increased leading to a delayed recruitment of mucosal and connective tissue mast cells. These changes may play a role in the increased incidence of hypersensitivity reactions associated with Giardia infection.

No abstract

Antigen challenge of jejunal epithelium from rats sensitized to egg albumin induces an active Cl- secretory process secondary to release of mucosal mast cell mediators. The present study was designed to define the relative role of these mast cell mediators and the enteric nervous system in the transport abnormalities associated with intestinal anaphylaxis. Net ion transport of stripped jejunal tissue from sensitized and sham-treated animals was studied in Ussing chambers. The Cl- secretory response induced by egg albumin during intestinal anaphylaxis was similar to that after addition of 5-hydroxytryptamine (5-HT), histamine, and prostaglandins D2 and E2 to jejunal tissue. Cinanserin, a 5-HT2-receptor antagonist, virtually abolished the response to 5-HT and totally abolished the response to egg albumin. Methysergide, a 5-HT1-receptor antagonist had no effect on either response. Indomethacin, an inhibitor of prostaglandin synthesis, significantly inhibited the 5-HT and egg albumin response. Diphenhydramine, an H1-receptor antagonist and cimetidine, an H2-receptor antagonist both significantly inhibited the histamine response but neither altered the response to egg albumin. Atropine, an anticholinergic, and tetrodotoxin, a nerve blocker, did not inhibit the antigen induced anaphylactic response. These results indicate that 5-HT, acting through 5-HT2 receptors is largely responsible for the transport abnormalities seen in intestinal anaphylaxis induced by egg albumin while prostaglandins appear to play a partial role. The findings do not support a role for the enteric nervous system for the egg albumin induced changes in Cl- secretion.