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Gut. Apr 2000; 46(4): 515–521.
PMCID: PMC1727902

Surface hydrophobicity of the rat colonic mucosa is a defensive barrier against macromolecules and toxins


BACKGROUND—Mucosal surface hydrophobicity is a key factor of the gastric acid defence barrier. In the colon, surface hydrophobicity is high but its biological function remains unexplored.
AIMS—To investigate the functional changes of the barrier due to removal of the surface active phospholipid layer by a detergent, or to reinforcement of the surface active phospholipid by local application of a suspension of lipids.
METHODS—Surface hydrophobicity (contact angle measurement), colonic permeability (lumen to blood clearance of mannitol and dextran), and mucosal resistance against luminal aggression (distal colitis induced by dextran sodium sulphate, DSS) were investigated in three study groups: (a) rats pretreated with a detergent (Brij 35) known to remove surfactant lipids; (b) rats pretreated with a suspension of surface active lipids (tripalmitin and dipalmitoyl-phosphatidylcholine); and (c) control rats pretreated with the corresponding vehicles.
RESULTS—In controls, surface hydrophobicity was low on the caecal mucosa and high in colon and rectum. Detergent treatment reduced surface hydrophobicity, and increased colonic permeability to mannitol and dextran. Conversely, treatment with lipids increased surface hydrophobicity, and reduced colonic permeability. Administration of DSS induced a progressive loss of colonic surface hydrophobicity, and an increase in permeability to mannitol and dextran. Detergent treatment increased susceptibility to epithelial damage and mucosal inflammation by DSS. Treatment with lipids reduced susceptibility to DSS colitis.
CONCLUSION—Colonic surface hydrophobicity modulates permeability to hydrophilic molecules and protects against toxins.

Keywords: mucosal surface hydrophobicity; mannitol; dextran

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Selected References

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Figures and Tables

Figure 1
Surface hydrophobicity of the colonic mucosa in control rats and in rats treated with 2% Brij 35 in the drinking water for two days. Data are presented as the mean (SEM) of five rats per group. *p<0.05 compared with control.
Figure 2
Surface hydrophobicity of the colonic mucosa in control rats and in rats treated with 2 ml of tripalmitin-phosphatidylcholine. Data are presented as the mean (SEM) of seven rats per group. *p<0.05 compared with control.
Figure 3
Surface hydrophobicity of the colonic mucosa in control rats, in rats treated with 1 ml 5% Brij 35 instilled into the colonic lumen, and in rats treated with 5% Brij 35 as above and 2 ml of a lipid suspension (tripalmitin-phosphatidylcholine) ...
Figure 4
Lumen to blood clearance of mannitol or dextran expressed as percentage of the dose administered intracolonically at time 0 to control rats and to rats treated with 2% Brij 35 in the drinking water for two days. Values are means (SEM) ...
Figure 5
Lumen to blood clearance of mannitol or dextran expressed as percentage of the dose administered intracolonically at time 0 to control rats and to rats treated with 2 ml of a lipid suspension (tripalmitin-phosphatidylcholine) instilled ...
Figure 6
Surface hydrophobicity of the colonic mucosa in control rats (day 0) and in rats treated with 4% dextran sodium sulphate (DSS) in the drinking water on days 1, 3, and 5 after exposure to DSS. Values are means (SEM) for five rats ...
Figure 7
Lumen to blood clearance of mannitol or dextran five hours after intracolonic administration of labelled probes in controls, and in rats treated with 4% dextran sodium sulphate (DSS) in the drinking water on days 1, 3, and 5 after ...
Figure 8
Colonic damage scores after administration of 4% DSS for five days in control rats, in rats pretreated with 2% Brij 35 for two days, and in rats treated with 2 ml enemas of a lipid suspension for three days before DSS and during the five ...

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