Intestinal microbial flora after feeding phytohemagglutinin lectins (Phaseolus vulgaris) to rats

Abstract

Incorporation of purified phytohemagglutinin (PHA) lectins derived from red kidney beans (Phaseolus vulgaris) in the diet of weanling rats will cause growth failure, malabsorption of nutrients, and bacterial overgrowth in the small intestine. These effects are not caused by feeding a similar quantity of PHA to germfree rats. To define the morphological and bacterial changes on the mucosal surfaces of the jejunum, ileum, and cecum in greater detail, we pair fed two groups of weanling rats isocaloric, isonitrogenous diets with or without 0.5% PHA protein. On the jejunal surfaces of control rats, the mucous layer was a confluent covering with sparsely scattered bacteria and protozoa. In PHA-treated rats, the mucous layer was thin and discontinuous, and the microvilious surface of the tissue was extensively populated by bacterial cells of two distinct morphotypes-a gram-negative rod and a gram-positive coccobacillus. In all PHA-treated animals, these bacteria formed adherent monospecific or mixed adherent microcolonies on the tissue surface. Tissue damage was observed in PHA-exposed jejunal tissue as evidenced by vesiculation of the microvillous plasma membrane and by damage to the brush border membrane. On the ileal surfaces of control rats, there was a thick mucous layer within which small numbers of bacteria and protozoa were seen. Segmented filamentous bacteria were anchored in the tissue surface. In PHA-treated rats, the ileal surface was only incompletely covered by a mucous layer, and the overlying mucosal surface was extensively covered by large numbers of protozoan cells (predominantly Hexamita muris). Most of the ileal surfaces not covered by the mucous layer were occupied and virtually occluded by an overgrowth of these protozoan cells with occasional cells of Giardia muris and the tissue-associated segmented bacillus. In the ceca of control rats, the mucosa was incompletely covered by a discontinuous mucous layer and colonized by an unnamed Spirillum sp., other bacteria, and occasional protozoa. The cecal surfaces of PHA-treated rats retained most of their incomplete overlying mucous layer, which was heavily colonized by the same type of Spirillum sp. seen in untreated animals; intestinal crypts were colonized. These descriptive morphological studies demonstrate that exposure to purified PHA in the diet caused characteristic changes in the microbial ecology of the small intestine. The changes in microbial flora contributed to the malabsorption of nutrients in the small intestines of PHA-fed animals.

Structure-function and application of plant lectins in disease biology and immunity

“…That is why plant lectins are used as a potent inhibitor of gastric secretion in a dose-dependent manner without affecting pepsin secretion (Kordás et al, 2000(Kordás et al, , 2001. Mucosal damage in microvilli resulting from bacterial overgrowth is also controlled by consuming purified PHA followed by better host defence mechanism by improving the gut bacterial flora (Banwell et al, 1985;Sharon and Lis, 1989).…”

Oral Administration of Raw White Kidney Beans (Phaseolus Vulgaris L. Var. Beldia) Induces Overgrowth of Fecal Coliforms and Lactobacilli in Wistar Rats

“…In other side, it increased as well the numbers of E. coli, lactic acid bacteria, and other Enterobacteriaceae in the feces. Previously, PHA has been reported to dose-dependently induce bacterial overgrowth in the intestine, which is associated with weight loss, malabsorption, and villus damage [2,6,40]. It has been suggested that PHA increases the turnover of epithelial cells, promoting the expression of mannosylated receptor glycans on the gut surface and thus leading to increased adhesion and subsequent proliferation of mannose-sensitive type 1-fimbriated Escherichia coli.…”

“…One of these factors is phytohemagglutinin (PHA), the heat-stable lectin from the kidney bean (Phaseolus vulgaris L.; Family: Fabaceae) [1], which, when ingested orally, results in diarrhea, impaired nutrition absorption, growth rate inhibition, and can even lead to the eventual death of PHA-fed animals [2,3]. These effects are believed to result from changes in the autochthonous microflora induced by the presence of PHA in the diet [2,[4][5][6][7]. Information is accumulating on the effects of PHA on intestinal microflora, but there is a marked lack of information regarding the significance of these effects on fecal microbiota.…”

Bowel Biofilms: Tipping Points between a Healthy and Compromised Gut?

“…Recent findings support the hypothesis that the appendix serves as a safe house for human intestinal microbes, and here biofilm-like structures may have a function (Box 2, Figure 1). Several reports mention the occurrence of small agglomerates of the gut microbiota, that is, microcolonies, in the gut [31][32][33][34]. Their formation is further supported by some major theoretical concerns that argue against the formation of thick biofilms in the gut [35].…”