Page 33 - Read Online

Son et al. Microbiome Res Rep. 2025;4:29 https://dx.doi.org/10.20517/mrr.2025.14 Page 13 of 19

IMPACTS OF F18 E. coli CHALLENGE ON JEJUNAL MORPHOLOGY
+
Jejunal morphology data from 14 studies involving F18 E. coli challenge were reviewed [9,23,27-30,36,37] . On
+
+
average, F18 E. coli challenge resulted in a 10.2% and 10.7% decrease in VH and VH-to-crypt depth (CD)
ratio (VH:CD), respectively, and a 0.9% and 35.4% increase in CD and crypt cell proliferation in the
jejunum [Table 5]. These parameters serve as indicators of morphological development and the extent of
damage caused by F18 E. coli infection. F18 E. coli reduces VH in the jejunum primarily through
+
+
inflammation- and oxidative stress-induced apoptosis, which in turn impairs nutrient absorption .
[9]
[19]
Although inflammation and oxidative stress could theoretically reduce CD as well , the reviewed studies
show inconsistent effects of F18 E. coli on CD. This inconsistency may be explained by structural
+
differences between villi and crypts: villi are finger-like projections exposed to both luminal digesta and the
mucosa surface, while crypts are located at the base of the villi and are less exposed to the luminal
+
environment. These characteristics may make crypts less susceptible to F18 E. coli-induced damage. The
observed reduction in the VH:CD ratio is mainly driven by the greater reduction in VH compared to the
+
increase in CD. Ki-67 cells, which are present in all active cell cycle phases except G0, serve as a marker of
+
+
cell proliferation. The increased proportion of Ki-67 proliferative cells in response to F18 E. coli suggests
tissue damage by the pathogen and a corresponding activation of repair mechanisms . The morphological
[108]
+
changes induced by F18 E. coli ultimately impair nutrient absorption and increase nutrient loss due to the
energy demands of tissue repair in nursery pigs.
IMPACTS OF F18 E. coli CHALLENGE ON OTHER PARTS OF THE INTESTINE IN PIGS
+
Although the jejunum is the primary site affected by F18 E. coli, the negative impacts of this infection on
+
the ileum - particularly those involving microbial alterations and inflammation - have also been
investigated, due to the presence of F18 receptors on the ileal epithelium. In a study by Li et al., the RA of
Escherichia and Enterobacteriaceae, which include pathogenic species, increased in response to F18 E. coli
+
challenge . Conversely, the RA of Lactobacillus, a genus comprising beneficial bacteria, was reduced in the
[33]
ileum of infected pigs. This microbial imbalance, or dysbiosis, may promote the secretion of pro-
inflammatory cytokines. The F18 E. coli challenge also elevated IL-8 levels and secretory IgA levels in the
+
ileal mucosa of nursery pigs . At the gene expression level, the relative mRNA levels of IL-6 and TNF-α in
[18]
+
the ileal mucosa were also upregulated following F18 E. coli challenge [33,109] . Inflammation induced by the
infection damaged ileal morphology and downregulated the expression of tight junction protein genes,
potentially compromising intestinal barrier integrity [18,109] .

Research focusing on the large intestine remains limited, as F18 E. coli primarily targets the small intestine
+
due to the distribution of the F18 receptor. However, Duarte et al. reported a reduction in the RA of
Prevotella stercorea in feces following F18 E. coli challenge . This species is considered beneficial due to its
[9]
+
role in fermenting dietary fiber and producing SCFAs. Similarly, the RA of Selenomonas lipolytica, another
[23]
SCFA-producing, fiber-fermenting bacterium, was also found to decrease . These reductions in beneficial
bacterial populations mirror those observed in the small intestine, although the specific genera affected
differ. These discrepancies may stem from inherent differences in the microbial community composition
and substrate availability between the small and large intestines .
[80]
CONCLUSION
This review outlines the mechanisms and consequences of F18 E. coli challenge on intestinal health in the
+
+
jejunal tissue and mucosa of nursery pigs. F18 E. coli interacts with the jejunal epithelium through its
structural components. The F18 fimbriae, unique to this strain, facilitate attachment and colonization
within the pig intestine. After colonization, the bacterium secretes enterotoxins, inducing diarrhea via
electrolyte imbalance and ultimately reducing pig productivity. According to the reviewed literature, F18
+