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Updated: Sep 28, 2025
A Murine Model of Fetal Exposure to Maternal Inflammation to Study the Effects of Acute Chorioamnionitis on Newborn Intestinal Development
Published on: June 24, 2020
Protective effects of recombinant lactoferrin with different iron saturations on enteritis injury in young mice
1Key Laboratory of Quality & Safety Control for Milk and Dairy Products of Ministry of Agriculture and Rural Affairs, Institute of Animal Science, Chinese Academy of Agricultural Sciences, Beijing 100193, P. R. China.
Insights
Apo-lactoferrin (apo-LF) significantly alleviates infant intestinal inflammation and injury caused by lipopolysaccharides (LPS). This form of lactoferrin (LF) demonstrates superior protective effects compared to holo-LF by regulating key inflammatory pathways.
Area of Science:
- Pediatrics
- Gastroenterology
- Immunology
Background:
- Infant intestines are vulnerable to infections, leading to developmental damage and enteritis.
- Lactoferrin (LF) shows potential in protecting infant intestines, but its iron saturation's role is unclear.
- Iron saturation differentiates apo-LF and holo-LF, potentially influencing their bioactivity.
Purpose of the Study:
- To investigate the protective effects of apo-LF and holo-LF against infant intestinal inflammation.
- To compare the efficacy of apo-LF versus holo-LF in an infant enteritis model.
- To elucidate the molecular mechanism of iron-saturated LF in mitigating intestinal inflammation.
Main Methods:
- Established young mouse models with lipopolysaccharide (LPS)-induced intestinal damage.
- Administered apo-LF and holo-LF to assess their protective effects in vivo and in vitro.
- Utilized Western blot assays to analyze inflammatory pathway regulation.
Main Results:
- Apo-LF significantly reduced disease activity, colon shortening, and histopathological scores compared to LPS and holo-LF groups.
- Apo-LF treatment led to decreased LPS concentration and gram-negative bacteria in the gut.
- Pro-inflammatory factor expression in colon tissue was downregulated in the apo-LF group.
Conclusions:
- Apo-LF effectively alleviates LPS-induced enteritis injury in infants.
- Apo-LF exerts its protective effects by modulating the PPAR-γ/PFKFB3/NF-κB inflammatory pathway.
Abstract:
Infant intestinal development is immature and, thus, is vulnerable to bacterial and viral infections, which damage intestinal development and even induce acute enteritis. Numerous studies have investigated that lactoferrin (LF) has protective effects on the intestine and may play a role in preventing intestinal inflammation in infants. Lactoferrin is divided into 2 types, namely apo-LF and holo-LF, depending on the degree of iron saturation, which may affect its bioactivities. However, the role of LF iron saturation in protecting infant intestinal inflammation has not been clearly clarified. Therefore, in this study, young mice models with intestinal damage induced by lipopolysaccharides (LPS) in vivo and primary intestinal epithelial cells in vitro were constructed to enteritis injury in infants for investigation. The apo-LF and holo-LF were subsequently applied to the mouse models to investigate and compare their levels of protection in the intestinal inflammatory injury, as well as to identify which LF was most active. Moreover, the specific mechanism of the LF with optimal iron saturation was further investigated through Western blot assay. Results demonstrated that disease activity index, shortened length of colon tissue, and histopathological score were significantly decreased in the apo-LF group compared with those of the LPS group and the holo-LF group. In the apo-LF group, the concentration of LPS in the intestinal tract and the number of gram-negative bacteria colonies decreased significantly and the expression levels of proinflammatory factors in the colon tissue were downregulated, in comparison with those in the LPS group. The findings of this study thus verify that apo-LF can significantly alleviate enteritis injury caused by LPS, through regulating the PPAR-γ/PFKFB3/NF-κB inflammatory pathway.
