Combined Lactoferrin and Osteopontin Treatment Attenuates LPS-Induced Inflammatory Responses and Intestinal Injury in Macrophages and Mice.
- 1College of Food Science and Nutritional Engineering, China Agricultural University, Beijing 100083, China.
- 2Key Laboratory of Precision Nutrition and Food Quality, Department of Nutrition and Health, China Agricultural University, Beijing 100193, China.
- 3National Center of Technology Innovation for Dairy, Hohhot 010000, China.
Abstract
This study explored the combined anti-inflammatory potential of lactoferrin (LF) and osteopontin (OPN) using both in vitro (LPS-challenged macrophages) and in vivo (LPS-induced intestinal injury) models. The LF-OPN combination demonstrated superior efficacy over monotherapies in suppressing pro-inflammatory mediator expression in macrophages. In vivo, co-administration markedly attenuated intestinal-barrier disruption and preserved mucosal architecture, evidenced by increased villus height, crypt depth, and goblet-cell counts, surpassing the effects of OPN alone. This structural protection was accompanied by significant immunomodulation; the combination treatment elevated systemic and local anti-inflammatory cytokines while reducing pro-inflammatory ones more effectively than either single protein. Notably, at LF:OPN ratios of 1:1, 5:1, and 10:1, murine intestinal Il10 concentrations rose by 44.25%, 54.46%, and 60.02%, respectively, relative to LF group; Tnfα concentrations fell by 33.73%, 52.27%, and 37.80% at the same three ratios when benchmarked against the OPN group (all p < 0.05). These data reveal a potent combined effect of LF and OPN against acute inflammatory insults, suggesting a promising therapeutic combined effect. Future work should focus on elucidating the underlying signaling mechanisms and evaluating efficacy in chronic disease models.
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BibTeX
@article{zhang2026combined,
title = {{Combined Lactoferrin and Osteopontin Treatment Attenuates LPS-Induced Inflammatory Responses and Intestinal Injury in Macrophages and Mice.}},
author = {Yijia Zhang and Chuangang Li and Wenrui Zhang and Yujuan Chen and Xinyuan Wang and Yifei Zhai and Yanqin Quan and Jian He and Yixuan Li and Yanan Sun},
journal = {Foods (Basel, Switzerland)},
year = {2026},
month = oct,
doi = {10.3390/foods15203746},
url = {https://europepmc.org/article/MED/42940383},
note = {CC BY},
}
RIS
TY - JOUR
TI - Combined Lactoferrin and Osteopontin Treatment Attenuates LPS-Induced Inflammatory Responses and Intestinal Injury in Macrophages and Mice.
AU - Yijia Zhang
AU - Chuangang Li
AU - Wenrui Zhang
AU - Yujuan Chen
AU - Xinyuan Wang
AU - Yifei Zhai
AU - Yanqin Quan
AU - Jian He
AU - Yixuan Li
AU - Yanan Sun
PY - 2026
DA - 2026/10/21
JO - Foods (Basel, Switzerland)
DO - 10.3390/foods15203746
UR - https://europepmc.org/article/MED/42940383
AB - This study explored the combined anti-inflammatory potential of lactoferrin (LF) and osteopontin (OPN) using both in vitro (LPS-challenged macrophages) and in vivo (LPS-induced intestinal injury) models. The LF-OPN combination demonstrated superior efficacy over monotherapies in suppressing pro-inflammatory mediator expression in macrophages. In vivo, co-administration markedly attenuated intestinal-barrier disruption and preserved mucosal architecture, evidenced by increased villus height, crypt depth, and goblet-cell counts, surpassing the effects of OPN alone. This structural protection was accompanied by significant immunomodulation; the combination treatment elevated systemic and local anti-inflammatory cytokines while reducing pro-inflammatory ones more effectively than either single protein. Notably, at LF:OPN ratios of 1:1, 5:1, and 10:1, murine intestinal Il10 concentrations rose by 44.25%, 54.46%, and 60.02%, respectively, relative to LF group; Tnfα concentrations fell by 33.73%, 52.27%, and 37.80% at the same three ratios when benchmarked against the OPN group (all p < 0.05). These data reveal a potent combined effect of LF and OPN against acute inflammatory insults, suggesting a promising therapeutic combined effect. Future work should focus on elucidating the underlying signaling mechanisms and evaluating efficacy in chronic disease models.
SN - 2304-8158
ER -