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Updated: Mar 8, 2026
Non-Invasive Model of Neuropathogenic Escherichia coli Infection in the Neonatal Rat
Published on: October 29, 2014
[Lactobacillus rhamnosus GG conditioned medium prevents E. coli meningitis by inhibiting nuclear factor-κB pathway]
Qing Zeng1, Xiao-Long He, Han-Sheng Xiao
1Department of Microbiology, School of Public healthy, Southern Medical University, Guangzhou 510515, China.E-mail: 870686982@qq.com.
Objective:
To investigate whether Lactobacillus rhamnosus GG conditioned medium(LGG-CM)has preventive effect against E. coli K1-induced neuropathogenicity in vitro by inhibiting nuclear factor-κB (NF-κB) signaling pathway.
Methods:
An in vitro blood-brain barrier (BBB) model was constructed using human brain microvascular endothelial cells (HBMECs). The effect of LGG-CM on E. coli-actived NF-κB signaling pathway was assayed using Western blotting. Invasion assay and polymorphonuclear leukocyte (PMN) transmigration assay were performed to explore whether LGG-CM could inhibit E. coli invasion and PMN transmigration across the BBB in vitro. The expressions of ZO-1 and CD44 were detected using Western blotting and immunofluorescence. The changes of trans-epithelial electric resistance (TEER) and bacterial translocation were determined to evaluate the BBB permeability.
Results:
Pre-treament with LGG-CM inhibited E. coli-activated NF-κB signaling pathway in HBMECs and decreased the invasion of E. coli K1 and transmigration of PMN. Western blotting showed that LGG-CM could alleviate E. coli-induced up-regulation of CD44 and down-regulation of ZO-1 expressions in HBMECs. In addition, pre-treatment with LGG-CM alleviated E. coli K1-induced reduction of TEER and suppressed bacterial translocation across the BBB in vitro.
Conclusion:
LGG-CM can block E. coli-induced activation of NF-κB signaling pathway and thereby prevents E. coli K1-induced neuropathogenicity by decreasing E. coli K1 invasion rates and PMN transmigration.
Insights
Lactobacillus rhamnosus GG conditioned medium (LGG-CM) prevents E. coli K1 neuropathogenicity by inhibiting the NF-κB pathway. This probiotic treatment reduces bacterial invasion and immune cell transmigration across the blood-brain barrier.
Area of Science:
- Neuroscience
- Microbiology
- Immunology
Background:
- Enterohemorrhagic Escherichia coli (E. coli) K1 can cause neuropathogenicity.
- The nuclear factor-κB (NF-κB) signaling pathway plays a role in inflammatory responses.
- The blood-brain barrier (BBB) is crucial for protecting the central nervous system.
Purpose of the Study:
- To investigate the preventive effect of Lactobacillus rhamnosus GG conditioned medium (LGG-CM) against E. coli K1-induced neuropathogenicity.
- To determine if LGG-CM inhibits the NF-κB signaling pathway in vitro.
- To assess LGG-CM's impact on BBB integrity and bacterial invasion.
Main Methods:
- An in vitro BBB model using human brain microvascular endothelial cells (HBMECs) was established.
- Western blotting was used to assay NF-κB pathway activation and protein expression (ZO-1, CD44).
- Invasion assays, polymorphonuclear leukocyte (PMN) transmigration assays, and trans-epithelial electric resistance (TEER) measurements evaluated BBB permeability and bacterial translocation.
Main Results:
- LGG-CM pre-treatment inhibited E. coli-activated NF-κB signaling in HBMECs.
- LGG-CM decreased E. coli K1 invasion and PMN transmigration across the BBB model.
- LGG-CM treatment mitigated E. coli-induced changes in ZO-1 and CD44 expression and maintained BBB integrity (TEER).
Conclusions:
- LGG-CM effectively blocks E. coli-induced NF-κB activation.
- LGG-CM prevents E. coli K1 neuropathogenicity by reducing bacterial invasion and PMN transmigration.
- LGG-CM demonstrates a protective effect on the blood-brain barrier against E. coli K1 infection.
