Evidence map›Paper›PMID 41591410›Full record

ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026

Recombinant TsP53 mitigates inflammation and blood-brain barrier disruption in CLP-induced septic mice.

Deng Zhezhi, Sun Zaiyuan, Lu Gengxin, Gong Wenqian, Guo Jifeng, Guo Li, Wei Lingyu, Xu Jia

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

Authors and funding

8 authors.

Deng Zhezhi *Department of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Sun Zaiyuan *Department of Emergency, The Seventh Affiliated Hospital, Sun Yat-Sen University, 628 Zhenyuan Road, Shenzhen, 518107, China.
Lu Gengxin *Department of Neurology, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Gong WenqianDepartment of Emergency, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China.
Guo JifengDepartment of Clinical Laboratory, Guangdong Women and Children Hospital, 521 Xingnan Road, Guangzhou, 511400, China.
Guo LiDepartment of Clinical Laboratory, Guangdong Women and Children Hospital, 521 Xingnan Road, Guangzhou, 511400, China. guoli88121@163.com.
Wei LingyuDepartment of Emergency, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China. weily29@mail.sysu.edu.cn.
Xu JiaDepartment of Emergency, The First Affiliated Hospital, Guangdong Provincial Key Laboratory of Diagnosis and Treatment of Major Neurological Diseases, National Key Clinical Department and Key Discipline of Neurology, Sun Yat-Sen University, No.58 Zhongshan Road 2, Guangzhou, 510080, China. xujia5@mail.sysu.edu.cn.

Funding

Basic and Applied Basic Research Foundation of Guangdong Province 2023A1515010491Guangzhou Municipal Science and Technology Project 2024A04J4565
6 · The paper itself

Abstract

backgroundSepsis-associated encephalopathy (SAE), a neurological complication of sepsis without direct CNS infection, currently lacks established pharmacological therapy. Key pathological features include excessive microglial activation and blood-brain barrier (BBB) disruption. Our prior work showed that recombinant Trichinella spiralis 53-kDa glycoprotein (rTsP53) modulates intestinal endothelial tight junctions in septic mice by downregulating inflammation.

methodsWe analyzed inflammatory factor levels and performed bioinformatics analysis on cerebrospinal fluid (CSF) from SAE patients. In a cecal ligation and puncture (CLP)-induced septic mouse model, we assessed brain inflammatory cytokines, BBB permeability, tight junction protein expression, microglial activation, and transcription factor p65 levels. Mice were prophylactically treated with rTsP53 prior to septic insult.

resultsCSF from SAE patients showed significantly elevated inflammatory factors and upregulated leukocyte migration/chemotaxis pathways. CLP-induced septic mice exhibited increased brain inflammatory cytokines, enhanced BBB permeability, reduced tight junction protein expression, microglial activation, and elevated p65. Prophylactic rTsP53 treatment decreased pro-inflammatory cytokines (IL-6, IL-17A) and p65, increased anti-inflammatory factors (IL-4, IL-13), and alleviated BBB damage.

conclusionProphylactic rTsP53 mitigates sepsis-induced brain inflammation and BBB disruption in mice by modulating the microglial response. These findings provide preclinical evidence supporting the further exploration of rTsP53 as a potential preventive agent for SAE.

Indexed as

Blood-Brain BarrierSepsisSepsis-Associated EncephalopathyAnimalsCecumCytokinesHumansInflammationMaleMiceMice, Inbred C57BLMicrogliaRecombinant ProteinsTrichinella spiralisCytokinesRecombinant ProteinsBlood–brain barrierMicrogliaSepsis-associated encephalopathyTrichinella spiralis antigens

Identifiers

PMID41591410

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.