Evidence map›Paper›PMID 41039397›Full record

ArticleJournal of neuroinflammation2025

Neuro-immune regulation of sepsis-associated delirium via the PBN-CeA-spleen axis.

Menglin Dong, Yu Zou, Zhiwen Ye, Wangyuan Zou, Lina Zhang, Yuhang Ai, Qianyi Peng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Menglin DongDepartment of Critical Care Medicine, Xiangya Hospital, Central South University, No 87 Xiangya Rd, Changsha, 410008, Hunan, China.
Yu ZouDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.
Zhiwen YeDepartment of Critical Care Medicine, Xiangya Hospital, Central South University, No 87 Xiangya Rd, Changsha, 410008, Hunan, China.
Wangyuan ZouDepartment of Anesthesiology, Xiangya Hospital, Central South University, Changsha, China.
Lina ZhangDepartment of Critical Care Medicine, Xiangya Hospital, Central South University, No 87 Xiangya Rd, Changsha, 410008, Hunan, China.
Yuhang AiDepartment of Critical Care Medicine, Xiangya Hospital, Central South University, No 87 Xiangya Rd, Changsha, 410008, Hunan, China.
Qianyi PengDepartment of Critical Care Medicine, Xiangya Hospital, Central South University, No 87 Xiangya Rd, Changsha, 410008, Hunan, China. 405905@csu.edu.cn.

Funding

the National Natural Science Foundation of China 82372199the Natural Science Foundation of Hunan Province , China 2024JJ5559
6 · The paper itself

Abstract

backgroundSepsis associated delirium (SAD) is the most prevalent manifestation of acute brain dysfunction in sepsis, yet its central regulatory mechanisms remain incompletely understood. As researchers have progressively explored the brain-spleen axis and neuroimmunity, this study aimed to investigate the role of the parabrachial nucleus (PBN)-central amygdala (CeA)-spleen axis in the pathogenesis of SAD.

methodsIn a mouse model of SAD induced by intraperitoneal injection of lipopolysaccharide (LPS, 10 mg/kg), we identified activation patterns in both the PBN and CeA using immunofluorescence analysis. We subsequently investigated direct anatomical connections between these regions through bidirectional neural tracing, followed by functional interrogation using fiber photometry and electrophysiological recordings. Finally, we evaluated the effect of targeted inhibition of the PBN-CeA pathway on delirium in septic mice through behavioral assays. Additionally, enzyme-linked immunosorbent assay (ELISA) and flow cytometry were employed for immunological profiling.

resultsWe observed a significant increase in c-Fos expression in both the PBN and CeA, and confirmed a direct anatomical connection between these regions. Fiber photometry and electrophysiological recordings revealed that LPS stimulation activated CeA neurons and splenic sympathetic nerves. In addition, targeted inhibition of the PBN-CeA pathway mitigated CeA calcium dynamics and reduced spontaneous splanchnic nerve discharge. Behavioral assays showed that splenic denervation and inhibition of the PBN-CeA pathway attenuated delirium-like behaviors in septic mice. ELISA and flow cytometry demonstrated that these interventions reversed splenic proinflammatory cytokines (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-1β, IL-6, and IL-10, interferon-gamma [IFN-γ]) and norepinephrine (NE) while restoring immune cell composition and enhancing natural killer (NK) cell function.

conclusionThe PBN-CeA-splenic axis plays a critical neuroimmune conduit linking central neural circuits to peripheral immune modulation, offering new mechanistic insight into the neural regulation of systemic inflammation and the pathogenesis of SAD.

Indexed as

DeliriumNeuroimmunomodulationSepsisSpleenAnimalsLipopolysaccharidesMaleMiceMice, Inbred C57BLLipopolysaccharidesCentral amygdalaNeuro-immunomodulationParabrachial nucleusPBN-CeA-splenic axisSepsis-associated delirium

Identifiers

PMID41039397
PMCPMC12492939

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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.