Effects of S100B neutralization on the long-term cognitive impairment and neuroinflammatory response in an animal model of sepsis
Open accessAbstract
The nervous system is one of the first systems to be affected during sepsis. Sepsis not only has a high risk of mortality, but could also lead to cerebral dysfunction and cognitive impairment in long-term survival patients. The receptor for advanced glycation end products (RAGE) can interact with several ligands, and its activation triggers a series of cell signaling events, resulting in the hyperinflammatory condition related to sepsis. Recent studies show that elevated levels of S100B (RAGE ligand) are associated with the pathophysiology of neurodegenerative disorders. They also participate in inflammatory brain diseases and may lead to an increased activation of microglia and astrocytes, leading to neuronal death. This study aimed to determine the effect of S100B inhibition on the neuroinflammatory response in sepsis. Sepsis was induced in Wistar rats by cecal ligation and perforation (CLP). There were three groups: Sham, CLP, and CLP + 10 μg/kg of monoclonal antibody (Anti-S100B) administered intracerebroventricularly. The animals were killed 30 days after sepsis following behavioral evaluation by open field, novel object recognition, and splash test. The hippocampus, prefrontal cortex, and amydgala were used for the determination of S100B and RAGE proteins by western blotting and for the evaluation of cytokine levels and verification of the number of microglial cells by immunohistochemistry. On day 30, both the Sham and CLP + anti-S100B groups were capable of recovering the habitual memory in the open field task. Regarding novel object recognition, Sham and CLP + anti-S100B groups increased the recognition index during the test session in comparison to the training session. There was a significant increase in the time of grooming in CLP + anti-S100B in comparison to the CLP group. There was a modulation of cytokine levels and immunohistochemistry showed that the CLP + anti-S100B group had a decrease in the number of microglial cells only in the hippocampus. These results helped to understand the role of S100B protein in the pathophysiology of sepsis-associated encephalopathy and could be helpful to further experimental studies regarding this subject.
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Sustained microglial activation triggered by the RAGE ligand S100B exacerbates abnormal BBB permeability.
“sustained activation triggered by the RAGE ligand S100B exacerbates abnormal BBB permeability [17,18].”
From Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy (2026) · cites this paper as [17]
The Introduction identifies S100B as a RAGE ligand, and the Discussion links S100B to neuroinflammation and reports effects of S100B neutralization on inflammatory cytokines in septic rats. The paper does not establish that sustained S100B-triggered microglial activation exacerbates blood–brain barrier permeability; the barrier claim is not supported by the passages found. Page numbers were not available in our copy. (LLM, conf=0.85)
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Research Advances in the Pathogenesis of Sepsis-Associated Encephalopathy
Tan, H., Su, W., & Niu, Z. (2026) · International Journal of Molecular Sciences · doi:10.3390/ijms27125390 · Cited by 1 · see citing works
“During sepsis, these cells undergo dynamic functional transformation: early activation exerts protective effects via Foxc1-mediated I κ B α /NF-κ B signaling regulation [16]; however, sustained activation triggered by the RAGE ligand S100B exacerbates abnormal BBB permeability [17,18].”
Valvassori, S. S., Della, T. P., Aguiar‐Geraldo, J. M., Sant'Ana, R. G., Dal-Pont, G. C., Pescador, B., Zugno, A. I., Quevedo, J., & Dal‐Pizzol, F. (2023) · European Journal of Neuroscience · doi:10.1111/ejn.16064
Self-citationBiomarkers of acute cerebral damage in complex diagnosis of sepsis-associated encephalopathy
Savvina, I. A., Dryagina, N. V., Bykova, K. M., Iablonskikh, D. D., Rodchenko, A. M., Rutkovskiy, R. V., Matakaeva, Z. A., Kasherininov, I. Y., Mazurok, V. A., & Shlyakhto, E. V. (2025) · Russian Journal of Anesthesiology and Reanimatology · doi:10.17116/anaesthesiology20250316
- Authors
- Rocha, M., Vieira, A., Michels, M., Borges, H., Goulart, A., Fernandes, F., Dominguini, D., Ritter, C., & Dal-Pizzol, F.
- Affiliations
- Universidade do Extremo Sul Catarinense (BR)
- ORCID
- Venue
- Neurochemistry International
- Publisher
- Elsevier BV
- Published
- 2021-01
- Volume
- 142
- Pages
- 104906
- ISSN
- 0197-0186 (ISSN-L)
- OpenAlex
- W3109789947
- Semantic Scholar
- 7aa2cbe308a4bd67111813d238a132d61af36309
- Cited by
- 20
- References
- 66
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 4 · 2023: 6 · 2022: 6 · 2021: 1
- FWCI
- 1.06
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neurochemistry International (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Coordenação de Aperfeiçoamento de Pessoal de Nível Superior
- Universidade do Extremo Sul Catarinense (826)
- Conselho Nacional de Desenvolvimento Científico e Tecnológico (404932/2016-9, 305829/2015-7)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › S100 Proteins and Annexins
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Advanced Glycation End Products research
- Health Sciences › Medicine › Epidemiology › Sepsis Diagnosis and Treatment
- Keywords
- S100B, sepsis, sepsis-associated encephalopathy, neuroinflammation, receptor for advanced glycation end products, cognitive impairment, memory, microglia, astrocytes, cytokines, hippocampus, cecal ligation and puncture, neuroprotection
- MeSH terms
- Animals, Anti-Inflammatory Agents, Brain, Disease Models, Animal, Male, Time Factors, Rats, Wistar, Oxidative Stress, Sepsis, Inflammation Mediators, Rats, Cognitive Dysfunction, S100 Calcium Binding Protein beta Subunit
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