ArticleFrontiers in neuroscience2026
Integrated transcriptomic and proteomic profiling reveals C3-associated hippocampal neuroimmune remodeling in sodium bicarbonate-treated sepsis-associated encephalopathy.
Article in Frontiers in neuroscience, 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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Abstract
Background: Sepsis-associated encephalopathy (SAE) is a neurological complication of sepsis characterized by cognitive impairment and persistent brain dysfunction. Although neuroinflammation and glial activation contribute to SAE pathogenesis, the molecular alterations underlying hippocampal neuroimmune dysfunction remain incompletely understood. The potential role of NaHCO₃ in SAE-associated neurological dysfunction remains unclear. Methods: An LPS-induced mouse model of SAE was established to investigate the effects of NaHCO₃ administration. Survival and cognitive function were evaluated using survival analysis, novel object recognition, open-field, and Y-maze tests. Hippocampal transcriptomic and proteomic profiling was performed, followed by cross-omics integration. Candidate molecules were further assessed by qRT-PCR, Western blotting, and immunofluorescence. Results: NaHCO₃ treatment improved survival and alleviated cognitive deficits in SAE mice. Transcriptomic and proteomic profiling revealed extensive hippocampal molecular alterations, with functional enrichment highlighting immune- and inflammation-related processes and pathways. Three-group cross-omics analysis identified 18 candidates meeting an FDR < 0.05 at both omics levels and showing a concordant SAE-associated increase followed by a decrease after NaHCO₃ treatment. Among these candidates, C3 was prioritized based on its cross-omics expression pattern and neuroimmune relevance. qRT-PCR and Western blot analyses supported increased hippocampal C3 expression during SAE and its responsiveness to NaHCO₃ treatment. Immunofluorescence analysis revealed increased spatial association between C3 and GFAP-positive astrocytic structures during SAE, which was attenuated following NaHCO₃ treatment. Conclusion: NaHCO₃ treatment was associated with improved neurological outcomes and altered hippocampal molecular profiles in LPS-induced SAE. Cross-omics analysis identified C3 among candidate molecules associated with SAE and NaHCO₃ responsiveness. The increased C3-GFAP spatial association suggests that complement-associated alterations accompany astrocytic responses during SAE. The causal role of C3 and the mechanisms underlying the effects of NaHCO₃ require further investigation.
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