ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Loss of C3 and CD14 reduces region-specific neuroinflammation in a murine polytrauma model.
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.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTBI-polytrauma (P-TBI) is associated with acute neurological deterioration, delirium, and poor prognosis. Systemic inflammatory mediators are thought to amplify the cerebral neuroimmune response, particularly microglial activation, with detrimental consequences.
methodsWe investigated the roles of complement factor C3 and the TLR co-receptor CD14 in a murine polytrauma model combining mild TBI with femur fracture, blunt thorax trauma, and resuscitated haemorrhagic shock, using mice lacking C3, CD14, or both.
resultsP-TBI induced a rapid, brain-wide increase in inflammatory cytokines with region-specific patterns. TNF and CCL2 mRNA were upregulated in microglia in the cortex, hippocampus, and striatum, and this response was abolished in C3
conclusionThus, C3 and CD14 are dispensable for the acute response at the injury site but differentially regulate microglial and neuronal activation in remote brain regions, representing potential targets to reduce P-TBI-associated encephalopathy.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.