Sex and stress paradigm influence behavioural, neuroimmune, and microbiome responses in pubertal CD-1 mice
In pubertal CD-1 mice, chronic stress favours anxiogenic behavioural and pro-inflammatory responses (via NLRP3) and alters the gut microbiome in a sex-dependent manner, with more pronounced effects in females.
| Population | CD-1 mice of both sexes during the pubertal period (≈ postnatal day 42) |
|---|---|
| Intervention | Chronic stress (repeated varied stressor paradigm) versus acute stress (single exposure) |
| Comparator | Non-stressed controls; cross-comparison by sex (males vs. females) |
| Outcome | Anxiety/depression-like behaviour; NLRP3 inflammasome activation; M1/M2 microglial polarisation; Gut microbiome composition; Sex-dependent response difference |
Summary of findings
| Outcome | Effect | 95% CI | Certainty | Clinical relevance | Notes |
|---|---|---|---|---|---|
| Anxiety/depression-like behaviour | No data available | — | Very low | — | |
| NLRP3 inflammasome activation | No data available | — | Very low | — | |
| M1/M2 microglial polarisation | No data available | — | Very low | — | |
| Gut microbiome composition | No data available | — | Very low | — | |
| Sex-dependent response difference | No data available | — | Very low | — |
Context
Puberty is a critical window for brain maturation and HPA axis reorganisation, with sexual dimorphism in stress responsivity. Chronic stress during this window may establish persistent neurobiological trajectories. The interaction between NLRP3-mediated neuroinflammation, gut microbiome, and behaviour as a function of sex remains poorly characterised experimentally.
What the study showed
The full text provided contains only the introduction repeated across all three sections (methods, results, discussion), with no original numerical data reported. No absolute or relative values, 95% CIs, or effect sizes are available in the submitted material. The study describes, at an introductory level, that chronic stress promotes M1 microglial polarisation via NLRP3 and anxious/depressive behaviours in pubertal murine models, with greater vulnerability in females — but without verifiable primary data in this text.
How it was done
Preclinical study in pubertal CD-1 mice comparing acute and chronic stress paradigms with sex stratification. The provided text does not contain a methods section with detailed experimental protocol, sample size, precise protocol duration, analytical techniques, or statistical design — only the introduction repeated across three sections.
Effect magnitude
No effect size with 95% CI can be extracted: the submitted text contains no primary quantitative data.
Risk of bias
The provided material does not allow formal risk-of-bias assessment (RoB 2 or ROBINS-I inapplicable due to absence of data). Inherent model limitations: single species (CD-1), restricted developmental window, absence of direct hormonal manipulation to isolate gonadal effects, inability to directly translate findings to humans. The text is truncated and repetitive, preventing complete critical analysis.
What this study does NOT prove
This study does NOT prove causality between microbiome alterations and pubertal neuroinflammation in humans. Results in CD-1 mice are not generalisable to other strains, species, or human adolescents.
In clinical practice
Findings are preclinical in rodents and do not support any direct clinical recommendations. Clinicians should await complete published data before drawing any inference regarding pubertal stress management or microbiome interventions.
Limitations
The provided material does not allow formal risk-of-bias assessment (RoB 2 or ROBINS-I inapplicable due to absence of data). Inherent model limitations: single species (CD-1), restricted developmental window, absence of direct hormonal manipulation to isolate gonadal effects, inability to directly translate findings to humans. The text is truncated and repetitive, preventing complete critical analysis.
What is still missing
Complete primary data are needed (behavioural outcomes, immunohistochemistry, microbial sequencing with statistics) for effect magnitude assessment, replication in other animal models, and subsequent translational studies in human adolescents.
Technical appendix
Version history
- 1.0 · 2026-09-22 — Auto-generated under Evidence Standard v1.0