ArticleFrontiers in immunology2024
Mendelian randomization suggests causal correlations between inflammatory cytokines and immune cells with mastitis.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Correlation does not equal causation: the imperative of causal inference in machine learning models for immunotherapy.Frontiers in immunology · 2025Pooled it
- Transcriptome-derived variants in milk reveal host response signatures to subclinical intramammary infection in Holstein cattle.Journal of animal science and biotechnology · 2026Article
- Unraveling the causal link between inflammatory cytokines and hypertensive renal disease: a Mendelian randomization analysis.International urology and nephrology · 2026Article
- Overexpression of mitofusin 2 ameliorates inflammation and oxidative stress in lipopolysaccharide-induced mastitis model by regulating phosphofurin acidic cluster sorting protein 2.Animal models and experimental medicine · 2026Article
- Evaluating the impact of gut microbiota, circulating cytokines and plasma metabolites on febrile seizure risk in Mendelian randomization study.Scientific reports · 2025Article
- Immune imbalance and autoimmune mechanisms in plasma cell mastitis: current perspectives.Frontiers in cell and developmental biology · 2025Review
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Authors and funding
6 authors.
Funding
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Abstract
Objectives: Previous studies have reported that immunoinflammatory responses have associations with mastitis. Here, we aimed to further figure out whether circulating inflammatory cytokines and immune cells causally impact mastitis liability. Methods: The two-sample Mendelian randomization made use of genetic variances of 91 inflammatory cytokines from a large publicly available genome-wide association study (GWAS) containing 14,824 participants, 731 immunophenotypes data from 3,757 individuals as exposures separately, and mastitis from a GWAS summary (1880 cases and 211699 controls of European ancestry) as outcome. The primary analysis applied the inverse-variance weighted (IVW) method to estimate causal influences, with MR-Egger, weighted median, weighted mode and simple mode as supplementary approaches. Heterogeneity and pleiotropy were evaluated by the Cochrane Q test, MR-Egger intercept test, and MR-PRESSO global test. Results: The results indicated that CX3CL1 may be suggestively relevant to the risk of mastitis (odds ratio, OR = 1.434, 95% CI = 1.142~1.800, Conclusion: Our study adds to current knowledge on the causal roles of inflammatory cytokines and immune cells on mastitis by genetic means, thus guiding future clinical research.
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