ArticleBrain, behavior, and immunity2018
TRIF is a key inflammatory mediator of acute sickness behavior and cancer cachexia.
Article in Brain, behavior, and immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- The underexplored links between cancer and the internal body climate: Implications for cancer prevention and treatment.Frontiers in oncology · 2022Pooled it
- Feeding Behaviour in the KPC Model of Pancreatic Cancer-Associated Cachexia: Alteration of Spontaneous and Evoked Feeding Behaviours.Journal of cachexia, sarcopenia and muscle · 2026Article
- Cancer cachexia: molecular basis and therapeutic advances.Signal transduction and targeted therapy · 2026Review
- Lower content of cerebrospinal fluid chemokines in patients with cancer cachexia.Acta cirurgica brasileira · 2026Article
- The Role of Prenatal Microglial Activation and Its Sex Differences in the Development of Neuropsychiatric Disorders and Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Blood-Brain Barrier-Penetrating Nanocarriers Enable Microglial-Specific Drug Delivery in Hypothalamic Neuroinflammation.Advanced healthcare materials · 2025Article
- Molecular Mechanisms of Cachexia: A Review.Cells · 2024Review
- MiRNA-338-3p Inhibits Neuroinflammation in the Corpus Callosum of LCV-LPS Rats Via STAT1 Signal Pathway.Cellular and molecular neurobiology · 2023Article
- Multi-Tissue Transcriptome Study of Innate Immune Gene Expression Profiling Reveals Negative Energy Balance Altered the Defense and Promoted System Inflammation of Dairy Cows.Veterinary sciences · 2023Article
- Lipopolysaccharide-induced hypothalamic inflammation in cancer cachexia-anorexia is amplified by tumour-derived prostaglandin E2.Journal of cachexia, sarcopenia and muscle · 2022Article
- Neurobiology of cancer: Definition, historical overview, and clinical implications.Cancer medicine · 2022Review
- Animal Models for Neuroinflammation and Potential Treatment Methods.Frontiers in neurology · 2022Review
- Sex differences in the behavioral and immune responses of mice to tumor growth and cancer therapy.Brain, behavior, and immunity · 2021Article
- Chronic cerebral lipocalin 2 exposure elicits hippocampal neuronal dysfunction and cognitive impairment.Brain, behavior, and immunity · 2021Article
- Neural Mechanisms of Cancer Cachexia.Cancers · 2021Review
- Growth differentiation factor 15 neutralization does not impact anorexia or survival in lipopolysaccharide-induced inflammation.iScience · 2021Article
- Lipocalin 2 mediates appetite suppression during pancreatic cancer cachexia.Nature communications · 2021Article
- Brain metabolites in cholinergic and glutamatergic pathways are altered by pancreatic cancer cachexia.Journal of cachexia, sarcopenia and muscle · 2020Article
- Melanocortin-4 receptor antagonist TCMCB07 ameliorates cancer- and chronic kidney disease-associated cachexia.The Journal of clinical investigation · 2020Article
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Authors and funding
6 authors at 1 institution in 1 country.
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Abstract
Hypothalamic inflammation is a key component of acute sickness behavior and cachexia, yet mechanisms of inflammatory signaling in the central nervous system remain unclear. Previous work from our lab and others showed that while MyD88 is an important inflammatory signaling pathway for sickness behavior, MyD88 knockout (MyD88KO) mice still experience sickness behavior after inflammatory stimuli challenge. We found that after systemic lipopolysaccharide (LPS) challenge, MyD88KO mice showed elevated expression of several cytokine and chemokine genes in the hypothalamus. We therefore assessed the role of an additional inflammatory signaling pathway, TRIF, in acute inflammation (LPS challenge) and in a chronic inflammatory state (cancer cachexia). TRIFKO mice resisted anorexia and weight loss after peripheral (intraperitoneal, IP) or central (intracerebroventricular, ICV) LPS challenge and in a model of pancreatic cancer cachexia. Compared to WT mice, TRIFKO mice showed attenuated upregulation of Il6, Ccl2, Ccl5, Cxcl1, Cxcl2, and Cxcl10 in the hypothalamus after IP LPS treatment, as well as attenuated microglial activation and neutrophil infiltration into the brain after ICV LPS treatment. Lastly, we found that TRIF was required for Ccl2 upregulation in the hypothalamus and induction of the catabolic genes, Mafbx, Murf1, and Foxo1 in gastrocnemius during pancreatic cancer. In summary, our results show that TRIF is an important inflammatory signaling mediator of sickness behavior and cachexia and presents a novel therapeutic target for these conditions.
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