ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Early life activation of toll-like receptor 4 reprograms neural anti-inflammatory pathways.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 86 citations in OpenAlex.
- Perinatal morphine exposure induces chromatin and transcriptomic remodeling to alter immune and metabolic function.Frontiers in immunology · 2026Article
- Maternal immune activation during the lactational period alters offspring behavior, reproductive development, and immune function in mice.Hormones and behavior · 2025Article
- Maternal immune activation during the lactational period alters offspring behavior, reproductive development, and immune function in mice.bioRxiv : the preprint server for biology · 2025Article
- From Childhood Woes to Adult Blues: Unmasking the Role of Early Traumas, P2X7 Receptor, and Neuroinflammation in Anxiety and Depression.International journal of molecular sciences · 2025Review
- Microbial orchestration of neuroimmune crosstalk: from homeostasis to disease.Frontiers in immunology · 2025Review
- Anxiolytic effects of Enterococcus faecalis 2001 on a mouse model of colitis.Scientific reports · 2024Article
- Pitfalls and potential: Translating the two-hit model of early life stress from pre-clinical non-human experiments to human samples.Brain, behavior, & immunity - health · 2024Article
- Review
- Prenatal Activation of Glucocorticoid Receptors Induces Memory Impairment in a Sex-Dependent Manner: Role of Cyclooxygenase-2.Molecular neurobiology · 2022Article
- Astrocytes and Microglia in Stress-Induced Neuroinflammation: The African Perspective.Frontiers in immunology · 2022Review
- Early life stress induces dysregulation of the heme pathway in adult mice.Physiological reports · 2021Article
- Microglia Phenotypes Following the Induction of Alcohol Dependence in Adolescent Rats.Alcoholism, clinical and experimental research · 2021Article
- Impact of inflammation on developing respiratory control networks: rhythm generation, chemoreception and plasticity.Respiratory physiology & neurobiology · 2020Review
- One bout of neonatal inflammation impairs adult respiratory motor plasticity in male and female rats.eLife · 2019Article
- Prenatal Inflammation Dampens Neurogenesis and Enhances Serotonin Transporter Expression in the Hippocampus of Adult Female Rats.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2019Article
- Role of TLR4 in the Modulation of Central Amygdala GABA Transmission by CRF Following Restraint Stress.Alcohol and alcoholism (Oxford, Oxfordshire) · 2018Article
- Cyclooxygenase enzyme activity does not impair respiratory motor plasticity after one night of intermittent hypoxia.Respiratory physiology & neurobiology · 2018Article
- Gut Microbiota and the Neuroendocrine System.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2018Review
- Impact of prenatal immune challenge on the demyelination injury during adulthood.CNS neuroscience & therapeutics · 2017Article
- Postnatal LPS Challenge Impacts Escape Learning and Expression of Plasticity Factors Mmp9 and Timp1 in Rats: Effects of Repeated Training.Neurotoxicity research · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
A single postnatal exposure to the bacterial endotoxin, lipopolysaccharide (LPS), reduces the neuroimmune response to a subsequent LPS exposure in the adult rat. The attenuated fever and proinflammatory response is caused by a paradoxical, amplified, early corticosterone response to LPS. Here we identify the mechanisms underlying the heightened corticosterone response to LPS in adults after early life exposure to LPS. In postnatal LPS-treated rats, hypothalamic corticotrophin-releasing hormone mRNA, pituitary proopiomelanocortin mRNA, and circulating adrenocorticotrophic hormone were all increased after adult exposure to LPS without significant modification to hippocampal or hypothalamic glucocorticoid receptor mRNA or protein or vagally mediated afferent signaling to the brain. Postnatal LPS administration did cause a persistent upregulation of the LPS Toll-like receptor-4 (TLR4) mRNA in liver and spleen, but not in brain, pituitary, or adrenal gland. In addition, cyclooxygenase-2 (COX-2), which is a prostaglandin biosynthetic enzyme and is normally undetectable in most peripheral tissue, was constitutively expressed in the liver. Adult immune activation of the upregulated TLR4 and COX-2 caused a rapid, amplified rise in circulating, but not brain, prostaglandin E(2) that induced an early, enhanced activation of the hypothalamic-pituitary-adrenal (HPA) axis. Thus, postnatal LPS reprograms the neuroimmune axis by priming peripheral tissues to create a novel, prostaglandin-mediated activation of the HPA axis brought about by increased constitutive expression of TLR4 and COX-2.
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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.