ArticleEMBO reports2016
Central CCL2 signaling onto MCH neurons mediates metabolic and behavioral adaptation to inflammation.
Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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Who cites it
34 citing papers in PubMed.
- Chronic activity-based anorexia triggers a glial response in the hippocampus independent of intestinal epithelial toll-like receptor 4.Journal of neuroinflammation · 2026Article
- Downregulation of neuronal DRD2 drives microglia synaptic pruning and results in cognitive deficits by promoting CCL2 release in a rat model of chronic migraine.The journal of headache and pain · 2026Article
- Mechanisms of postoperative anorexia in surgical patients: a narrative review.Frontiers in neuroscience · 2026Review
- Dependence of energy balance and hypothalamic neuropeptide gene expression on initial tumor load in mice.Frontiers in oncology · 2026Article
- The function of chemokine-driven glial-neuronal interaction in chronic pain.Frontiers in neuroscience · 2026Review
- Systemic inflammation during the neonatal period and BMI at 1 year in infants with gastroschisis: a retrospective cohort study.European journal of pediatrics · 2025Article
- Autophagy Suppresses CCL2 to Preserve Appetite and Prevent Lethal Cachexia.bioRxiv : the preprint server for biology · 2025Article
- Chemokine associations with blood cerebrospinal fluid (CSF) barrier permeability and delirium.Brain, behavior, & immunity - health · 2025Article
- Angiostrongylus cantonensis induces energy imbalance and dyskinesia in mice by reducing the expression of melanin-concentrating hormone.Parasites & vectors · 2024Article
- Prostaglandin EProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Anti-inflammatory actions of β-funaltrexamine in a mouse model of lipopolysaccharide-induced inflammation.Inflammopharmacology · 2023Article
- Exercise Restores Hypothalamic Health in Obesity by Reshaping the Inflammatory Network.Antioxidants (Basel, Switzerland) · 2023Review
- Glial cells as integrators of peripheral and central signals in the regulation of energy homeostasis.Nature metabolism · 2022Review
- Infections, Pandemics, and Sleep Disorders.Neuroscience and behavioral physiology · 2022Article
- The feeding behaviour of Amyotrophic Lateral Sclerosis mouse models is modulated by the CaBritish journal of pharmacology · 2021Article
- Multifaceted actions of melanin-concentrating hormone on mammalian energy homeostasis.Nature reviews. Endocrinology · 2021Review
- Fasting increases microbiome-based colonization resistance and reduces host inflammatory responses during an enteric bacterial infection.PLoS pathogens · 2021Article
- Targeting the CCL2-CCR2 axis in depressive disorders.Pharmacological reports : PR · 2021Review
- Microglia-Neuron Crosstalk in Obesity: Melodious Interaction or Kiss of Death?International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
14 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sickness behavior defines the endocrine, autonomic, behavioral, and metabolic responses associated with infection. While inflammatory responses were suggested to be instrumental in the loss of appetite and body weight, the molecular underpinning remains unknown. Here, we show that systemic or central lipopolysaccharide (LPS) injection results in specific hypothalamic changes characterized by a precocious increase in the chemokine ligand 2 (CCL2) followed by an increase in pro-inflammatory cytokines and a decrease in the orexigenic neuropeptide melanin-concentrating hormone (MCH). We therefore hypothesized that CCL2 could be the central relay for the loss in body weight induced by the inflammatory signal LPS. We find that central delivery of CCL2 promotes neuroinflammation and the decrease in MCH and body weight. MCH neurons express CCL2 receptor and respond to CCL2 by decreasing both electrical activity and MCH release. Pharmacological or genetic inhibition of CCL2 signaling opposes the response to LPS at both molecular and physiologic levels. We conclude that CCL2 signaling onto MCH neurons represents a core mechanism that relays peripheral inflammation to sickness behavior.
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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.