Current status of chemokines in the adult CNS

Goazigo, Annabelle Réaux‐Le; Steenwinckel, Juliette Van; Rostène, William; Parsadaniantz, Stéphane Melik

doi:10.1016/j.pneurobio.2013.02.001

Cited by 211 publications

(179 citation statements)

References 355 publications

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“…This complex is also important as a molecular signal in the crosstalk among neuronal and glial cells and immune resident cells in the nervous system (e.g., microglia) [99,100]. Since chemokines have the capacity to target different types of receptor, they can modulate different cell processes, including cell adhesion and proliferation, phagocytosis, apoptosis, angiogenesis, cytokine secretion, and T cell activation [101].…”

Section: Neuroimmune Alterations In Asd: From Patients To the Vpa Animentioning

confidence: 99%

Neuroimmune Alterations in Autism: A Translational Analysis Focusing on the Animal Model of Autism Induced by Prenatal Exposure to Valproic Acid

Deckmann

Schwingel

Fontes-Dutra

et al. 2018

Neuroimmunomodulation

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Autism spectrum disorder (ASD) is a highly prevalent developmental disorder characterized by deficits in communication and social interaction and in stereotyped or repetitive behaviors. Besides the classical behavioral dyad, several comorbidities are frequently present in patients with ASD, such as anxiety, epilepsy, sleep disturbances, and gastrointestinal tract dysfunction. Although the etiology of ASD remains unclear, there is supporting evidence for the involvement of both genetic and environmental factors. Valproic acid (VPA) is an anticonvulsant and mood stabilizer that, when used during the gestational period, increases the risk of ASD in the offspring. The animal model of autism induced by prenatal exposure to VPA demonstrates important structural and behavioral features that can be observed in individuals with autism; it is thus an excellent tool for testing new drug targets and developing novel behavioral and drug therapies. In addition, immunological alterations during pregnancy could affect the developing embryo because immune molecules can pass through the placental barrier. In fact, exposure to pathogens during the pregnancy is a known risk factor for ASD, and maternal immune activation can lead to autistic-like features in animals. Interestingly, neuroimmune alterations are common in both autistic individuals and in animal models of ASD. We summarize here the important alterations in inflammatory markers, such as cytokines and chemokines, in patients with ASD and in the VPA animal model.

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Section: Neuroimmune Alterations In Asd: From Patients To the Vpa Animentioning

confidence: 99%

Neuroimmune Alterations in Autism: A Translational Analysis Focusing on the Animal Model of Autism Induced by Prenatal Exposure to Valproic Acid

Deckmann

Schwingel

Fontes-Dutra

et al. 2018

Neuroimmunomodulation

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“…Proinflammatory chemokines are responsible for migration of immune cells to the infection site [7] and homeostatic chemokines are responsible for recruiting cells for tissue repair and maintenance [8] . Recent studies suggest novel, brain-specific functions of chemokines, including the regulation of neuroendocrine functions, the modulation of neurotransmitter systems, and neurodegeneration [9] . Elevated levels of chemokines in serum or cerebrospinal fluid are additionally associated with psychiatric disorders including depression, bipolar disorder, and schizophrenia [6,10,11] .…”

Section: Introductionmentioning

confidence: 99%

Macrophage-Derived Chemokine: A Putative Marker of Pharmacological Therapy Response in Major Depression?

Milenkovic¹,

Sarubin

Hilbert

et al. 2017

Neuroimmunomodulation

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Introduction: Inflammatory processes play an important and complex role in the pathophysiology of major depressive disorder (MDD), but, so far, no specific investigation of chemokines exists. Methods: In this study, we investigated the changes of plasma chemokine levels (eotaxin-1, eotaxin-3, IP-10, MCP-1, MCP-4, MDC, MIP-1α, MIP-1β, and TARC) in 47 MDD patients before (PRE) and after 1 and 6 weeks of pharmacological treatment (POST1 and POST6) in relation to the response to antidepressive therapy. We hypothesized that the direction of alterations in levels of chemokines would significantly differ between the 2 groups, responders and nonresponders. Results: Among the investigated chemokines, only the level of macrophage-derived chemokine (MDC) changed significantly in relation to therapy response. MDC levels were significantly elevated in the responder group at POST6. Discussion: MDC is a constitutively expressed chemokine involved in the pathophysiology of infectious and neoplastic diseases. This is the first study providing valuable hints that MDC might serve as a marker of pharmacological therapy response in MDD.

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“…These homeostatic functions take on added significance within the context of neuroinflammatory disease, as the CXCL12/CXCR4 signaling axis aids recovery by promoting survival of mature neurons, recruitment of neural and glial progenitor cells (6)(7)(8), and neuronal-glial communication (9).…”

Section: Introductionmentioning

confidence: 99%

Neuronal ferritin heavy chain and drug abuse affect HIV-associated cognitive dysfunction

Pitcher¹,

Abt²,

Myers³

et al. 2014

J. Clin. Invest.

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Interaction of the chemokine CXCL12 with its receptor CXCR4 promotes neuronal function and survival during embryonic development and throughout adulthood. Previous studies indicated that μ-opioid agonists specifically elevate neuronal levels of the protein ferritin heavy chain (FHC), which negatively regulates CXCR4 signaling and affects the neuroprotective function of the CXCL12/CXCR4 axis. Here, we determined that CXCL12/CXCR4 activity increased dendritic spine density, and also examined FHC expression and CXCR4 status in opiate abusers and patients with HIV-associated neurocognitive disorders (HAND), which is typically exacerbated by illicit drug use. Drug abusers and HIV patients with HAND had increased levels of FHC, which correlated with reduced CXCR4 activation, within cortical neurons. We confirmed these findings in a nonhuman primate model of SIV infection with morphine administration. Transfection of a CXCR4-expressing human cell line with an iron-deficient FHC mutant confirmed that increased FHC expression deregulated CXCR4 signaling and that this function of FHC was independent of iron binding. Furthermore, examination of morphine-treated rodents and isolated neurons expressing FHC shRNA revealed that FHC contributed to morphine-induced dendritic spine loss. Together, these data implicate FHC-dependent deregulation of CXCL12/CXCR4 as a contributing factor to cognitive dysfunction in neuroAIDS.

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Current status of chemokines in the adult CNS

Cited by 211 publications

References 355 publications

Neuroimmune Alterations in Autism: A Translational Analysis Focusing on the Animal Model of Autism Induced by Prenatal Exposure to Valproic Acid

Neuroimmune Alterations in Autism: A Translational Analysis Focusing on the Animal Model of Autism Induced by Prenatal Exposure to Valproic Acid

Macrophage-Derived Chemokine: A Putative Marker of Pharmacological Therapy Response in Major Depression?

Neuronal ferritin heavy chain and drug abuse affect HIV-associated cognitive dysfunction

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