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Cited by 639Neuroinflammation and Neurodegeneration MechanismsPain Mechanisms and TreatmentsTryptophan and brain disorders

Cytokines and chemokines at the crossroads of neuroinflammation, neurodegeneration, and neuropathic pain

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Ramesh, Geeta, MacLean, Andrew G., Philipp, Mario T.·2013·Mediators of Inflammation
DOI 10.1155/2013/480739PMC PMC3753746
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Abstract

Cytokines and chemokines are proteins that coordinate the immune response throughout the body. The dysregulation of cytokines and chemokines is a central feature in the development of neuroinflammation, neurodegeneration, and demyelination both in the central and peripheral nervous systems and in conditions of neuropathic pain. Pathological states within the nervous system can lead to activation of microglia. The latter may mediate neuronal and glial cell injury and death through production of proinflammatory factors such as cytokines and chemokines. These then help to mobilize the adaptive immune response. Although inflammation may induce beneficial effects such as pathogen clearance and phagocytosis of apoptotic cells, uncontrolled inflammation can result in detrimental outcomes via the production of neurotoxic factors that exacerbate neurodegenerative pathology. In states of prolonged inflammation, continual activation and recruitment of effector cells can establish a feedback loop that perpetuates inflammation and ultimately results in neuronal injury. A critical balance between repair and proinflammatory factors determines the outcome of a neurodegenerative process. This review will focus on how cytokines and chemokines affect neuroinflammation and disease pathogenesis in bacterial meningitis and brain abscesses, Lyme neuroborreliosis, human immunodeficiency virus encephalitis, and neuropathic pain.

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  • This infection can lead to the activation of microglial cells, which mediate neuron communication through the production of proinflammatory factors such as cytokines including IL-1β, IL-10, TNF-α, and IFN-γ ultimately facilitating the migration of immune cells across the blood-brain barrier.

    “This infection can lead to the activation of microglial cells, which mediate neuron communication through the production of proinflammatory factors such as cytokines including IL-1β, IL-10, TNF-α, and IFN-γ ultimately facilitating the migration of immune cells across the blood-brain barrier (BBB) (Ramesh et al., 2013).”

    From Arbovirus infection increases the risk for the development of neurodegenerative disease pathology in the murine model (2024) · cites this paper as Ramesh et al., 2013

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Authors
Ramesh, G., MacLean, A. G., & Philipp, M. T.
Affiliations
Tulane University (US)
Corresponding author
Ramesh, Geeta
ORCID
Venue
Mediators of Inflammation
Publisher
Wiley
Published
2013
Volume
2013
Pages
1-20
ISSN
  • 0962-9351 (ISSN-L)
  • 1466-1861
DOI
10.1155/2013/480739
PMC
PMC3753746
OpenAlex
W2119337283
Cited by
639
References
254
Citations by year
2026: 26 · 2025: 62 · 2024: 57 · 2023: 63 · 2022: 55 · 2021: 76 · 2020: 54 · 2019: 43 · 2018: 51 · 2017: 47 · 2016: 35 · 2015: 42 · 2014: 24 · 2013: 3
FWCI
3.37
Type
journal article
Language
en
Open access
Licence
Locations
  • Mediators of Inflammation (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Institutes of Health (51OD011104/P51RR000164, NS048952, MH077544)
  • National Institute of Neurological Disorders and Stroke (51OD011104/P51RR000164, NS048952, MH077544)
  • National Institute of Mental Health (51OD011104/P51RR000164, NS048952, MH077544)
Topics
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Health Sciences › Medicine › Physiology › Pain Mechanisms and Treatments
  • Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
Keywords
cytokines, chemokines, neuroinflammation, neurodegeneration, neuropathic pain, microglial activation, demyelination, bacterial meningitis, brain abscess, Lyme neuroborreliosis, HIV encephalitis, neurotoxicity, adaptive immune response
MeSH terms
Animals, Astrocytes, Brain Abscess, Encephalitis, Humans, Inflammation, Meningitis, Pneumococcal, Neuralgia, Phagocytosis, Staphylococcus aureus, Signal Transduction, HIV Infections, Cytokines, Meningitis, Bacterial, Microglia, Chemokines, Neurodegenerative Diseases, Lyme Neuroborreliosis

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