title: Role of TNF in mast cell neuroinflammation and pain.
abstract: Inflammatory mediators, such as cytokines, chemokines and arachidonic acid compounds, lead to vascular permeability and dilation and increase sensitization and pain receptors. Proinflammatory cytokines, including tumor necrosis factor, are involved in the etiology of clinical neurological disorders. These cytokines activate nuclear factor-κB (NF-κB) which leads to the activation of different inflammatory genes. TNF implicated in neurological disorders has an important role in the activation of microglia and astrocytes. The inhibition of TNF may lead to the decrease of microglia activation and can be useful for therapeutic intervention. TNF, at the site of nerve injury may activate mast cells (MCs) which mediate pathologic events such as headache and pain. TNF is the only cytokine stored in mast cells and can be rapidly released along with biogenic amines after MC stimulation. Activation of MCs leads to NF-κB and AP1 generation with release of many cytokines including TNF, IL-33 and IL-1. In this paper we discuss the role of TNF in MC activation, mediating pain and neurological disorders.
authors.affiliation: Radiotherapy Ward 3, The First Affiliated Hospital of Zhengzhou, Zhengzhou, Henan, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Gu
authors.affiliation: Compositive Thermotherapy Center, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
authors.forename: D K
authors.initials: DK
authors.lastname: Yang
authors.affiliation: Department of Surgery and dontostomatological Sciences, University of Cagliari, Italy.
authors.forename: E
authors.initials: E
authors.lastname: Spinas
authors.affiliation: Department of Microbiology and Infectious Diseases, School of Veterinary Medicine, Aristotle University of Thessaloniki, Macedonia, Greece.
authors.forename: S K
authors.initials: SK
authors.lastname: Kritas
authors.affiliation: Department of Dermatology, University of Rome Tor Vergata, Rome, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Saggini
authors.affiliation: Orthopedic Division, University of Perugia, Perugia, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Caraffa
authors.affiliation: Orthopedic Division, University of Perugia, Perugia, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Antinolfi
authors.affiliation: Department of Neurosciences and Imaging, Faculty of Medicine and Surgery, G. DAnnunzio University Chieti-Pescara, Chieti, Italy.
authors.forename: R
authors.initials: R
authors.lastname: Saggini
authors.affiliation: Immunology Division, Post Graduate School of Medicine, Chieti, Italy.
authors.forename: P
authors.initials: P
authors.lastname: Conti
mesh_terms: D001927:Brain Diseases / Q000209:etiology*; D006801:Humans; D007249:Inflammation / Q000209:etiology*; D008407:Mast Cells / Q000502:physiology*; D016328:NF-kappa B / Q000502:physiology; D010146:Pain / Q000209:etiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
chemical_list: D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha