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ISSN:2171-6625
September 18-19, 2017 | Dallas, USA
4th International Conference on
NEUROLOGY AND NEUROIMMUNOLOGY
Chronic inflammation of mucosal surface is an aberrant
immune response to different chemical, environmental
insults as well as luminal microbial which generate an array of
cytokineandchemokines andoxygen radicals leading totissue
destruction and loss of function, as noted in pancreatitis,
hepatitis, inflammatory bowel diseases (IBD), periodontitis,
arthritis and temporomandibular joint disorders (TMJD).
Patients with TMJD and arthritis often have a combined
etiology of hereditary and microenvironmental factors
contributing to joint pain. Multiple clinical and animal studies
have proven “dual-hit phenomenon” as inflammatory insults
to initiate chronic response in joints and in other related as
well as unrelated organs. As, the initial inflammatory insult
primes the immune system, the succeeding insult/s amplify/s
deleterious responses. Pro-inflammatory cytokine, tumor
necrosis factor α (TNFα) up-regulates various inflammatory
markers, cytokines and chemokines to initiate acute and
chronic stages of inflammation and pain related sensation
in patients and model for pancreatitis, hepatitis and IBD,
as well as neuropathy. TNFα is released mainly by activated
macrophages, astroglia, microglia, CD4+ lymphocytes,
natural killer cells, and neurons. The biological action of
TNFα is through two gene family receptors, TNFR1 and
TNFR2. Dysregulation of TNFα contributes to development
of colitis, hepatitis, pancreatitis, headache, periodontal,
temporomandibular and neuropathic pain. Trigeminal
neuropathic pain is common following trigeminal nerve
damage post-surgical procedures and maxillofacial injuries.
Soluble TNFR1 and R2 neutralize circulating TNFα to alleviate
pain related responses such as allodynia, hyperalgesia or
peripheral nerve injuries. Murine with genetic deletion of
TNFα receptors (TNFR1/R2 deficient) develop severe chronic
inflammatory symptoms including pancreatitis and orofacial
trigeminal inflammatory compression (TIC) nerve injuries
compared in WT animals. In addition, TNFR1/R2 deficient
animals after recovering from initial inflammatory insult, such
as knee joint arthritis or unilateral into temporomandibular
joint (TMJ), when exposed to second but unrelated, colonic
inflammatory, insult, develop recrudescence chronic
secondary hypersensitivity which continued for over 4-6
months duration of studies. Analysis of proteomic profiling
at multiple time points identified several altered levels of
inflammatory cytokines and chimokines. This presentation
will discuss in detail relationship between TNFα and its
receptors to provoke chronic inflammatory and neuropathic
disorders and further to expose their association with
several other inflammatory markers through proteomic
profiling. In addition, various pharmacological interventions
will be scrutinized for efficacy in these chronic hypersensitive
models.
e:
Tumor necrosis factor receptor 1 and 2 (TNFR1/R2) deletion provoke inflammatory chemokines,
cytokines and pain related hypersensitivity
Helieh S Oz
UK Medical Center, USA
J Neurol Neurosci, 8:5
DOI: 10.21767/2171-6625-C1-003