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Current Trends in Immunology   Volumes    Volume 16 
Abstract
The role of cytokine-related inflammatory biomarkers in medical conditions of physical trauma and injury: Assessment of serum levels of human interleukin-1β (hIL-1β) quantified by sandwich enzyme-linked immunosorbent assay (S-ELISA)
John J. Haddad
Pages: 27 - 37
Number of pages: 11
Current Trends in Immunology
Volume 16 

Copyright © 2015 Research Trends. All rights reserved

ABSTRACT
 
The serological patterns of pro-inflammatory biomarkers associated with physically traumatic and injurious conditions pre- and post-rehabilitation are not well characterized. These conditions, which usually require physical rehabilitation and interventional therapy, among other diagnostic/prognostic procedures, may exhibit inflammatory symptomatic reactions that are often associated with the release of inflammatory markers such as cytokines. Cytokines such as interleukins are crucial physiologic and inflammatory mediators of remodeling and injury. This study investigated the pre-habilitation/therapy serological patterns of human interleukin (IL)-1β (hIL-1β) in physically traumatic and injurious conditions, including rotator cuff tendinitis (RCT), adhesive capsulitis (AC), hemiparesis/hemiplegia (HH), lumbago/lumbalgia (LL), tennis elbow/lateral epicondylitis (TELE), meniscal tear (MT), radiculopathy (RD), sciatic nerve injury (SNI), supraspinatus tear (ST), cervicalgia/neck pain (CNP), cervical spondylitis (CS), osteoarthritis (OS), Colle’s fracture (CF) and osteoporosis (OP). Whilst the serum levels of hIL-1β were negligible or undetectable in RCT, AC, HH, MT, RD, CNP, CS and OS, the levels of hIL-1β were significantly upregulated in LL (4-fold), TELE (2-fold), SNI (3-fold), ST (14-fold), CF (4-fold), and OP (2-fold). These results clearly indicate that physically traumatic and injurious conditions are variably associated with the upregulation of inflammatory biomarkers in pre-habilitation therapeutic status, and that the immunotherapeutic seropositive patterns of hIL-1β may contribute to exacerbating the condition by regulating localized and/or systemic inflammation.  

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