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B Cell–Activating Factor Is Associated with Testosterone and Smoking Status in Non-Ambulatory Men with Chronic Spinal Cord Injury
Author(s) -
Ricardo Battaglino,
Nguyen Nguyen,
Megan Summers,
Leslie R. Morse
Publication year - 2019
Publication title -
journal of neurotrauma
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.653
H-Index - 149
eISSN - 1557-9042
pISSN - 0897-7151
DOI - 10.1089/neu.2018.6221
Subject(s) - b cell activating factor , medicine , spinal cord injury , ambulatory , testosterone (patch) , cytokine , immunology , endocrinology , spinal cord , b cell , antibody , psychiatry
B cell-mediated autoimmunity may contribute to poor neurological outcomes after spinal cord injury (SCI). B cell-activating factor (BAFF) is a key cytokine involved in B cell development, proliferation, activation, and survival whose expression is elevated in men with chronic SCI. The aim of this study was to assess factors associated with circulating BAFF in non-ambulatory males with chronic SCI. We assessed the association between clinical and demographic factors, health habits, and circulating BAFF levels in a convenience sample of 43 non-ambulatory men with chronic spinal cord injury (≥ 1 year post-injury). Serum BAFF and total testosterone levels were quantified by enzyme-linked immunosorbent assay. Body composition was determined by whole body dual-energy X-ray absorptiometry. In multivariable models, active smokers had significantly greater BAFF levels than former/nonsmokers (871 pg/mL vs. 665 pg/ml, p  = 0.002). BAFF decreased 36 ± 11.1 pg/mL for every 1 ng/mL increase in total testosterone ( p  = 0.002). This model explained 41% of the variation in circulating BAFF levels (model p  < 0.0001). Our findings suggest that modifiable health habits may be associated with elevated BAFF levels in men with non-ambulatory chronic SCI. Further, the significant and independent negative association between testosterone levels and BAFF would suggest a link between androgen deficiency and autoimmunity observed in SCI via modulation of BAFF and B cell numbers. This points toward BAFF as a potential biomarker of injury severity and a target of therapies designed to reduce neuroinflammation and improve neurological outcomes after SCI.

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