Pilot investigation of the association between serum stress neuropeptide levels and lymphocyte expression of fas and fas ligand in critical illness
Journal
Biological Research for Nursing
Date Issued
2015
DOI
10.1177/1099800414542871
Abstract
In critical illness, apoptotic loss of immunocytes is associated with immunosuppression. Aim:to explore
expression of Fas/Fas ligand (FasL) on B and T cells from critically ill patients without sepsis compared to matched controls and associations with disease severity and neuropeptide Y (NPY), cortisol, adrenocorticotropic hormone (ACTH), and prolactin (PRL) levels. Methods: Repeated-measures correlational design with 36 critically ill patients (14-day follow-up) and 36 controls. Disease severity was assessed using the Multiple Organ Dysfunction Score (MODS) and Multi Organ Failure scale.Fas/FasL values were standardized for viable cell counts. An enzyme-linked immunosorbent assay (NPY) and electrochemiluminescence immunoassay (cortisol, ACTH, and PRL) were employed. Results: Fas and FasL expression on T-helper (p < .0001–.03)and T-cytotoxic cells (p < .0001–.002) and Fas expression on B cells (p < .0001–.03) were higher in patients. MODS severity was associated with FasL expression on cytotoxic T cells (r ¼ .752–.902, p ¼ .023–.037). There was an inverse association between Day 1 NPY levels and Fas expression on T-helper cells (r ¼ .447, p ¼ .019). On the day of maximum severity, we report for the
first time an inverse association between NPY levels and FasL expression on helper (r ¼ .733, p ¼ .016) and cytotoxic (r ¼.862, p ¼ .003) T cells. Cortisol levels were positively associated with counts of FasL-positive helper (r ¼ .828) and cytotoxic(r ¼ .544, p < .05) T cells. Conclusion: Results suggest a potential role for stress neuropeptides in lymphocyte survival and activation in critical illness.
expression of Fas/Fas ligand (FasL) on B and T cells from critically ill patients without sepsis compared to matched controls and associations with disease severity and neuropeptide Y (NPY), cortisol, adrenocorticotropic hormone (ACTH), and prolactin (PRL) levels. Methods: Repeated-measures correlational design with 36 critically ill patients (14-day follow-up) and 36 controls. Disease severity was assessed using the Multiple Organ Dysfunction Score (MODS) and Multi Organ Failure scale.Fas/FasL values were standardized for viable cell counts. An enzyme-linked immunosorbent assay (NPY) and electrochemiluminescence immunoassay (cortisol, ACTH, and PRL) were employed. Results: Fas and FasL expression on T-helper (p < .0001–.03)and T-cytotoxic cells (p < .0001–.002) and Fas expression on B cells (p < .0001–.03) were higher in patients. MODS severity was associated with FasL expression on cytotoxic T cells (r ¼ .752–.902, p ¼ .023–.037). There was an inverse association between Day 1 NPY levels and Fas expression on T-helper cells (r ¼ .447, p ¼ .019). On the day of maximum severity, we report for the
first time an inverse association between NPY levels and FasL expression on helper (r ¼ .733, p ¼ .016) and cytotoxic (r ¼.862, p ¼ .003) T cells. Cortisol levels were positively associated with counts of FasL-positive helper (r ¼ .828) and cytotoxic(r ¼ .544, p < .05) T cells. Conclusion: Results suggest a potential role for stress neuropeptides in lymphocyte survival and activation in critical illness.