Independent
effect of depression on inflammatory markers as
compared to natural killer cell
activity
It
is recognized that the functioning of the immune
system is altered in major depressive disorder
which leads to an increased risk of infectious
disease and incidence of inflammatory disorders.
A reduction of natural killer (NK) cell activity
in depression has been reported by some studies,
whereas increases of inflammatory markers have
been found in others. However, NK activity and
inflammation, and their potential association
have never been simultaneously examined in
depression. A study evaluated levels of NK
activity and markers of immune activation in
depressed patients compared to age-, gender, and
body weight matched controls.
The total sample included 25 patients with
current major depressive disorder and 25 control
subjects, all individuals were male. Mononuclear
cells were isolated from peripheral blood and NK
cell activity was assayed. Serum levels of
interleukin-6 (IL-6), soluble interleukin-2
receptor (sIL-2R), and acute phase proteins
(haptoglobin, alpha-1-anti-trypsin (AAT), and
alpha-1-acid glycoprotein (AAG)) were
measured.
Compared to controls, NK activity was
significantly lower in the depressed patients (p
= 0.05). In contrast, circulating levels of IL-6
were elevated in the depressives compared to
controls (p < 0.05). Serum levels of sIL-2R,
haptoglobin, AAT, and AAG did not differ between
the two groups. There was no correlation between
NK activity and levels of IL-6, sIL-2R,
haptoglobin, AAT or AAG.
From these results there is evidence for
increased inflammatory markers in major
depression which is not correlated with
reduction of NK cell responses. The independent
effect of depression on NK immune responses as
compared to inflammatory markers may explain the
different individual reactions to the major
depressive disorder, particularly the
differences in its adverse health effects. Pike
JL, Irwin MR. Dissociation of inflammatory
markers and natural killer cell activity in
major depressive disorder. Brain Behav Immun
2006, 20:169-174.