fnins-13-00384 April 19, 2019 Time: 17:29 # 1
published: 24 April 2019
Federal University of São Paulo, Brazil
Charles Barnet Nemeroff,
The University of Texas at Austin,
University of Texas Dell
Medical School, United States,
in collaboration with reviewer CBN
Centre Hospitalier Universitaire
de Grenoble, France
This article was submitted to
a section of the journal
Frontiers in Neuroscience
Received: 10 January 2019
Accepted: 02 April 2019
Published: 24 April 2019
Maydych V (2019) The Interplay
Between Stress, Inﬂammation,
and Emotional Attention: Relevance
Front. Neurosci. 13:384.
The Interplay Between Stress,
Inﬂammation, and Emotional
Attention: Relevance for Depression
Department Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors, TU
Dortmund (IfADo), Dortmund, Germany
Depression is among the most signiﬁcant public mental health issues. A growing body
of research implicates inﬂammation in the etiology and pathophysiology of depression.
Yet, the results are somewhat inconsistent, leading to burgeoning attempts to identify
associations between components of innate immune system involved in inﬂammation
and speciﬁc symptoms of depression, including attention to emotional information.
Negative attentional bias, deﬁned as a tendency to direct attention toward negatively
valenced information, is one of the core cognitive features of depression and is reliably
demonstrated in depressed and vulnerable individuals. Altered attentional processing of
emotional information and immunological changes are often precipitated by stressful
events. Psychological stress triggers inﬂammatory activity and affective-cognitive
changes that play a critical role in the onset, maintenance, and recurrence of depression.
Using various designs, recent studies have reported a positive relationship between
markers of inﬂammation and negative attentional bias on behavioral and neural levels,
suggesting that the association between inﬂammation and emotional attention might
represent a neurobiological pathway linking stress and depression. This mini-review
summarizes current research on the reciprocal relationships between different types of
stressors, emotional attention, inﬂammation, and depression, and discusses potential
neurobiological mechanisms underlying these interactions. The integration provided
aims to contribute toward understanding how biological and psychological processes
interact to inﬂuence depression outcomes.
Keywords: inﬂammation, cytokines, psychological stress, emotional attention, attentional bias, negative bias,
depression, depressive disorders
Depression is a highly prevalent mood disorder in modern society and is associated with signiﬁcant
impairments in the patients’ quality of life. A multitude of basic research and clinical studies have
been performed, with the aim of understanding the interaction between biological, psychological,
and environmental factors involved in the etiology of depression. There is growing evidence
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Maydych Stress, Inﬂammation and Emotional Attention
implicating increased levels of markers of inﬂammation in
the pathogenesis of depressive disorders (Raison et al., 2006).
Inﬂammation is a part of the innate immune system’s response
to infection or injury. The main mediators of the inﬂammatory
response, proinﬂammatory cytokines, such as interleukin (IL)-
1β, interleukin (IL)-1 receptor antagonist (RA), interleukin
(IL)- 6, tumor necrosis factor (TNF)-α, and interferon (IFN)-
γ, have been recently shown to communicate with the brain
and aﬀect neurotransmission, neuroendocrine activity, and
brain structure and functions, thereby inducing emotional,
cognitive, and behavioral changes (Haroon et al., 2012). If the
inﬂammatory response remains unresolved, the chronic release
of proinﬂammatory cytokines can promote pathology, including
depression. Diﬀerent studies using a variety of study designs and
populations have found positive associations between increased
levels of proinﬂammatory cytokines and symptoms of depression
(Dowlati et al., 2010;Valkanova et al., 2013). However, ﬁndings
have not been entirely consistent for all types of depression
(Rothermundt et al., 2001), raising the need for identifying
more speciﬁc links between inﬂammation and diﬀerent somatic
and aﬀective-cognitive symptoms, rather than merely testing
associations between increased inﬂammation and categorically
According to cognitive models of depression, one of the
key features of depressed and vulnerable individuals is biased
cognitive processing of emotional and social information.
Cognitive biases manifest themselves in a consistent shift
toward (self-referential) negative or threatening information
in all aspects of cognition, including perception, attention,
interpretation, memory, or sensitivity to feedback (Miskowiak
and Carvalho, 2014). Negatively biased processing of emotional
information is usually regarded both as a neuropsychiatric
symptom and as a lingering trait factor that confers cognitive
vulnerability to depression and may, when triggered by adverse
environmental factors (e.g., stress), initiate the development
or reoccurrence of depression (Ingram et al., 1998). The
following mini-review focuses primarily on one cognitive
Heightened inﬂammation and negative attentional bias (AB)
are often the results of psychological stress. Acute stressful
challenges lead to increases in inﬂammatory activity and
other neurophysiological changes that modulate aﬀective,
cognitive, and behavioral processes (Allen et al., 2014;
Slavich and Irwin, 2014). Chronic exposure to stressors causes
endocrine and immune system dysfunction that contributes
to sustained low-grade inﬂammation, which is involved in
the pathogenesis of depressive symptoms (Rohleder, 2014). In
parallel, acute stress has been shown to trigger aﬀective and
cognitive changes similar to biased information processing
characteristic to depression (Gotlib and Joormann, 2010).
This evidence has recently led to promising attempts to
investigate interactions between emotional attention and
inﬂammation in the context of stress, thereby identifying
speciﬁc neurocognitive pathways that may be relevant for the
etiology of depression and development of novel treatments.
The aim of this mini-review is to summarize independent lines
of inquiry focusing on the eﬀects of stress (1) on inﬂammation
and (2) emotional attention as well as the potential link
between stress-inﬂammation and stress-cognition pathways
(3), and depression.
INFLAMMATION, STRESS, AND
A considerable body of evidence suggests that individuals
with diagnosed depression exhibit signiﬁcantly higher
levels of IL-1, IL-6, TNF-α, and C-reactive protein (CRP)
compared to non-depressed counterparts (Howren et al., 2009;
Dowlati et al., 2010). Concurrently, depressive symptoms
are more frequent in patients with conditions involving
inﬂammation (e.g., autoimmune diseases) and can be reversed
through the use of anti-inﬂammatory drugs (Kojima et al.,
2009;Köhler et al., 2014). Notably, increased inﬂammatory
activity has been documented only in some patients with
depression. This indicates that the depression-inﬂammation
link may be modulated by further vulnerability factors,
such as genes or cognitive vulnerability. Alternatively,
since depression is a heterogeneous disorder, it is also
plausible that the association between cytokine-mediated
inﬂammatory processes and depression is more nuanced
in terms of the groups of depressive symptoms (somatic
vs. aﬀective-cognitive). In support of this notion, a large
data set has documented mechanistic links between somatic
symptoms of depression and increased inﬂammation in animals
and humans (DellaGioia and Hannestad, 2010); however,
studies are lacking in aﬀective-cognitive changes related to
inﬂammatory activity. There is some evidence that inﬂammatory
processes may have diﬀerential eﬀects on somatic and aﬀective-
cognitive depressive symptoms that are based on distinct
neurophysiological mechanisms. For example, studies examining
the development of depressive symptoms during the course
of IFN-αtherapy found that all patients developed somatic
symptoms, including fatigue, altered sleep and appetite, motor
slowing, during the ﬁrst weeks of therapy (Capuron and
Miller, 2004). In contrast, only 30–50% of patients developed
aﬀective-cognitive symptoms such as negative mood, anhedonia,
or cognitive impairment during the later stages of therapy.
Strikingly, the development of this group of symptoms could
be prevented by prophylactic antidepressant administration
(Musselman et al., 2001).
There is considerable evidence that psychological stress can
activate the inﬂammatory response. Diﬀerent types of stressors
are capable of eliciting increases in inﬂammatory activity in
a manner that may promote depressive symptoms (Slavich
and Irwin, 2014). Moreover, the link between stressor-evoked
increases in CRP and proinﬂammatory cytokines and depression
appears to be bidirectional, as chronic stressors and current
depressive symptoms, both associated with neurophysiological
changes (e.g., glucocorticoid resistance), were found to increase
stress reactivity, including cytokine changes in response to
One of the most robust predictors of increased levels of
proinﬂammatory cytokines is early life adversity (ELA). Usually
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Maydych Stress, Inﬂammation and Emotional Attention
indicated by parental maltreatment and low socioeconomic
status during childhood, ELA is considered as a chronic and
severe stressor causing long-lasting psychological and biological
abnormalities that considerably increase the risk of depression
(Hostinar et al., 2018). Psychological alterations are manifested
in exaggerated reactivity to negative information and stress;
biological abnormalities include HPA axis activity dysregulation
(in most cases hyperactivity leading to glucocorticoid resistance),
low parasympathetic activity, and frontolimbic circuit alterations
that promote reactivity to threatening stimuli (Callaghan
and Tottenham, 2016). For example, individuals exposed to
ELA showed stronger increases in proinﬂammatory cytokines
in response to laboratory stress than those who were not
(Pace et al., 2006). Moreover, exposure to ELA was prospectively
and retrospectively associated with an increased inﬂammation
in later life (Danese et al., 2008;Kiecolt-Glaser et al., 2011;
Coelho et al., 2014).
The causal role of stress in inﬂammatory activity was also
examined in laboratory settings that enable the assessment of
temporal patterns of cytokine responses and use of standardized
stress induction procedures such as the Trier Social Stress Test
(TSST) (Kirschbaum et al., 1993;Slavich and Irwin, 2014).
Laboratory studies showed that acute stress was associated
with signiﬁcant increases in IL-1β(Yamakawa et al., 2009),
IL-1RA and IL-6 (Goebel et al., 2000;O’Donnell et al.,
2008;Hackett et al., 2012), and TNF-α(O’Donnell et al.,
2008), with IL-β, IL-6, and TNF-αdemonstrating the most
robust increases (Marsland et al., 2017). At the same time,
higher cytokine levels were reported to be associated with
increases in negative mood and anxiety in some studies
(Yamakawa et al., 2009;Moons et al., 2010;Carroll et al.,
2011). The notion that increases in inﬂammatory activity
can lead to negative emotional states was also supported
by studies that induced low-grade inﬂammation through
the injection of bacterial endotoxin (i.e., lipopolysaccharide,
LPS) or vaccines (i.e., ﬂu, typhoid). Stimulated increases in
proinﬂammatory cytokines were associated with symptoms such
as fatigue, negative mood, anhedonia, cognitive impairment,
social withdrawal, motor slowing – a variety of symptoms
collectively referred to as sickness behavior and resembling
those of aﬀective-cognitive and somatic symptoms of depression
(Dantzer et al., 2008;Eisenberger et al., 2010). Moreover,
the associations between inﬂammatory activity and sickness
behavior were not restricted to the laboratory, but also
predicted depressive symptoms and cognitive impairment 1 week
later (Kuhlman et al., 2018). Similarly, increases in IL-1β
in response to TSST predicted the increase of depressive
symptoms 1 year later (Aschbacher et al., 2012). Individuals
with diagnosed depression have demonstrated stronger increases
in proinﬂammatory cytokines in response to laboratory stress
than non-depressed individuals (Weinstein et al., 2010;Fagundes
et al., 2013), indicating an increased inﬂammatory stress
responsiveness in depression. Although the aforementioned
studies provide interesting ﬁndings, the ecological validity of
most results is limited due to laboratory settings and mainly
samples of healthy young adults. Future research could seek
to examine whether naturalistic stressor-induced increases in
proinﬂammatory cytokines are prospectively associated with
EMOTIONAL ATTENTION, STRESS, AND
Cognitive symptoms of depression include attentional biases
(AB) toward negative information (Mathews and MacLeod,
2005). A number of studies using diﬀerent attention allocation
tasks (MacLeod et al., 1986) demonstrated that compared
to non-depressed counterparts, depressed individuals exhibit
increased diﬃculty in disengaging their attention from negative
stimuli than from positive or neutral stimuli, especially when
negative material is related to depression (e.g., feelings of
worthlessness, guilt) (Gotlib et al., 2004a,b;Koster et al., 2005;
Caseras et al., 2007). Negative AB has been also documented in
patients with remitted depression and in individuals exposed to
ELA (Luecken and Appelhans, 2005;Joormann and Gotlib, 2007;
Raymond et al., 2018).
The common assumption of cognitive stress-diathesis models
is that depression is a result of the interaction between cognitive
vulnerability and stressful life events (Ingram et al., 1998).
Therefore, given cognitive vulnerability, experiencing stressful
events can initiate a depressive episode. Although the causal
role of stress and cognitive biases that jointly increase the
subsequent depression risk is theoretically now well-established,
surprisingly few studies have examined this etiological pathway
with assessments of stressful events and attention measures
that do not rely on the participants’ self-report. A number
of laboratory-based studies have examined whether laboratory
stress would increase negative AB and whether attention shift
would be associated with mood change. Indeed, AB toward
negative vs. neutral material has been shown to be increased
after a stressful challenge (Ellenbogen et al., 2002;Tsumura
and Shimada, 2012). Moreover, attention shift toward negative
information was associated with mood lowering (Ellenbogen
et al., 2002, 2006) cortisol responses (Ellenbogen et al., 2010;
Roelofs et al., 2007) in healthy participants and slower stress
recovery in a depressed cohort (Sanchez et al., 2017). Although
these results suggest a causal link between stressor-evoked AB
and negative mood, the main limitation of this work is that
stress eﬀects on AB and mood change reﬂect short-term prime
eﬀects rather than providing ecologically valid evidence of the
stress-diathesis hypothesis. To examine the long-term eﬀects,
several studies examined whether baseline or stressor-related
negative AB shifts would prospectively predict depressive
symptoms. These studies reported that AB shift following
induction of negative mood interacted with subsequent stressful
events in predicting increases in dysphoria 7 weeks later
in dysphoric students (Beevers and Carver, 2003). Similarly,
negative AB was predictive of the exacerbation of depressive
symptoms in adults with subclinical depression after 5 weeks
(Disner et al., 2017). Finally, a signiﬁcant interaction eﬀect
of stressful life events and dysfunctional attitudes on clinical
depression incidence after 12 months has been reported
(Lewinsohn et al., 2001).
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Maydych Stress, Inﬂammation and Emotional Attention
STRESS, INFLAMMATION, AND
As outlined in previous sections, distinct lines of research
show that diﬀerent stressors can trigger inﬂammatory activity
and increase the attentional processing of negative information.
Both inﬂammatory processes and cognitive stressor-evoked
changes were associated with mood lowering and an increase in
anxiety and depressive symptoms. Stressor-evoked elevations in
proinﬂammatory cytokines and attention shift toward negative
information can represent stress responses at multiple levels that
independently contribute to depressive symptoms. Alternatively,
inﬂammatory and cognitive stress responses may act together,
potentiating one another’s impact on promoting depression. The
following section provides a summary of studies that examined
the relationship between AB and markers of inﬂammation.
To analyze an association between negative AB and increased
inﬂammatory activity, several cross-sectional and clinical studies
examined performance in attention tasks using emotional
material and tested for relationships with inﬂammatory markers.
Levels of CRP were reported to positively correlate with increased
AB toward sad vs. happy and angry faces in breast cancer
survivors (Boyle et al., 2017). In addition, hepatitis C patients
showed an AB away from positive vs. neutral and fearful faces
and an increase in symptoms of depression, anxiety, and fatigue
6–7 weeks after commencing IFN-αtherapy (Cooper et al., 2018).
Concurrently, a greater increase in AB toward self-referential
positive vs. negative words and improvement of aﬀective-
cognitive and somatic depressive symptoms was observed after
completion of anti-TNF-αtherapy in patients with inﬂammatory
bowel disease (Gray et al., 2018). This preliminary evidence
suggests that aﬀective processing and depressive symptoms may,
at least, be partially driven by inﬂammatory activity. The pattern
of AB toward negative and away from positive information is
consistent with AB usually observed in depression. However,
the inﬂuence of disease or environmental confounding factors
cannot be ruled out in these studies.
To examine whether a causal relationship exists between
stressor-evoked inﬂammatory response and AB, a number of
experimental studies investigated the eﬀects of acute stress or
mood induction on cytokine levels and emotional attention
in healthy and depressed individuals; however, the ﬁndings
have been mixed. Signiﬁcant increases in both pro- and
anti-inﬂammatory cytokines following laboratory stress were
reported by some studies (Boyle, 2018;Maydych et al., 2018).
Elevations of cytokine levels were, in turn, positively associated
with increased AB toward negative and decreased AB toward
positive information. While these ﬁndings provide support for
the notion that stressor-evoked cytokine increases may drive,
at least, short-term changes in attention processing with these
eﬀects depending on the valence of emotional material, other
studies could not conﬁrm this hypothesis (Benson et al., 2017;
Niemegeers et al., 2019). The inconsistency of the ﬁndings may
stem from methodological and design issues, especially from
diﬀerences in stress/mood induction procedures, the timing
of cytokine assessments, and types of attention tasks. It is
also plausible that endogenous concentrations of cytokines, in
particular in healthy samples, even after a stressful challenge,
may be too low to map on behavioral attention measures.
Alternatively, attention tasks may not be sensitive enough to the
cognitive changes produced by cytokines.
Increased inﬂammatory activity appears not only to be
associated with AB toward negative information but has also
been suggested to increase stress reactivity (Dooley et al.,
2018). As outlined earlier, depressed individuals and those
exposed to ELA exhibit higher increases in proinﬂammatory
cytokines in response to acute stress. Thus, it is possible that
exogenously induced inﬂammation prior to stress manipulation
would increase stress reactivity and drive even stronger changes
in emotional processing than individual treatments. Increases in
IL-6 levels have been demonstrated to be positively associated
with negative AB only in response to typhoid vaccine in women
with partially remitted depression, but not in response to
laboratory stress or both treatments (Niemegeers et al., 2019).
In another study, slower processing of negative information was
observed in response to LPS treatment and at a trend level in
combined LPS and negative mood induction condition in healthy
males (Benson et al., 2017).
In summary, the ﬁndings from various behavioral studies
indicate that stressor-related or endotoxin-induced increases in
inﬂammatory activity may aﬀect emotional attention similar to
AB in depression. Yet, there were some inconsistent results and
null results, which can reﬂect methodological diﬀerences between
studies. In addition, the results obtained in laboratory studies
do not allow for conclusions on long-term causal relationships
between immune and cognitive processes. Future studies should
determine whether increased inﬂammation can prospectively
predict alterations in emotional attention.
FUNCTIONAL NEUROIMAGING STUDIES
Although the literature is rather sparse at present, the eﬀects
of inﬂammation on neural activity and functional connectivity
during the processing of emotional stimuli have also been
the subject of investigation. The experimental designs of these
studies induced increased inﬂammation through either LPS,
vaccines, or laboratory stress and measured neural activity
and connectivity during exposure to emotional stimuli or
receiving social feedback. LPS-induced inﬂammation was shown
to increase amygdala activity while viewing negative facial
expression images (Inagaki et al., 2012). Furthermore, peripheral
levels of IL-6 were associated with increased activation of
the amygdala and increased functional connectivity between
the amygdala and dorsomedial prefrontal cortex (dmPFC) in
response to negative social feedback (Muscatell et al., 2015).
Laboratory stressor-evoked increases in the soluble TNF-α
receptor (sTNFαRII) have been shown to be positively correlated
with increased activation in dorsal anterior cingulate cortex
(dACC) and anterior insula (AI) in response to social rejection
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Maydych Stress, Inﬂammation and Emotional Attention
(Slavich et al., 2010;Muscatell et al., 2016). Comparatively, the
LPS-stimulated increase in IL-6 was positively associated with
increased activation of the bilateral amygdala, dACC, and dorsal
prefrontal cortex (dPFC) in response to negative feedback from
the confederate based on a 10-min interview previously provided
by participants (Muscatell et al., 2016). Other studies reported on
the enhanced activity of right inferior orbitofrontal cortex (iOFC)
(Kullmann et al., 2013) and subgenual ACC (Harrison et al., 2009)
in response to viewing emotional pictures and faces, respectively.
Although the data is not yet suﬃcient to draw generalized
conclusions, the majority of studies have documented the
increased activity of amygdala and dACC in response to increases
in inﬂammatory activity and negative social stimuli/feedback.
This is consistent with the literature on AB in depressive or at-risk
individuals (e.g., those exposed to ELA) that found enhanced and
long-lasting activity of amygdala in response to negative material
(Disner et al., 2011). A simultaneous activation increase in of PFC
and ACC was attributed to cortical insuﬃciency and abnormal
frontolimbic circuit function (Wagner et al., 2006;Matsuo et al.,
2007). Along with amygdala and AI, dACC was suggested to
constitute a so-called “neural alarm system,” which is responsible
for the detection of environmental threats and the regulation of
responses to danger including SNS system and HPA axis response
(Muscatell and Eisenberger, 2012).
MECHANISMS LINKING INFLAMMATION
TO EMOTIONAL ATTENTION
Peripherally released cytokines communicate with the brain and
are capable of eliciting changes in emotional processing that
mimic aﬀective-cognitive symptoms of depression. Research has
identiﬁed several pathways by which cytokine signals can access
the brain (Haroon et al., 2012). Brieﬂy, cytokines can enter the
brain through leaky regions in the blood-brain barrier (e.g.,
circumventricular organs) or activated monocytes/macrophages
recruited to the brain. In addition, cytokine release can be
stimulated through brain blood vessel cells (e.g., endothelial
cells). Furthermore, aﬀerent vagus nerve ﬁbers can be stimulated
to transduce cytokine signals from the periphery into the brain,
where the cytokine signals activate cytokine-producing glia cells.
One of the most important molecular mechanisms
linking inﬂammation to emotional cognition is the cytokine
eﬀect on the serotonergic system (Capuron and Castanon,
2016). Proinﬂammatory cytokines activate indoleamine-2,3-
dioxygenase (IDO), an enzyme involved in the synthesis of
kynurenine from dietary tryptophan. Central and peripheral
activation of IDO causes increased catabolism of tryptophan, an
important precursor of serotonin, leading to serotonin deﬁciency
(O’connor J. et al., 2009;O’Connor J.C. et al., 2009). Furthermore,
the products of kynurenine metabolism, such as quinolinic acid,
stimulate the N-methyl-D-aspartate (NMDA) receptor, thereby
unfolding neurotoxic eﬀects leading to neuronal damage
(Campbell et al., 2014).
Another mechanism linking inﬂammation with cognition
is the eﬀect of cytokines on the HPA axis. Cytokines can
act on glucocorticoid receptors and indirectly upregulate
the synthesis of corticotrophin-releasing hormone (CRH),
adrenocorticotropic hormone (ACTH), and cortisol (Raison
and Miller, 2003). The extent to which cytokines induce
the release of ACTH and cortisol is predictive of the
development of aﬀective-cognitive but not of somatic symptoms
of depression (Capuron et al., 2003). This implies that HPA axis
sensitivity to inﬂammatory stimulation is particularly relevant for
the development of aﬀective-cognitive symptoms of depression.
Finally, the parasympathetic nervous system has been
suggested to modulate aﬀective-cognitive and immune processes
involved in stress cascade and depression (Thayer and Sternberg,
2006;Ondicova et al., 2010). Lower activity of the vagus nerve
is predictive of higher levels of cortisol and cytokine acute
stress response (Hamer and Steptoe, 2007;Smeets, 2010;Woody
et al., 2017) as well as slower stress recovery (Weber et al.,
2010). In addition, the vagal tone has been implicated in the
detection and (down-) regulation of inﬂammatory processes.
The anti-inﬂammatory eﬀects are mediated by the vagal release
of acetylcholine, which activates a7 nicotinic Ach receptors in
macrophages, thereby inhibiting the release of proinﬂammatory
cytokines from these lymphocytes (the mechanism referred to
as “cholinergic anti-inﬂammatory reﬂex”) (Rosas-Ballina and
Tracey, 2009). It has been also suggested that reduced activity of
the vagus nerve is associated with disturbed emotion regulation
and further aﬀective-cognitive symptoms that stem from the
impaired inhibitory control of the prefrontal cortex over the
limbic system (Thayer and Sternberg, 2006;Thayer et al., 2012)
as well as deﬁciency in monoamines (Dorr and Debonnel, 2006).
In summary, preliminary evidence suggests that acute and
chronic stress is associated with increased inﬂammatory activity
and enhanced attentional processing of negative information.
Both are predictive of negative mood and depression symptoms
that, in turn, increase inﬂammatory and cognitive stress
reactivity. Increased inﬂammation was associated with a pattern
of attentional changes characteristic to depression, whereas
aﬀective-cognitive states were predictive of inﬂammatory stress
responses. These ﬁndings indicate that immune and aﬀective-
cognitive processes are interconnected and may potentiate
one another’s impact on depression onset, maintenance or
recurrence. An improved understanding of the interplay between
inﬂammatory activity and emotional cognition in the context of
stress may help to optimize treatment strategies for depression.
VM has conceptualized and written the manuscript.
The author thanks Dr. Thomas Kleinsorge for proofreading of the
ﬁrst version of the manuscript. The publication of this article was
funded by the Open Access Fund of the Leibniz Association.
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Maydych Stress, Inﬂammation and Emotional Attention
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