Key result
Acute active psychological stress decreased classical monocyte proportions (89.4% to 87.0%; p=0.007) and altered nonclassical monocyte proportions compared to baseline.
Why the study?
Psychological stress is a modifiable CVD risk factor possibly by promoting inflammation, but the impact of acute active and passive psychological stress on monocyte subsets remains to be defined.
Does acute active or passive psychological stress alter monocyte subsets and leukocyte count ratios in human participants?
Does acute active or passive psychological stress alter monocyte subsets and leukocyte count ratios in human participants?
Acute active, but not passive, psychological stress promotes a pro-inflammatory shift in monocyte subsets, highlighting a potential mechanism linking stress to cardiovascular disease.
Answers are grounded in this paper and cite their sources.
Active stress may promote pro-inflammatory monocyte shifts; leaves open whether stress-type interventions modify CVD risk.
OBJECTIVE: Psychological stress exposure is a modifiable risk factor for cardiovascular disease (CVD), possibly through promoting a heightened inflammatory milieu. Under psychological stress, changes in monocyte subsets from classical (CM) to intermediate (IM) and nonclassical (NCM) could indicate a more pro-inflammatory environment. We investigated the impact of acute psychological stress (active and passive) on monocyte subsets and leukocyte count ratios. METHODS: Twenty-four participants completed a 20-minute baseline period, followed by a passive [International Affective Picture System (IAPS)] and active stress task [socially evaluative paced auditory serial addition test (PASAT)] with 90-minute recovery after each task. Blood samples were collected to determine changes in: CM, IM and NCM count/proportions, Systemic Inflammation Response Index (SIRI) and neutrophil:lymphocyte ratio (NLR). RESULTS: CM proportions decreased (89.4% to 87.0%; p = .007) and NCM proportions increased (6.8% to 2.1%; p = .035) from baseline to immediately post-PASAT. There were no differences in monocyte subsets from baseline to post-IAPS (CM% p > .99; IM% p > .99; NCM% p > .99). NLR and SIRI did not differ from baseline in response to either the PASAT or IAPS ( p > .05). CONCLUSIONS: Acute active, but not passive, psychological stress promoted a transition in monocyte subsets towards a more pro-inflammatory environment, which may be an important advancement in markers used to assess the inflammatory response to acute psychological stress.
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Linsley et al. (2025) studied this question. Acute active psychological stress (PASAT) vs. Baseline and passive stress (IAPS) was evaluated on Classical monocyte (CM) proportions (p=0.007). Acute active psychological stress decreased classical monocyte proportions (89.4% to 87.0%; p=0.007) and altered nonclassical monocyte proportions compared to baseline.
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