Elevated levels of systemic inflammation are associated with altered reward-related brain function in ventral striatal areas of the brain like the nucleus accumbens (NAcc). In adolescents, cross-sectional research indicates that exposure to early life stress (ELS) can moderate the relation between inflammation and neural activation, which may contribute to atypical reward function; however, no studies have tested whether this moderation by ELS of neuroimmune associations persists over time. Here, we conducted a cross-sectional analysis and the first exploratory longitudinal analysis testing whether cumulative severity of ELS moderates the association of systemic inflammation with reward-related processing in the NAcc in adolescents (n = 104; 58F/46M; M[SD] age = 16.00[1.45] years; range = 13.07-19.86 years). For the cross-sectional analysis, we modeled a statistical interaction between ELS and levels of C-reactive protein (CRP) predicting NAcc activation during the anticipation and outcome phases of a monetary reward task. We found that higher CRP was associated with blunted NAcc activation during the outcome of reward in youth who experienced higher levels of ELS (β = -0.31; p = 0.006). For the longitudinal analysis, we modeled an interaction between ELS and change in CRP predicting change in NAcc activation across 2 years. This analysis similarly showed that increasing CRP over time was associated with decreasing NAcc during reward outcomes in youth who experienced higher levels of ELS (β = -0.47; p = 0.022). Both findings support contemporary theoretical frameworks involving associations among inflammation, reward-related brain function, and ELS exposure, and suggest that experiencing ELS can have significant and enduring effects on neuroimmune function and adolescent neurodevelopment.
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http://dx.doi.org/10.1038/s41386-023-01708-y | DOI Listing |
Orv Hetil
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J Infect Dev Ctries
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Department of Emergency Medicine, Faculty of Medicine, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.
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BDJ Open
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Department of Orthodontics, Institute of Dentistry, Medical Faculty, Jagiellonian University, Kraków, Poland.
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Department of Rheumatology and Immunology, Peking University People's Hospital, No. 11, Xizhimen South Street, Xicheng District, Beijing, 100044, China; Beijing Key Laboratory for Rheumatism Mechanism and Immune Diagnosis (BZ0135), No. 11, Xizhimen South Street, Xicheng District, Beijing, 100044, China; Division of Rheumatology, Department of Medicine, University of Colorado, No. 11, Xizhimen South Street, Xicheng District, Aurora, CO, 80045, USA. Electronic address:
Rheumatoid arthritis (RA) is a complex autoimmune disease with growing evidence implicating the microbiota as a critical contributor to its pathogenesis. This review explores the multifaceted roles of microbial dysbiosis in RA, emphasizing its impact on immune cell modulation, autoantibody production, gut barrier integrity, and joint inflammation. Animal models reveal how genetic predisposition and environmental factors interact with specific microbial taxa to influence disease susceptibility.
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Renal Physiopathology Laboratory, Department of Nephrology, Instituto Investigación Sanitaria Gregorio Marañón, Hospital General Universitario Gregorio Marañón, Madrid, Spain; Department of Physiology, School of Medicine, Universidad Complutense, Madrid, Spain. Electronic address:
Sepsis is a systemic inflammatory response to infection, and its occurrence is associated with a poor prognosis in the context of multiorgan dysfunction syndrome (MODS). Although there are several animal models for the study of its etiology, the cecal ligation and puncture (CLP) model has been considered the "Gold standard" because it shows a high degree of similarity to the progression of human sepsis. Currently, it is one of the most frequently chosen options to search for therapeutic alternatives to diminish the progression and organ damage induced by sepsis.
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