Associations between childhood maltreatment and inflammatory markers

Palmos, Alish; Watson, Stuart; Hughes, Tom; Finkelmeyer, Andreas; McAllister-Williams, R. Hamish; Ferrier, Nicol; Anderson, Ian; Nair, Rajesh; Young, Allan H.; Strawbridge, Rebecca; Cleare, Anthony J.; Chung, Raymond T.; Frissa, Souci; Goodwin, Laura; Hotopf, Matthew; Hatch, Stephani L.; Wang, Hong; Collier, David A.; Thuret, Sandrine; Breen, Gerome; Powell, Timothy R.

doi:10.1192/bjo.2018.80

Cited by 18 publications

(23 citation statements)

References 26 publications

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“…Informed written consent was obtained from all participants at the time of sample collection. The 35 inflammatory markers represent adequately expressed cytokines from an initial panel of 42, which were originally assayed in relation to major depression risk, as described previously 48 . The mean age of our sample was 48.7 ± 15.1 (standard deviation), with a mean body mass index of 27.3 ± 5.5.…”

Section: Methodsmentioning

confidence: 99%

“…The first phase aimed to assess common physical and mental disorders in South East London; the second, to examine the roles of historical social context and policy in shaping patterns of health inequalities; and the third, to collect biological specimens from a subset of participants, including blood for serum separation and DNA for genotyping. Serum and DNA were extracted and stored at −80 °C until use, as described previously 47,48 .…”

Section: Methodsmentioning

confidence: 99%

“…Quantification and analysis of cytokines. Serum levels (pg/mL) of 35 blood-based markers were assessed in blood samples from the SELCoH cohort using multiplex ELISA-based technology provided by the Meso Scale Discovery Biomarker kits, as described previously 48 . For each marker, we adjusted for the effects of assay run, age, gender, body mass index (BMI), smoking (never, current, former) and ethnicity, by taking standardized residuals (z-scores).…”

Section: Methodsmentioning

confidence: 99%

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The behavioral, cellular and immune mediators of HIV-1 acquisition: New insights from population genetics

Powell

Duarte

Hotopf

et al. 2020

Sci Rep

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Millions are exposed to the human immunodeficiency virus type 1 (HIV-1) every year, but not all acquire the virus, suggesting a potential role for host genetics in the moderation of HIV-1 acquisition. Here, we analyzed summary statistics from the largest genome-wide association study of HIV-1 acquisition todate, consisting of 6,334 infected patients and 7,247 population controls, to advance our understanding of the genetic mechanisms implicated in this trait. We found that HIV-1 acquisition is polygenic and heritable, with SNP heritability estimates explaining 28-42% of the variance in this trait at a population level. Genetic correlations alongside UK Biobank data revealed associations with smoking, prospective memory and socioeconomic traits. Gene-level enrichment analysis identified EF-hand calcium binding domain 14 as a novel susceptibility gene for HIV-1 acquisition. We also observed that susceptibility variants for HIV-1 acquisition were significantly enriched for genes expressed in T-cells, but also in striatal and hippocampal neurons. Finally, we tested how polygenic risk scores for HIV-1 acquisition influence blood levels of 35 inflammatory markers in 406 HIV-1-negative individuals. We found that higher genetic risk for HIV-1 acquisition was associated with lower levels of C-C motif chemokine ligand 17. Our findings corroborate a complex model for HIV-1 acquisition, whereby susceptibility is partly heritable and moderated by specific behavioral, cellular and immunological parameters.Around 38 million people currently live with the human immunodeficiency virus type 1 (HIV-1) worldwide 1 , and millions more are exposed to potential infection every year through sexual contact, vertical transmission, or via the parenteral route 2,3 . First-line prevention strategies against acquisition comprise of the use of condoms and pre-exposure prophylaxis (PrEP), or abstinence from drugs or sex 4 . However, epidemiological studies have identified varying degrees of susceptibility to HIV-1, suggesting that host genetics may play a role in moderating acquisition, which could be explored in the context of preventive strategies. For example, studies conducted prior to the development of antiretroviral therapy observed that less than a third of babies born from HIV-1-positive mothers acquire HIV-1 5 and, similarly, that a proportion of highly exposed individuals are resistant to infection 6 . Supporting this hypothesis, homozygosity of the Δ32 mutation of the C-C chemokine receptor type 5 (CCR5) gene has been shown to protect against HIV-1 infection 7-9 , as the encoded protein is a co-receptor needed for viral entry. However, it remains unknown whether common genetic risk factors are also involved in host susceptibility to acquisition.HIV-1 acquisition is a complex phenotype that consists of behavioral risk parameters and biological factors moderating viral entry and replication. A better understanding of both behavioral and biological factors influencing acquisition has the potential to improve our basic comprehension of ...

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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The behavioral, cellular and immune mediators of HIV-1 acquisition: New insights from population genetics

Powell

Duarte

Hotopf

et al. 2020

Sci Rep

Self Cite

View full text Add to dashboard Cite

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“…According to the tools guidelines studies can be categorised as low quality (<20), moderate quality (20)(21)(22)(23)(24)(25)(26)(27)(28)(29), and high quality (30+). All papers were rated by 1 reviewer, and the 2 nd reviewer independently quality rated a sub-sample of 25% of papers.…”

Section: Methods Of Reviewmentioning

confidence: 99%

“…BMI-Body mass index, CM-Child Maltreatment, CRP-C-reactive protein, CTQ-Childhood Trauma Questionnaire, EA-Emotional abuse, EN-Emotional neglect, ETI-Early Trauma Inventory, FEP-First Episode Psychosis, MDD-Major Depressive Disorder, PA-Physical abuse, PN-Physical abuse, SA-Sexual abuse, UHR-Ultra-high riskAll papers reporting clinical samples were retrospective and all but one used CTQ to record CM. Four studies did not find any association between CM and CRP[24][25][26][27]. A further two studies found initially significant associations between CM measures and CRP, which attenuated to non-significance on adjustment for BMI[28,29].…”

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confidence: 99%

The association of child maltreatment and systemic inflammation in adulthood: A systematic review

Kerr

McDonald

Minnis

2020

Preprint

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IntroductionChild maltreatment (CM) is associated with mental and physical health disorders in adulthood. Some studies have identified elevated markers of systemic inflammation in adult survivors of CM, and inflammation may mediate the association between CM with later health problems. However, there are methodological inconsistencies in studies of the association between CM and systemic inflammation and findings are conflicting. We performed a systemic review to examine the association of CM with systemic inflammation in adults.MethodsA systematic review was performed following PRISMA . Medline, Embase, Scopus and PsychInfo were searched for studies of the association of CM with blood markers of inflammation in adults. Quality was assessed using the Crowe Critical Appraisal Tool. We had intended to perform a meta-analysis but this was not possible due to variation in study design and reporting.ResultsForty-six articles met criteria for inclusion in the review. The most widely reported biomarkers were C-Reactive Protein (CRP) (n=29), interleukin-6 (n=25) and Tumour Necrosis Factor-alpha (TNF-a). Four studies were prospective (all relating to CRP) and the remainder were retrospective. 85% of studies were based in Western settings. In the prospective studies, CM was associated with elevated CRP in adulthood. Results of retrospective studies were conflicting. Methodological issues relating to the construct of CM, methods of analysis, and accounting for confounding or mediating variables (particularly Body Mass Index) may contribute to the uncertainty in the field.ConclusionsThere is some robust evidence from prospective studies that CM is associated with elevated CRP in adulthood. We have identified significant methodological issues in the literature and have proposed measures that future researchers could employ to improve consistency across studies. Further prospective, longitudinal, research using robust and comparable measures of CM with careful consideration of confounding and mediating variables are required to bring clarity to this field.

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Genetic risk for severe COVID‐19 correlates with lower inflammatory marker levels in a SARS‐CoV‐2‐negative cohort

et al. 2021

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Objectives It remains unknown how inflammatory marker levels differ amongst individuals susceptible to coronavirus disease 2019 (COVID‐19), prior to severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection and the onset of the cytokine storm. We used genetic risk scores to model how susceptibility to severe COVID‐19 correlates with baseline levels of 35 inflammatory markers, by testing their impact in a SARS‐CoV‐2‐negative population cohort. Because of the established effects of age and body mass index on severe COVID‐19 risk, we further considered how these variables interacted with genetic risk to affect inflammatory marker levels. Methods We accessed data on 406 SARS‐CoV‐2‐negative individuals as part of a UK population study. Multiplex electrochemiluminescence methods were applied to blood serum, and 35 inflammatory markers were assayed. Corresponding genotype data, alongside results from a large genome‐wide association study of severe COVID‐19, allowed us to construct genetic risk scores and to test their impact on inflammatory protein levels. Results Our results revealed that a higher genetic risk for severe COVID‐19 was associated with lower blood levels of interferon gamma (IFN‐γ), vascular endothelial growth factor D (VEGF‐D) and tumor necrosis factor alpha (TNF‐α). Inflammatory profiles of those with high genetic risk increasingly diverge from the norm in association with age and obesity. Conclusion Our results support the theory that individuals at risk of severe COVID‐19 have a deficient innate immunity marked by reduced levels of inflammatory markers at baseline, including IFN‐γ, VEGF‐D and TNF‐α. We hypothesise that a secondary overactive adaptive immune response may subsequently explain the high levels of cytokines observed in SARS‐CoV‐2‐positive COVID‐19 patients.

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Associations between childhood maltreatment and inflammatory markers

Cited by 18 publications

References 26 publications

The behavioral, cellular and immune mediators of HIV-1 acquisition: New insights from population genetics

The behavioral, cellular and immune mediators of HIV-1 acquisition: New insights from population genetics

The association of child maltreatment and systemic inflammation in adulthood: A systematic review

Genetic risk for severe COVID‐19 correlates with lower inflammatory marker levels in a SARS‐CoV‐2‐negative cohort

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