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Glucocorticoid dysfunction in children with severe malaria. | LitMetric

AI Article Synopsis

  • Malaria continues to be a significant health issue, particularly severe malaria (SM), which is linked to high mortality rates and involves immune and metabolic disturbances; this study focuses on the role of glucocorticoids (GCs) in children with uncomplicated malaria (UM), severe malaria, and asymptomatic controls (AC).
  • Researchers examined how leukocytes respond to GCs by analyzing the levels of specific molecules (GILZ and FKBP5) and metabolic changes in blood cells of malaria patients.
  • Results indicated that while cortisol levels were higher in SM patients, their responsiveness to GCs was lower compared to asymptomatic individuals, suggesting that reduced GC sensitivity may worsen disease severity in malaria.

Article Abstract

Introduction: Malaria remains a widespread health problem with a huge burden. Severe or complicated malaria is highly lethal and encompasses a variety of pathological processes, including immune activation, inflammation, and dysmetabolism. Previously, we showed that adrenal hormones, in particular glucocorticoids (GCs), play critical roles to maintain disease tolerance during infection in mice. Here, GC responses were studied in Cameroon in children with uncomplicated malaria (UM), severe malaria (SM) and asymptomatic controls (AC).

Methods: To determine the sensitivity of leukocytes to GC signaling on a transcriptional level, we measured the induction of glucocorticoid induced leucine zipper (GILZ) and FK506-binding protein 5 (FKBP5) by GCs in human and murine leukocytes. Targeted tracer metabolomics on peripheral blood mononuclear cells (PBMCs) was performed to detect metabolic changes induced by GCs.

Results: Total cortisol levels increased in patients with clinical malaria compared to AC and were higher in the SM versus UM group, while cortisol binding globulin levels were unchanged and adrenocorticotropic hormone (ACTH) levels were heterogeneous. Induction of both GILZ and FKBP5 by GCs was significantly reduced in patients with clinical malaria compared to AC and in malaria-infected mice compared to uninfected controls. Increased activity in the pentose phosphate pathway was found in the patients, but this was not affected by stimulation with physiological levels of hydrocortisone. Interestingly, hydrocortisone induced increased levels of cAMP in AC, but not in clinical malaria patients.

Discussion: Altogether, this study shows that patients with SM have increased cortisol levels, but also a decreased sensitivity to GCs, which may clearly contribute to the severity of disease.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10364055PMC
http://dx.doi.org/10.3389/fimmu.2023.1187196DOI Listing

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