Inflammatory Cytokines Are Associated with Cognitive Dysfunction and Depressive State during Acute Bacterial Infections and the Recovery Phase

Int J Mol Sci. 2023 Sep 18;24(18):14221. doi: 10.3390/ijms241814221.

Abstract

During a bacterial infection, individuals may present with behavioral changes referred to as sickness behavior, which has been suggested is induced by the inflammatory markers that are released because of the infective immunological challenge. However, few studies have explored this multidimensional phenomenon in naturally occurring conditions. A longitudinal observational study was conducted to explore the role of inflammatory cytokines in mediating the sickness behavior during a bacterial infection. There were 13, 11 and 37 participants in the infection, hospital control and healthy groups, respectively. They were all followed up for 6 weeks and their inflammatory markers were quantified throughout those weeks. Cognitive function and depressive state were assessed by means of the Mini-Mental State Examination (MMSE) and Cornell Scale for Depression in Dementia (CSDD). Reductions in proinflammatory markers C-Reactive protein (CRP), interleukin - 6 (IL6) and tumor necrosis factor-α (TNFα) and increments in anti-inflammatory markers (interleukin - 4 (IL4)) were associated with an improvement in CSDD and MSEE in patients recovering from a bacterial infection. The correlation between inflammatory makers and CSDD was statistically significant for the CRP (r = 0.535, p = 0.001), the IL6 (r = 0.499, p < 0.001), the TNFα (r = 0.235, p = 0.007) and the IL4 (r = -0.321, p = 0.018). Inflammatory cytokines may mediate sickness behavior during acute illness. These results may enhance the understanding of the pathophysiology and potential treatment strategies to palliate this sickness behavior.

Keywords: acute bacterial infections; cytokines; sickness behavior.

Publication types

  • Observational Study

MeSH terms

  • Bacterial Infections* / complications
  • C-Reactive Protein
  • Cognitive Dysfunction* / etiology
  • Cytokines
  • Humans
  • Infections*
  • Interleukin-4
  • Interleukin-6
  • Tumor Necrosis Factor-alpha

Substances

  • Cytokines
  • Interleukin-6
  • Interleukin-4
  • Tumor Necrosis Factor-alpha
  • C-Reactive Protein

Grants and funding

This research was funded by the Medicine for Older People Department, Royal Bournemouth Hospital (University Hospitals Dorset, Bournemouth). The APC was funded by the CIBEROBN, Instituto de Salud Carlos III.