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  3. Urinary Tract Infection Exaggerates Cognitive Deficits And Region-specific Neuroinflammation Following Traumatic Brain Injury.
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  3. Urinary Tract Infection Exaggerates Cognitive Deficits And Region-specific Neuroinflammation Following Traumatic Brain Injury.

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Investigations on Alterations of Hippocampal Circuit Function Following Mild Traumatic Brain Injury
10:59

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Urinary Tract Infection Exaggerates Cognitive Deficits and Region-Specific Neuroinflammation Following Traumatic

Zachary Zimomra1,2,3, Christina Lepak1,2,4, Rebecca Boland1,2,3

  • 1Department of Neuroscience, College of Medicine, Wexner Medical Center, The Ohio State University, Columbus, Ohio, USA.

Journal of Neurotrauma
|June 26, 2026

View abstract on PubMed

Summary
This summary is machine-generated.

Urinary tract infection (UTI) following traumatic brain injury (TBI) worsens cognitive deficits and alters neuroinflammation. This study reveals that post-TBI bladder infection negatively impacts brain injury outcomes, highlighting a critical link between infections and neurological health.

Keywords:
memoryneuroinflammationtraumatic brain injuryurinary tract infection

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Area of Science:

  • Neuroscience
  • Immunology
  • Infectious Diseases

Background:

  • Traumatic brain injury (TBI) increases susceptibility to infections like urinary tract infections (UTIs).
  • UTIs, often caused by Uropathogenic Escherichia coli (UPEC), are common and can affect vulnerable populations.
  • The neuroimmune and cognitive consequences of UTIs following TBI are not well understood.

Purpose of the Study:

  • To investigate the biological effects of bladder infection subsequent to TBI in a pre-clinical model.
  • To determine if UTI exacerbates long-term outcomes after TBI.
  • To explore the neuroimmune responses and cognitive changes associated with combined TBI and UTI.

Main Methods:

  • Female mice underwent either sham injury or lateral fluid percussion TBI.
  • Three days post-injury, mice were inoculated with vehicle or UPEC to induce UTI.
  • Behavioral tests (Y-maze, open-field), flow cytometry, ELISA, and immunohistochemistry were used to assess outcomes.

    • Main Results:

    • TBI induced spatial memory deficits, which were significantly worsened by subsequent UTI.
    • TBI elevated plasma IL-6, but UTI following TBI appeared to dampen this systemic inflammatory marker.
    • TBI increased microglial reactivity and monocyte infiltration in the brain, with UTI further modulating microglial activation markers (CD68) in a region-specific manner.

    Conclusions:

    • UTI following TBI is detrimental to overall outcome, exacerbating cognitive impairments.
    • Post-injury UTI alters the neuroimmune landscape in the brain, independent of systemic inflammation.
    • Further research is warranted to elucidate the signaling pathways connecting bladder infection and neuroinflammation after TBI.