A pre-existing Toxoplasma gondii infection exacerbates the pathophysiological response and extent of brain damage after traumatic brain injury in mice

Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological response to TBI. It is estimated that one-third of the human population is incurably infected with...

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Published inJournal of neuroinflammation Vol. 21; no. 1; p. 14
Main Authors Baker, Tamara L, Wright, David K, Uboldi, Alessandro D, Tonkin, Christopher J, Vo, Anh, Wilson, Trevor, McDonald, Stuart J, Mychasiuk, Richelle, Semple, Bridgette D, Sun, Mujun, Shultz, Sandy R
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 09.01.2024
BioMed Central
BMC
Subjects
Analysis
Animals
Brain
Brain damage
Brain Injuries - complications
Brain Injuries, Traumatic - complications
Brain research
Bupivacaine
Care and treatment
Cats
Central nervous system
Chronic infection
Complications and side effects
Craniotomy
Custom design
Diagnosis
Excitotoxicity
Female
Females
Food contamination & poisoning
Gene expression
Glutamatergic transmission
Humans
Immune response
Infection
Infections
Inflammation
Injuries
Magnetic resonance imaging
Male
Males
Medical research
Mice
Morbidity
Mortality
Neuroinflammation
Neuroinflammatory Diseases
Neurotoxicity
Oxidative stress
Protozoa
Risk factors
Sex
Spleen
Substantia alba
Toxoplasma gondii
Toxoplasmosis
Toxoplasmosis - complications
Traumatic brain injury
Canada
United States > US
Oxidative stress
Immune response
MRI
Excitotoxicity
Sex
Neuroinflammation
Behavior
Females
Online AccessGet full text

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Abstract Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological response to TBI. It is estimated that one-third of the human population is incurably infected with the feline-borne parasite, Toxoplasma gondii, which can invade the central nervous system and result in chronic low-grade neuroinflammation, oxidative stress, and excitotoxicity-all of which are also important pathophysiological processes in TBI. Considering the large number of TBI patients that have a pre-existing T. gondii infection prior to injury, and the potential mechanistic synergies between the conditions, this study investigated how a pre-existing T. gondii infection modified TBI outcomes across acute, sub-acute and chronic recovery in male and female mice. Gene expression analysis of brain tissue found that neuroinflammation and immune cell markers were amplified in the combined T. gondii + TBI setting in both males and females as early as 2-h post-injury. Glutamatergic, neurotoxic, and oxidative stress markers were altered in a sex-specific manner in T. gondii + TBI mice. Structural MRI found that male, but not female, T. gondii + TBI mice had a significantly larger lesion size compared to their uninfected counterparts at 18-weeks post-injury. Similarly, diffusion MRI revealed that T. gondii + TBI mice had exacerbated white matter tract abnormalities, particularly in male mice. These novel findings indicate that a pre-existing T. gondii infection affects the pathophysiological aftermath of TBI in a sex-dependent manner, and may be an important modifier to consider in the care and prognostication of TBI patients.
AbstractList Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological response to TBI. It is estimated that one-third of the human population is incurably infected with the feline-borne parasite, Toxoplasma gondii, which can invade the central nervous system and result in chronic low-grade neuroinflammation, oxidative stress, and excitotoxicity—all of which are also important pathophysiological processes in TBI. Considering the large number of TBI patients that have a pre-existing T. gondii infection prior to injury, and the potential mechanistic synergies between the conditions, this study investigated how a pre-existing T. gondii infection modified TBI outcomes across acute, sub-acute and chronic recovery in male and female mice. Gene expression analysis of brain tissue found that neuroinflammation and immune cell markers were amplified in the combined T. gondii + TBI setting in both males and females as early as 2-h post-injury. Glutamatergic, neurotoxic, and oxidative stress markers were altered in a sex-specific manner in T. gondii + TBI mice. Structural MRI found that male, but not female, T. gondii + TBI mice had a significantly larger lesion size compared to their uninfected counterparts at 18-weeks post-injury. Similarly, diffusion MRI revealed that T. gondii + TBI mice had exacerbated white matter tract abnormalities, particularly in male mice. These novel findings indicate that a pre-existing T. gondii infection affects the pathophysiological aftermath of TBI in a sex-dependent manner, and may be an important modifier to consider in the care and prognostication of TBI patients.
Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological response to TBI. It is estimated that one-third of the human population is incurably infected with the feline-borne parasite, Toxoplasma gondii, which can invade the central nervous system and result in chronic low-grade neuroinflammation, oxidative stress, and excitotoxicity—all of which are also important pathophysiological processes in TBI. Considering the large number of TBI patients that have a pre-existing T. gondii infection prior to injury, and the potential mechanistic synergies between the conditions, this study investigated how a pre-existing T. gondii infection modified TBI outcomes across acute, sub-acute and chronic recovery in male and female mice. Gene expression analysis of brain tissue found that neuroinflammation and immune cell markers were amplified in the combined T. gondii  + TBI setting in both males and females as early as 2-h post-injury. Glutamatergic, neurotoxic, and oxidative stress markers were altered in a sex-specific manner in T. gondii  + TBI mice. Structural MRI found that male, but not female, T. gondii  + TBI mice had a significantly larger lesion size compared to their uninfected counterparts at 18-weeks post-injury. Similarly, diffusion MRI revealed that T. gondii  + TBI mice had exacerbated white matter tract abnormalities, particularly in male mice. These novel findings indicate that a pre-existing T. gondii infection affects the pathophysiological aftermath of TBI in a sex-dependent manner, and may be an important modifier to consider in the care and prognostication of TBI patients.
Abstract Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological response to TBI. It is estimated that one-third of the human population is incurably infected with the feline-borne parasite, Toxoplasma gondii, which can invade the central nervous system and result in chronic low-grade neuroinflammation, oxidative stress, and excitotoxicity—all of which are also important pathophysiological processes in TBI. Considering the large number of TBI patients that have a pre-existing T. gondii infection prior to injury, and the potential mechanistic synergies between the conditions, this study investigated how a pre-existing T. gondii infection modified TBI outcomes across acute, sub-acute and chronic recovery in male and female mice. Gene expression analysis of brain tissue found that neuroinflammation and immune cell markers were amplified in the combined T. gondii + TBI setting in both males and females as early as 2-h post-injury. Glutamatergic, neurotoxic, and oxidative stress markers were altered in a sex-specific manner in T. gondii + TBI mice. Structural MRI found that male, but not female, T. gondii + TBI mice had a significantly larger lesion size compared to their uninfected counterparts at 18-weeks post-injury. Similarly, diffusion MRI revealed that T. gondii + TBI mice had exacerbated white matter tract abnormalities, particularly in male mice. These novel findings indicate that a pre-existing T. gondii infection affects the pathophysiological aftermath of TBI in a sex-dependent manner, and may be an important modifier to consider in the care and prognostication of TBI patients.
Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and their presence could modify the physiological response to TBI. It is estimated that one-third of the human population is incurably infected with the feline-borne parasite, Toxoplasma gondii, which can invade the central nervous system and result in chronic low-grade neuroinflammation, oxidative stress, and excitotoxicity--all of which are also important pathophysiological processes in TBI. Considering the large number of TBI patients that have a pre-existing T. gondii infection prior to injury, and the potential mechanistic synergies between the conditions, this study investigated how a pre-existing T. gondii infection modified TBI outcomes across acute, sub-acute and chronic recovery in male and female mice. Gene expression analysis of brain tissue found that neuroinflammation and immune cell markers were amplified in the combined T. gondii + TBI setting in both males and females as early as 2-h post-injury. Glutamatergic, neurotoxic, and oxidative stress markers were altered in a sex-specific manner in T. gondii + TBI mice. Structural MRI found that male, but not female, T. gondii + TBI mice had a significantly larger lesion size compared to their uninfected counterparts at 18-weeks post-injury. Similarly, diffusion MRI revealed that T. gondii + TBI mice had exacerbated white matter tract abnormalities, particularly in male mice. These novel findings indicate that a pre-existing T. gondii infection affects the pathophysiological aftermath of TBI in a sex-dependent manner, and may be an important modifier to consider in the care and prognostication of TBI patients. Keywords: Neuroinflammation, Immune response, Oxidative stress, Excitotoxicity, Females, Sex, MRI, Behavior
ArticleNumber 14
Audience Academic
Author Shultz, Sandy R
Tonkin, Christopher J
Vo, Anh
Sun, Mujun
Wright, David K
Uboldi, Alessandro D
Mychasiuk, Richelle
McDonald, Stuart J
Baker, Tamara L
Wilson, Trevor
Semple, Bridgette D
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  surname: Semple
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  givenname: Mujun
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  fullname: Shultz, Sandy R
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  organization: Health Sciences, Vancouver Island University, Nanaimo, BC, Canada. sandy.shultz@monash.edu
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Issue 1
Keywords Oxidative stress
Immune response
MRI
Excitotoxicity
Sex
Neuroinflammation
Behavior
Females
Language English
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  publication-title: J Biomed Res
  doi: 10.7555/JBR.32.20170033
  contributor:
    fullname: X Yang
– volume: 13
  year: 2022
  ident: 3014_CR82
  publication-title: Front Immunol
  doi: 10.3389/fimmu.2022.822567
  contributor:
    fullname: BL Castaño
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Snippet Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI patients, and...
Abstract Traumatic brain injury (TBI) is a key contributor to global morbidity that lacks effective treatments. Microbial infections are common in TBI...
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StartPage 14
SubjectTerms Analysis
Animals
Brain
Brain damage
Brain Injuries - complications
Brain Injuries, Traumatic - complications
Brain research
Bupivacaine
Care and treatment
Cats
Central nervous system
Chronic infection
Complications and side effects
Craniotomy
Custom design
Diagnosis
Excitotoxicity
Female
Females
Food contamination & poisoning
Gene expression
Glutamatergic transmission
Humans
Immune response
Infection
Infections
Inflammation
Injuries
Magnetic resonance imaging
Male
Males
Medical research
Mice
Morbidity
Mortality
Neuroinflammation
Neuroinflammatory Diseases
Neurotoxicity
Oxidative stress
Protozoa
Risk factors
Sex
Spleen
Substantia alba
Toxoplasma gondii
Toxoplasmosis
Toxoplasmosis - complications
Traumatic brain injury
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Title A pre-existing Toxoplasma gondii infection exacerbates the pathophysiological response and extent of brain damage after traumatic brain injury in mice
URI https://www.ncbi.nlm.nih.gov/pubmed/38195485
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