PMID- 38234880
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20240119
IS  - 2405-8440 (Print)
IS  - 2405-8440 (Electronic)
IS  - 2405-8440 (Linking)
VI  - 10
IP  - 1
DP  - 2024 Jan 15
TI  - Toxoplasma gondii infection and brain inflammation: A two-sample mendelian 
      randomization analysis.
PG  - e24228
LID - 10.1016/j.heliyon.2024.e24228 [doi]
LID - e24228
AB  - BACKGROUND: Toxoplasma gondii is an opportunistic parasitic protozoan that can 
      cause highly fatal toxoplasmic encephalitis when the host immune system is 
      compromised. However, the transition from chronic to acute infection remains 
      poorly understood. In this study, we conducted a 180-day observation of tissue 
      damage and inflammation in the brains of mice infected with T. gondii. 
      Subsequently, we investigated the inflammatory factors that T. gondii infection 
      may alter using two-sample Mendelian randomization (MR) analysis. METHODS: We 
      first established a mouse model of T. gondii infection. Subsequently, the mice 
      were euthanized, the brain tissue collected, and immunohistochemistry and 
      hematoxylin and eosin staining performed to observe tissue damage and 
      inflammatory conditions at various time points. Our study also included a 
      published large-scale genome-wide association study meta-analysis that 
      encompassed the circulating concentrations of 41 cytokines. This dataset included 
      8293 individuals from three independent population cohorts in Finland. Genetic 
      association data for T. gondii were sourced from the Integrative Epidemiology 
      Unit and European Bioinformatics Institute datasets, which included 5010 and 559 
      individuals of European ancestry, respectively. To assess the causal relationship 
      between T. gondii infection and inflammatory biomarkers, we applied a two-sample 
      MR. RESULTS: Inflammation and damage resulting from T. gondii infection varied 
      among the distinct regions of the mouse brain. Based on the MR analysis results, 
      three inflammatory biomarkers were chemically assigned to Chemokines and Others, 
      including IP10 (interferon gamma inducible protein-10), MCP1 (monocyte 
      chemoattractant protein-1), and TRAIL (TNF-related apoptosis-inducing ligand). 
      CONCLUSION: Our study commenced with the assessment of tissue damage and 
      progression of inflammation in distinct regions of the mouse brain after T. 
      gondii infection. Subsequently, using MR analysis, we detected potential 
      alterations in inflammatory factors associated with this infection. These 
      findings offer valuable insights into the mechanisms underlying toxoplasmic 
      encephalitis and suggest directions for the prevention and treatment of T. gondii 
      infections.
CI  - (c) 2024 The Authors.
FAU - Yao, Yong
AU  - Yao Y
AD  - Department of Immunology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, China.
AD  - College of Life Sciences, Anhui Medical University, Hefei, 230032, China.
FAU - Shi, Taiyu
AU  - Shi T
AD  - First Clinical Medical College of Anhui Medical University, Hefei, China.
FAU - Shu, Panyin
AU  - Shu P
AD  - State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, 
      China.
FAU - Zhang, Yixin
AU  - Zhang Y
AD  - First Clinical Medical College of Anhui Medical University, Hefei, China.
FAU - Gu, Hao
AU  - Gu H
AD  - Department of Immunology, School of Basic Medical Sciences, Anhui Medical 
      University, Hefei, China.
LA  - eng
PT  - Journal Article
DEP - 20240106
PL  - England
TA  - Heliyon
JT  - Heliyon
JID - 101672560
PMC - PMC10792577
OTO - NOTNLM
OT  - Inflammatory biomarkers
OT  - Mendelian randomization study
OT  - Pathological examination
OT  - Toxoplasma gondii
OT  - Toxoplasmic encephalitis
COIS- There is no declaration of Interest Statement.
EDAT- 2024/01/18 06:42
MHDA- 2024/01/18 06:43
PMCR- 2024/01/06
CRDT- 2024/01/18 04:15
PHST- 2023/09/19 00:00 [received]
PHST- 2024/01/04 00:00 [revised]
PHST- 2024/01/04 00:00 [accepted]
PHST- 2024/01/18 06:43 [medline]
PHST- 2024/01/18 06:42 [pubmed]
PHST- 2024/01/18 04:15 [entrez]
PHST- 2024/01/06 00:00 [pmc-release]
AID - S2405-8440(24)00259-7 [pii]
AID - e24228 [pii]
AID - 10.1016/j.heliyon.2024.e24228 [doi]
PST - epublish
SO  - Heliyon. 2024 Jan 6;10(1):e24228. doi: 10.1016/j.heliyon.2024.e24228. eCollection 
      2024 Jan 15.