PMID- 34578186
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20211001
IS  - 2076-0817 (Print)
IS  - 2076-0817 (Electronic)
IS  - 2076-0817 (Linking)
VI  - 10
IP  - 9
DP  - 2021 Sep 8
TI  - An Exaggerated Immune Response in Female BALB/c Mice Controls Initial Toxoplasma 
      gondii Multiplication but Increases Mortality and Morbidity Relative to Male 
      Mice.
LID - 10.3390/pathogens10091154 [doi]
LID - 1154
AB  - Studies indicate that female mice are more susceptible to T. gondii infection, as 
      defined by higher mortality rates in comparison to male mice. However, whether 
      this is due to an inability to control initial parasite multiplication or due to 
      detrimental effects of the immune system has not been determined. Therefore, the 
      following studies were undertaken to determine the influence of sex on early 
      parasite multiplication and the immune response during T. gondii infection and to 
      correlate this with disease outcome. Early parasite replication was studied 
      through applying an in vivo imaging system (IVIS) with luciferase expressing T. 
      gondii. In parallel immunological events were studied by cytometric bead array to 
      quantify key immunological mediators. The results confirmed the previous findings 
      that female mice are more susceptible to acute infection, as determined by higher 
      mortality rates and weight loss compared with males. However, conflicting with 
      expectations, female mice had lower parasite burdens during the acute infection 
      than male mice. Female mice also exhibited significantly increased production of 
      Monocyte Chemoattractant Protein-1 (MCP-1), Interferon (IFN)-gamma, and Tumour 
      Necrosis Factor (TNF)-alpha than male mice. MCP-1 was found to be induced by T. 
      gondii in a dose dependent manner suggesting that the observed increased levels 
      detected in female mice was due to a host-mediated sex difference rather than due 
      to parasite load. However, MCP-1 was not affected by physiological concentration 
      of estrogen or testosterone, indicating that MCP-1 differences observed between 
      the sexes in vivo are due to an as yet unidentified intermediary factor that in 
      turn influences MCP-1 levels. These results suggest that a stronger immune 
      response in female mice compared with male mice enhances their ability to control 
      parasite replication but increases their morbidity and mortality.
FAU - Alonaizan, Rasha
AU  - Alonaizan R
AD  - Strathclyde Institute of Pharmacy & Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
AD  - Faculty of Science, King Saud University, P.O. Box 2455, Riyadh 11451, Saudi 
      Arabia.
FAU - Woods, Stuart
AU  - Woods S
AUID- ORCID: 0000-0002-3798-2074
AD  - Strathclyde Institute of Pharmacy & Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
FAU - Hargrave, Kerrie E
AU  - Hargrave KE
AD  - Strathclyde Institute of Pharmacy & Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
AD  - Centre for Immunobiology, Institute of Infection, Immunity and Inflammation, 120 
      University Place, University of Glasgow, Glasgow G12 8QQ, UK.
FAU - Roberts, Craig W
AU  - Roberts CW
AUID- ORCID: 0000-0002-0653-835X
AD  - Strathclyde Institute of Pharmacy & Biomedical Sciences, University of 
      Strathclyde, 161 Cathedral Street, Glasgow G4 0RE, UK.
LA  - eng
GR  - BB/J013854/1/BB_/Biotechnology and Biological Sciences Research Council/United 
      Kingdom
PT  - Journal Article
DEP - 20210908
PL  - Switzerland
TA  - Pathogens
JT  - Pathogens (Basel, Switzerland)
JID - 101596317
PMC - PMC8470933
OTO - NOTNLM
OT  - IVIS
OT  - MCP-1
OT  - Toxoplasma gondii
OT  - immune endocrine
OT  - immune response
OT  - parasite burdens
OT  - sex differences
COIS- The authors declare no conflict of interest. The funders had no role in the 
      design of the study; in the collection, analyses, or interpretation of data; in 
      the writing of the manuscript; or in the decision to publish the results.
EDAT- 2021/09/29 06:00
MHDA- 2021/09/29 06:01
PMCR- 2021/09/08
CRDT- 2021/09/28 01:25
PHST- 2021/07/28 00:00 [received]
PHST- 2021/08/19 00:00 [revised]
PHST- 2021/08/23 00:00 [accepted]
PHST- 2021/09/28 01:25 [entrez]
PHST- 2021/09/29 06:00 [pubmed]
PHST- 2021/09/29 06:01 [medline]
PHST- 2021/09/08 00:00 [pmc-release]
AID - pathogens10091154 [pii]
AID - pathogens-10-01154 [pii]
AID - 10.3390/pathogens10091154 [doi]
PST - epublish
SO  - Pathogens. 2021 Sep 8;10(9):1154. doi: 10.3390/pathogens10091154.