TY - JOUR
T1 - Toxoplasma gondii-induced long-term changes in the upper intestinal microflora during the chronic stage of infection
AU - Prandovszky, Emese
AU - Li, Ye
AU - Sabunciyan, Sarven
AU - Steinfeldt, Curtis B.
AU - Avalos, Lauro Nathaniel
AU - Gressitt, Kristin L.
AU - White, James R.
AU - Severance, Emily G.
AU - Pletnikov, Mikhail V.
AU - Xiao, Jianchun
AU - Yolken, Robert H.
N1 - Funding Information:
)e authors thank Jodie Franklin, codirector, JHMI Synthesis and Sequencing Facility, for performing the MiSeq sequencing and Frank Boellmann, PhD, Regional Marketing Specialist, Informatics (Illumina), for helpful discussion on the analyses of the MiSeq sequencing results. )e authors also thank Vernon B. Carruthers, PhD, Professor, University of Michigan Medical School, and Christopher D. O’Donnell, PhD, for helpful advice. )is work was supported by the Stanley Medical Research Institute and the NIMH P50 Silvio O. Conte Center at Johns Hopkins (grant no MH-94268).
Publisher Copyright:
Copyright © 2018 Emese Prandovszky et al.
PY - 2018
Y1 - 2018
N2 - Toxoplasma gondii is an obligate intracellular parasite with worldwide distribution. Felines are the definitive hosts supporting the complete life cycle of T. gondii. However, other warm-blooded animals such as rodents and humans can also be infected. Infection of such secondary hosts results in long-term infection characterized by the presence of tissue cysts in the brain and other organs. While it is known that T. gondii infection in rodents is associated with behavioral changes, the mechanisms behind these changes remain unclear. Alterations of the host intestinal microflora are recognized as a prominent role player in shaping host behavior and cognition. It has been shown that acute T. gondii infection of mice results in microflora changes as a result of gastrointestinal inflammation in inbred mouse models. The long-term effects of chronic T. gondii infection on microbial communities, however, are unknown. In this study, after we verified using our model in terms of measuring microflora changes during an acute episode of toxoplasmosis, we assessed the microbiome changes that occur during a long-term infection; then we further investigated these changes in a follow-up study of chronic infection. Thse analyses were performed by constructing and sequencing 16S rRNA amplicon DNA libraries from small intestine fecal specimens. We found that acute infection with the GT1 strain of T. gondii caused an enrichment of Bacteroidetes compared with controls in CD1 mice. Strikingly, this enrichment upheld throughout longterm chronic infection. The potential biological consequences of this alteration in rodents and humans should be subjected to further exploration.
AB - Toxoplasma gondii is an obligate intracellular parasite with worldwide distribution. Felines are the definitive hosts supporting the complete life cycle of T. gondii. However, other warm-blooded animals such as rodents and humans can also be infected. Infection of such secondary hosts results in long-term infection characterized by the presence of tissue cysts in the brain and other organs. While it is known that T. gondii infection in rodents is associated with behavioral changes, the mechanisms behind these changes remain unclear. Alterations of the host intestinal microflora are recognized as a prominent role player in shaping host behavior and cognition. It has been shown that acute T. gondii infection of mice results in microflora changes as a result of gastrointestinal inflammation in inbred mouse models. The long-term effects of chronic T. gondii infection on microbial communities, however, are unknown. In this study, after we verified using our model in terms of measuring microflora changes during an acute episode of toxoplasmosis, we assessed the microbiome changes that occur during a long-term infection; then we further investigated these changes in a follow-up study of chronic infection. Thse analyses were performed by constructing and sequencing 16S rRNA amplicon DNA libraries from small intestine fecal specimens. We found that acute infection with the GT1 strain of T. gondii caused an enrichment of Bacteroidetes compared with controls in CD1 mice. Strikingly, this enrichment upheld throughout longterm chronic infection. The potential biological consequences of this alteration in rodents and humans should be subjected to further exploration.
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U2 - 10.1155/2018/2308619
DO - 10.1155/2018/2308619
M3 - Article
C2 - 30515345
AN - SCOPUS:85062440544
SN - 2090-908X
VL - 2018
JO - Scientifica
JF - Scientifica
M1 - 2308619
ER -