Infection of Mouse Neural Progenitor Cells by Toxoplasma gondii Reduces Proliferation, Migration, and Neuronal Differentiation in Vitro.

Congenital toxoplasmosis constitutes a major cause of pre- and postnatal complications. Fetal infection with Toxoplasma gondii influences development and can lead to microcephaly, encephalitis, and neurologic abnormalities. Systematic studies concerning the effects of neural progenitor cell infection with T.

P2X7 Receptor Modulation of the Gut Microbiota and the Inflammasome Determines the Severity of -Induced Ileitis.

In mice, oral infection induces severe ileitis. The aim of the present study was to investigate the impact of the P2X7 receptor (P2X7) on the inflammatory response to -induced ileitis. Cysts of the ME49 strain of were used to induce ileitis.

Impact of collaborative actions of subpopulations on the infection profile.

This study focuses on the role of the population structure of spp. on the adaptive capacity of the parasite. Herein, we investigate the contribution of subpopulations of the Thor strain (Thor03, Thor10 and Thor22) in the profile of murine macrophages infection.

In the Acute Phase of Infection, Liver Lymphoid and Myeloid Cells Display an Ambiguous Phenotype Combining Pro- and Anti-Inflammatory Markers.

Multiple cell populations, cellular biochemical pathways, and the autonomic nervous system contribute to maintaining the immunological tolerance in the liver. This tolerance is coherent because the organ is exposed to high levels of bacterial pathogen-associated molecular pattern (PAMP) molecules from the intestinal microbiota, such as lipopolysaccharide endotoxin (LPS). In the case of infection, although there is a dramatic acute immune response in the liver, we observed intrahepatic cell populations combining pro- and anti-inflammatory markers.

ZIKV replication is differential in explants and cells of human placental which is suppressed by HSV-2 coinfection.

During the Zika fever outbreak in Brazil in 2015-2016, only some babies from infected mothers had teratogenic effects, suggesting that cofactors may influence congenital transmission. We investigated the ZIKV infection profile in explants and isolated cells from full-term human placenta to infection with the Brazilian Zika virus strain (ZIKV) and the effect of coinfection with the Brazilian Human alphaherpesvirus 2 strain (HSV-2) on ZIKV replication. We found that the ZIKV infect the explants of amniotic and chorionic membranes, as well as chorionic villi core, but not the trophoblasts layer.