A Theorem on Matroid Homomorphism

This note generalizes a result contained in a previous paper [ J. Sanders, Circuit preserving edge maps II, J. Combin. Theory Ser. B 42 (1987), 146-155].Comment: 5 pages, 0 figure

Selected known secreted proteins with similar expression in sporozoites and tachyzoites.

<p>Selected known secreted proteins with similar expression in sporozoites and tachyzoites.</p

Top 50 genes with significantly higher expression in tachyzoites compared to sporozoites.

<p>Top 50 genes with significantly higher expression in tachyzoites compared to sporozoites.</p

Rat genes with significantly higher expression in IECs infected with tachyzoites but not with sporozoites.

<p>Rat genes with significantly higher expression in IECs infected with tachyzoites but not with sporozoites.</p

Host pathways significantly enriched in IECs infected with sporozoites or tachyzoites.

<p>Host pathways significantly enriched in IECs infected with sporozoites or tachyzoites.</p

Differentially expressed genes encoding IMC proteins.

<p>Differentially expressed genes encoding IMC proteins.</p

Expression dynamics of oocyst-associated genes from unsporulated oocysts to intracellular sporozoites.

<p>Expression dynamics of oocyst-associated genes from unsporulated oocysts to intracellular sporozoites.</p

Metabolic pathways differentially enriched in intracellular sporozoites vs. tachyzoites.

<p>Metabolic pathways differentially enriched in intracellular sporozoites vs. tachyzoites.</p

An <i>in vitro</i> model of intestinal infection reveals a developmentally regulated transcriptome of <i>Toxoplasma sporozoites</i> and a NF-κB-like signature in infected host cells

<div><p>Toxoplasmosis is a zoonotic infection affecting approximately 30% of the world’s human population. After sexual reproduction in the definitive feline host, <i>Toxoplasma</i> oocysts, each containing 8 sporozoites, are shed into the environment where they can go on to infect humans and other warm-blooded intermediate hosts. Here, we use an <i>in vitro</i> model to assess host transcriptomic changes that occur in the earliest stages of such infections. We show that infection of rat intestinal epithelial cells with mature sporozoites primarily results in higher expression of genes associated with Tumor Necrosis Factor alpha (TNFα) signaling via NF-κB. Furthermore, we find that, consistent with their biology, these mature, invaded sporozoites display a transcriptome intermediate between the previously reported day 10 oocysts and that of their tachyzoite counterparts. Thus, this study uncovers novel host and pathogen factors that may be critical for the establishment of a successful intracellular niche following sporozoite-initiated infection.</p></div

Experimental layout for <i>in vitro</i> infection of the intestine.

<p>Confluent rat intestinal epithelial cells (IEC-18) were infected with either sporozoites (SPZ) or tachyzoites in the absence (TZ) or presence (TZ+fzSPZ) of frozen-thawed sporozoites for 8 hours at 37°C. As a control for possible effects of oocyst/sporocyst wall components and MA-104 cells debris, sporozoites inactivated by freezing (fzSPZ) or MA-104 cell lysates (Mock) were added to IEC-18 cells, respectively. All experiments were performed in biological duplicate (i.e., starting with individual populations of sporozoites) and with two technical replicates. Total RNA was extracted and RNA sequencing was performed using the Illumina NextSeq platform. SAMseq analysis was used to identify differentially regulated genes of both host and parasite origin in various pairwise comparisons.</p