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Polar infection of Echovirus 30 causes differential barrier affection and gene regulation at the blood-CSF barrier

ABSTRACT: Among the non-polio enterovirus (NPEV) Echovirus-30 (E-30) is responsible for extensive global outbreaks of meningitis in children. To gain access to the central nervous system (CNS), E-30 first have to cross one of the two main barriers, the epithelial blood-cerebrospinal fluid (CSF) barrier (BCSFB) or the endothelial blood-brain barrier (BBB). Previously it has been shown that several meningitis causing bacteria preferentially infect human choroid plexus papilloma cells (HIBCPP) in a polar fashion from the basolateral cell side. Here, we investigated the polar infection with E-30 of HIBCPP cells. Both, apical and basolateral infections caused a significant decrease of the transepithelial resistance (TEER) of HIBCPP cells in a dose-dependent manner. However, to reach the same TEER decrease the multiplicity of infection (MOI) of the apical infection had to be 20 times higher than the basolateral infection. In line with this finding the number of infected cells at respective time-points after basolateral infection was significantly higher compared to apical infection. Cytotoxic effects of E-30 on HIBCPP cells during basolateral infection were observed following prolonged infection, and appeared more drastically compared to the apical infection. Evaluation of massive analysis of cDNA ends (MACE) RNA data comparing basolateral versus apical infection, revealed a distinct pattern of up- and down-regulated genes depending on the side of infection. Especially, the down-regulation of ITGα5 upon basolateral infection can be correlated with a more drastic impact of E-30 on the HIBCPP cells when compared to apical infection, leading to structural changes. Also, type 3 interferon genes might be a factor involved in the polar effect of E-30 on HIBCPP. Altogether, the data highlights the polar effect of E-30 in HIBCPP cells as an important factor for an efficient infection.

ORGANISM(S): Homo sapiens

PROVIDER: GSE146890 | GEO | 2020/10/02

REPOSITORIES: GEO

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Project description:Purpose: In the last decades, the advancements of nanotechnologies lead to a massive increase of engineered nanoparticles in consumer products, which translates in an increased human and environmental exposure to nanomaterials. For humans, inhalation is considered as the main exposure route to nanomaterials, which is the reason why lung toxicity studies should be considered as a priority. Inhalation studies are often performed in vivo in rodents. Therefore, in vitro models may represent a valid and efficient alternative to predict the acute toxicity effects of inhaled NPs on human health. The model used in this study represents the human alveolar barrier; it is constituted by four different human pulmonary cell lines (EA.hy 296 on the basolateral side; A549, HMC-1 and macrophage-like cells in the apical side). The cells in the apical side were cultivated at the air-liquid-interface (ALI) and they have been exposed to AuNPs with the VitroCell® Cloud System. Results: We describe the effects after 24 hours of exposure to three different gold nanoparticles (AuNPs) in order to evaluate the suitability of our model to assess the toxicological effects of particles. The set of PEGylated AuNPs used included spheres (GNPs), rods (GNRs) and stars (GNSs). The exposure did not cause any significant decrease of viability; all the AuNPs caused cytotoxicity and increase of IL-8 levels at the highest dose. The AuNP were up-taken by the cells in the apical side and they also translocated in the basolateral side. Regarding the global transcript, among differentially expressed genes (DEG) were found genes related to the enhancement of immune cells. Conclusion: AuNPs in the used range of concentrations did not cause severe effects on the co-culture, but different effects were observed for the different types of AuNPs supporting the role of the physico-chemical NP parameters in NP-cell interactions. In addition, our model resulted perfectly suitable to investigate the biological effects of particles especially in terms of inflammatory response and translocation.

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Polar infection of Echovirus 30 causes differential barrier affection and gene regulation at the blood-CSF barrier

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