Abstract
Retinal infection with Toxoplasma gondii—ocular toxoplasmosis—is a common cause of vision impairment worldwide. Pathology combines parasite-induced retinal cell death and reactive intraocular inflammation. Müller glial cells, which represent the supporting cell population of the retina, are relatively susceptible to infection with T. gondii. We investigated expression of long non-coding RNAs (lncRNAs) with immunologic regulatory activity in Müller cells infected with virulent T. gondii strains—GT1 (haplogroup 1, type I) and GPHT (haplogroup 6). We first confirmed expression of 33 lncRNA in primary cell isolates. MIO-M1 human retinal Müller cell monolayers were infected with T. gondii tachyzoites (multiplicity of infection = 5) and harvested at 4, 12, 24, and 36 h post-infection, with infection being tracked by the expression of parasite surface antigen 1 (SAG1). Significant fold-changes were observed for 31 lncRNAs at one or more time intervals. Similar changes between strains were measured for BANCR, CYTOR, FOXD3-AS1, GAS5, GSTT1-AS1, LINC-ROR, LUCAT1, MALAT1, MIR22HG, MIR143HG, PVT1, RMRP, SNHG15, and SOCS2-AS1. Changes differing between strains were measured for APTR, FIRRE, HOTAIR, HOXD-AS1, KCNQ1OT1, LINC00968, LINC01105, lnc-SGK1, MEG3, MHRT, MIAT, MIR17HG, MIR155HG, NEAT1, NeST, NRON, and PACER. Our findings suggest roles for lncRNAs in regulating retinal Müller cell immune responses to T. gondii, and encourage future studies on lncRNA as biomarkers and/or drug targets in ocular toxoplasmosis.
Highlights
Toxoplasma gondii is a ubiquitously distributed protozoan parasite that may infect any warm blooded animal [1]
Because of the large number of cells needed for the infectivity studies, it was necessary to use a cell line, and, this first stage of our work served to confirm that the long non-coding RNAs (lncRNAs) to be studied in the MIO-M1 cell line were expressed by primary Müller cells
Little research has been published on the response of human retinal Müller cells to infection with T. gondii, these cells are the key supporting cells within the retina, and ocular toxoplasmosis is a common retinal infection
Summary
Toxoplasma gondii is a ubiquitously distributed protozoan parasite that may infect any warm blooded animal [1]. Ocular toxoplasmosis follows the entry of T. gondii into and replication within the retina, which is associated with a vigorous inflammatory reaction; the inflammation may reach other ocular tissues, such as choroid, vitreous, or more rarely the optic nerve [1,2]. In Western Europe and North America, where 2% of the T. gondii seropositive population have retinal lesions, most of the parasite strains belong to type I, II, and III, and haplogroup 12 clonal lineages [6,7]. In South America, many non-clonal haplogroups are found [8,9,10], which are linked to more severe presentations and a higher prevalence of retinal lesions, reaching as high as 17% [11,12,13]
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