ArticlePLoS neglected tropical diseases2025
Distinct strategies of epithelial cell barrier disruption by Leptospira interrogans isolated from human patients in Okinawa, Japan.
Article in PLoS neglected tropical diseases, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Abstract
backgroundLeptospirosis is a bacterial infection common in tropical and subtropical regions, which causes feverish conditions. Although approximately half of human leptospirosis cases in Japan are reported in Okinawa, a subtropical area, the pathogenic mechanisms of clinical isolates from this region remain unknown. This study aimed to identify the infection mechanisms of L. interrogans isolates from Okinawa (Oki-strains) in human renal proximal tubule epithelial cells (RPTECs). METHODOLOGY/PRINCIPAL
findingsThe transepithelial electrical resistance (TEER) measurements of 11 Oki-strains in infected renal proximal tubule epithelial cells (RPTECs) showed that all strains caused a decrease in TEER by 48 hours post-infection. Imaging analysis of RPTECs infected with two selected strains (Oki53 and Oki65) revealed that both strains induced the displacement of adherens junction (AJ) proteins E-cadherin, α-catenin, afadin, and nectin-2 and cytoskeletal F-actin disorganization. However, western blotting analysis revealed that AJ protein levels were not reduced, except for afadin-an important protein for linking F-actin to AJs. Chemical inhibition revealed that the proteosome inhibitors MG132 and bortezomib and pan-caspase inhibitor Z-VAD-FMK prevented the Oki53-induced TEER decrease, AJ protein mislocalization, afadin degradation, and F-actin disorganization. However, in Oki65-infected RPTECs, the inhibitors partially prevented these effects. Thus, the AJ-F-actin link and epithelial barrier were fully preserved in Oki53-infected RPTECs pretreated with these inhibitors at 24 h post-infection (~TEER 130% of initial TEER), whereas in Oki65-infected cells, the AJ-F-actin link was maintained only partially (~TEER 70%). CONCLUSIONS/SIGNIFICANCE: Our findings suggest that the maintenance of epithelial barrier integrity requires both the afadin-F-actin and α-catenin-F-actin links, and that Oki53 and Oki65 employ distinct strategies to disrupt the AJ-F-actin link and, thus, the epithelial barrier.
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