OmpF porin from Yersinia ruckeri as pathogenic factor: Surface antigenic sites and biological properties

TY - JOUR

T1 - OmpF porin from Yersinia ruckeri as pathogenic factor: Surface antigenic sites and biological properties

AU - Portnyagina, Olga

AU - Chistyulin, Dmitry

AU - Dyshlovoy, Sergey

AU - Davidova, Viktoriya

AU - Khomenko, Valentina

AU - Shevchenko, Ludmila

AU - Novikova, Olga

N1 - Copyright © 2020 Elsevier Ltd. All rights reserved.

PY - 2021/1

Y1 - 2021/1

N2 - Bacterium Yersinia ruckeri as a pathogen induces causative agent of intestinal fish disease called enteric redmouth disease (ERM) is known. In this study, outer membrane OmpF porin from the Y. ruckeri (YrOmpF) has been identified as a pathogenic factor which affects host macrophage activation and life cycle of eukaryotic cells. Using synthetic peptides corresponding to the sequences of the outer loops of YrOmpF L1 loop of the porin is most involved in the structure of B epitopes on the surface of the microbial cell it was found. T epitopes of the isolated YrOmpF trimer not only by linear, but also by discontinuous determinants, which is due to the secondary structure of the protein are represented. It was shown that YrOmpF was twice more cytotoxic to THP-1 cells (human monocytes, cancer cells) in comparison with CHH-1 cells (Oncorhynchus keta cardiac muscle cell, non-cancer cells). It was found YrOmpF induce cell cycle S-phase arrest in both normal CHH-1 and cancer THP-1 cells. In the cancer cells observed effect was most pronounce. In addition, we have observed an induction of apoptosis in THP-1 cell line treated with YrOmpF for 48 h at IC50 (48.6 μg/ml). Significant cytotoxic effect of YrOmpF on primary mouse peritoneal macrophages been detected as well. Of note, co-incubation of macrophages with anti-YrOmpF antibodies could decrease the amount of lactate dehydrogenase, while the number of living cells significantly increased. YrOmpF stimulates the activity of the phagocytic bactericidal systems especially of the oxygen-independent subsystem it was found. Antibodies against YrOmpF decreased MPO release and CP synthesis by peritoneal macrophages and increased their viability.

AB - Bacterium Yersinia ruckeri as a pathogen induces causative agent of intestinal fish disease called enteric redmouth disease (ERM) is known. In this study, outer membrane OmpF porin from the Y. ruckeri (YrOmpF) has been identified as a pathogenic factor which affects host macrophage activation and life cycle of eukaryotic cells. Using synthetic peptides corresponding to the sequences of the outer loops of YrOmpF L1 loop of the porin is most involved in the structure of B epitopes on the surface of the microbial cell it was found. T epitopes of the isolated YrOmpF trimer not only by linear, but also by discontinuous determinants, which is due to the secondary structure of the protein are represented. It was shown that YrOmpF was twice more cytotoxic to THP-1 cells (human monocytes, cancer cells) in comparison with CHH-1 cells (Oncorhynchus keta cardiac muscle cell, non-cancer cells). It was found YrOmpF induce cell cycle S-phase arrest in both normal CHH-1 and cancer THP-1 cells. In the cancer cells observed effect was most pronounce. In addition, we have observed an induction of apoptosis in THP-1 cell line treated with YrOmpF for 48 h at IC50 (48.6 μg/ml). Significant cytotoxic effect of YrOmpF on primary mouse peritoneal macrophages been detected as well. Of note, co-incubation of macrophages with anti-YrOmpF antibodies could decrease the amount of lactate dehydrogenase, while the number of living cells significantly increased. YrOmpF stimulates the activity of the phagocytic bactericidal systems especially of the oxygen-independent subsystem it was found. Antibodies against YrOmpF decreased MPO release and CP synthesis by peritoneal macrophages and increased their viability.

U2 - 10.1016/j.micpath.2020.104694

DO - 10.1016/j.micpath.2020.104694

M3 - SCORING: Journal article

C2 - 33359075

VL - 150

SP - 104694

JO - MICROB PATHOGENESIS

JF - MICROB PATHOGENESIS

SN - 0882-4010

ER -