scholarly journals Faculty Opinions recommendation of Vibrio cholerae Outer Membrane Vesicles Inhibit Bacteriophage Infection.

Author(s):  
Chris Waters
Toxins ◽  
2019 ◽  
Vol 11 (4) ◽  
pp. 207 ◽  
Author(s):  
Elnaz Rasti ◽  
Angela Brown

Cholera toxin (CT), the major virulence factor of Vibrio cholerae, is an AB5 toxin secreted through the type II secretion system (T2SS). Upon secretion, the toxin initiates endocytosis through the interaction of the B pentamer with the GM1 ganglioside receptor on small intestinal cells. In addition to the release of CT in the free form, the bacteria secrete CT in association with outer membrane vesicles (OMVs). Previously, we demonstrated that strain 569B releases OMVs that encapsulate CT and which interact with host cells in a GM1-independent mechanism. Here, we have demonstrated that OMV-encapsulated CT, while biologically active, does not exist in an AB5 form; rather, the OMVs encapsulate two enzymatic A-subunit (CTA) polypeptides. We further investigated the assembly and secretion of the periplasmic CT and found that a major fraction of periplasmic CTA does not participate in the CT assembly process and instead is continuously encapsulated within the OMVs. Additionally, we found that the encapsulation of CTA fragments in OMVs is conserved among several Inaba O1 strains. We further found that under conditions in which the amount of extracellularly secreted CT increases, the concentration of OMV-encapsulated likewise CTA increases. These results point to a secondary mechanism for the secretion of biologically active CT that does not depend on the CTB-GM1 interaction for endocytosis.


2016 ◽  
Vol 8 (3) ◽  
pp. 269-283 ◽  
Author(s):  
Kyaw Min Aung ◽  
Annika E. Sjöström ◽  
Ulrich von Pawel-Rammingen ◽  
Kristian Riesbeck ◽  
Bernt Eric Uhlin ◽  
...  

Cholera epidemics are caused by Vibrio cholerae serogroups O1 and O139, whereas strains collectively known as non-O1/non-O139 V. cholerae are found in cases of extraintestinal infections and bacteremia. The mechanisms and factors influencing the occurrence of bacteremia and survival of V. cholerae in normal human serum have remained unclear. We found that naturally occurring IgG recognizing V. cholerae outer membrane protein U (OmpU) mediates a serum-killing effect in a complement C1q-dependent manner. Moreover, outer membrane vesicles (OMVs) containing OmpU caused enhanced survival of highly serum-sensitive classical V. cholerae in a dose-dependent manner. OMVs from wild-type and ompU mutant V. cholerae thereby provided a novel means to verify by extracellular transcomplementation the involvement of OmpU. Our data conclusively indicate that loss, or reduced expression, of OmpU imparts resistance to V. cholerae towards serum killing. We propose that the difference in OmpU protein levels is a plausible reason for differences in serum resistance and the ability to cause bacteremia observed among V. cholerae biotypes. Our findings provide a new perspective on how naturally occurring antibodies, perhaps induced by members of the microbiome, may play a role in the recognition of pathogens and the provocation of innate immune defense against bacteremia.


2011 ◽  
Vol 205 (3) ◽  
pp. 412-421 ◽  
Author(s):  
Anne L. Bishop ◽  
Abdullah A. Tarique ◽  
Bharathi Patimalla ◽  
Stephen B. Calderwood ◽  
Firdausi Qadri ◽  
...  

2008 ◽  
Vol 76 (10) ◽  
pp. 4554-4563 ◽  
Author(s):  
Stefan Schild ◽  
Eric J. Nelson ◽  
Andrew Camilli

ABSTRACT The gram-negative bacterium Vibrio cholerae releases outer membrane vesicles (OMVs) during growth. In this study, we immunized female mice by the intranasal, intragastric, or intraperitoneal route with purified OMVs derived from V. cholerae. Independent of the route of immunization, mice induced specific, high-titer immune responses of similar levels against a variety of antigens present in the OMVs. After the last immunization, the half-maximum total immunoglobulin titer was stable over a 3-month period, indicating that the immune response was long lasting. The induction of specific isotypes, however, was dependent on the immunization route. Immunoglobulin A, for example, was induced to a significant level only by mucosal immunization, with the intranasal route generating the highest titers. We challenged the offspring of immunized female mice with V. cholerae via the oral route in two consecutive periods, approximately 30 and 95 days after the last immunization. Regardless of the route of immunization, the offspring was protected against colonization with V. cholerae in both challenge periods. Our results show that mucosal immunizations via both routes with OMVs derived from V. cholerae induce long-term protective immune responses against this gastrointestinal pathogen. These findings may contribute to the development of “nonliving,” OMV-based vaccines against V. cholerae and other enteric pathogens, using the oral or intranasal route of immunization.


2015 ◽  
Vol 6 ◽  
Author(s):  
Deborah R. Leitner ◽  
Sabine Lichtenegger ◽  
Philipp Temel ◽  
Franz G. Zingl ◽  
Desiree Ratzberger ◽  
...  

Vaccine ◽  
2018 ◽  
Vol 36 (2) ◽  
pp. 322-330 ◽  
Author(s):  
Rezaei Adriani ◽  
Seyed Latif Mousavi Gargari ◽  
Shahram Nazarian ◽  
Samaneh Sarvary ◽  
Nafiseh Noroozi

2010 ◽  
Vol 78 (10) ◽  
pp. 4402-4420 ◽  
Author(s):  
Anne L. Bishop ◽  
Stefan Schild ◽  
Bharathi Patimalla ◽  
Brian Klein ◽  
Andrew Camilli

ABSTRACTVibrio choleraeis the causative agent of cholera, a severe diarrheal disease that remains endemic in many parts of the world and can cause outbreaks wherever sanitation and clean water systems break down. Prevention of disease could be achieved through improved sanitation and clean water provision supported by vaccination.V. choleraeserogroup O1 is the major cause of cholera; O1 serotypes Inaba and Ogawa have similar disease burdens, while O139 is the only non-O1 serogroup to cause epidemics. We showed previously that immunization of adult female mice with purifiedV. choleraeouter membrane vesicles (OMVs) elicits an antibody response that protect neonates from oralV. choleraechallenge and that suckling from an immunized dam accounts for the majority of protection fromV. choleraecolonization. Here we report that lipopolysaccharide (LPS) is the major OMV protective antigen. Mucosal immunization with OMVs from Inaba or Ogawa provides significant cross-serotype protection fromV. choleraecolonization, although serotype-specific antigens are dominant. OMVs from O1 or O139 do not provide cross-serogroup protection, but by immunization with a mixture of O1 and O139 OMVs, cross-serogroup protection was achieved. Neonatal protection is not associated with significant bacterial death but may involve inhibition of motility, as antibodies from OMV-immunized mice inhibitV. choleraemotilityin vitro, with trends that parallelin vivoprotection. Motility assays also reveal that a higher antibody titer is required to immobilize O139 compared to O1, a phenotype that is O139 capsule dependent.


2010 ◽  
Vol 60 (1) ◽  
pp. 18-27 ◽  
Author(s):  
Nivedita Roy ◽  
Soumik Barman ◽  
Amit Ghosh ◽  
Amit Pal ◽  
Krishnendu Chakraborty ◽  
...  

Author(s):  
Manijeh Sedaghat ◽  
Seyed Davar Siadat ◽  
Esmat Mirabzadeh ◽  
Malihe Keramati ◽  
Farzam Vaziri ◽  
...  

Background and Objectives: Cholera disease remains an important global health problem affecting 3-5 million subjects worldwide. Outer membrane vesicles (OMVs) have been found in a variety of Gram-negative bacteria and act as protective transport vesicles. The aim of this study was to evaluate Immune responses against Vibrio cholerae O1 El Tor clinical strain OMV and compare it with killed whole cell (KWC), complex of (KWC-OMV) as well as the internationally licensed oral cholera vaccine, Dukoral, in serum and intestinal secretions of mice. Materials and Methods: OMVs were prepared by using modified detergent-centrifugation procedure from V. cholerae O1 El Tor clinical strain from 2005 outbreak. The ultrastructure and content of OMVs were investigated via the Scanning Elec- tron Microscopy (SEM) and SDS-PAGE analysis. Three doses of oral immunization were adjusted and total IgG and IgA in serum and intestinal secretion were measured by enzyme-linked immunosorbent assay (ELISA). Results: Extracted OMVs from the V. cholerae were spherical vesicles with a size ranging from 10 to 300 nm. OMV-im- munized mice showed an increased level of total IgG and IgA both in serum and intestinal secretion when compared to the negative controls. Also, there existed a higher level of secretory IgA than the total IgG, suggesting the most of protection against V. cholerae colonization provided by sIgA. Conclusion: Our findings revealed that oral immunization with V. cholerae OMVs might induce a long-term immunity, es- pecially when administered in combination with KWC. This study tested the adjuvant activity of OMVs and may be useful in future nano vaccine research.


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