Local and Systemic Antibody Responses in Mice Immunized Intranasally with Native and Detergent-Extracted Outer Membrane Vesicles from<i>Neisseria meningitidis</i>

Guthrie, Terry; Wong, Siew Yee; Liang, Bin; Hyland, Lisa; Hou, Sam; Høiby, E. Arne; Andersen, Svein Rune

doi:10.1128/iai.72.5.2528-2537.2004

Cited by 25 publications

(15 citation statements)

References 52 publications

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“…In particular, using detergent-treated OMVs as a vaccine agent against N. meningitidis has been proposed and is being developed for clinical trial (32)(33)(34). Detergent-treated OMVs have the advantage in terms of increase in OMV yield, as treatment of detergent to bacteria increases vesicle release (34,37,38). However, studies comparing the protein composition of detergenttreated OMVs and native OMVs have shown a difference in the proteomic profiles (39).…”

Section: Discussionmentioning

confidence: 99%

Immunization with Escherichia coli Outer Membrane Vesicles Protects Bacteria-Induced Lethality via Th1 and Th17 Cell Responses

Kim

Hong

Park

et al. 2013

The Journal of Immunology

144

113

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Outer membrane vesicles (OMVs), secreted from Gram-negative bacteria, are spherical nanometer-sized proteolipids enriched with outer membrane proteins. OMVs, also known as extracellular vesicles, have gained interests for use as nonliving complex vaccines and have been examined for immune-stimulating effects. However, the detailed mechanism on how OMVs elicit the vaccination effect has not been studied extensively. In this study, we investigated the immunological mechanism governing the protective immune response of OMV vaccines. Immunization with Escherichia coli–derived OMVs prevented bacteria-induced lethality and OMV-induced systemic inflammatory response syndrome. As verified by adoptive transfer and gene-knockout studies, the protective effect of OMV immunization was found to be primarily by the stimulation of T cell immunity rather than B cell immunity, especially by the OMV-Ag–specific production of IFN-γ and IL-17 from T cells. By testing the bacteria-killing ability of macrophages, we also demonstrated that IFN-γ and IL-17 production is the main factor promoting bacterial clearances. Our findings reveal that E. coli–derived OMV immunization effectively protects bacteria-induced lethality and OMV-induced systemic inflammatory response syndrome primarily via Th1 and Th17 cell responses. This study therefore provides a new perspective on the immunological detail regarding OMV vaccination.

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Section: Discussionmentioning

confidence: 99%

Immunization with Escherichia coli Outer Membrane Vesicles Protects Bacteria-Induced Lethality via Th1 and Th17 Cell Responses

Kim

Hong

Park

et al. 2013

The Journal of Immunology

144

113

View full text Add to dashboard Cite

show abstract

“…Immunization with OMVs generates strong antigenspecific IgG and/or IgA antibody responses in the serum and in mucosal compartments 22,[76][77][78][79][80][81] . When introduced into the body, OMV antigens are presented by antigenpresenting cells (APCs) to CD4 + T cells 45,70,81,82 , which leads to the generation of antigen-specific B cell responses 45,78,82,83 .…”

Section: Presentation Of Omv Antigens Generation Of Protective Immunementioning

confidence: 99%

Immune modulation by bacterial outer membrane vesicles

2015

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Gram-negative bacteria shed extracellular outer membrane vesicles (OMVs) during their normal growth both in vitro and in vivo. OMVs are spherical, bilayered membrane nanostructures that contain many components found within the parent bacterium. Until recently, OMVs were dismissed as a by-product of bacterial growth; however, findings within the past decade have revealed that both pathogenic and commensal bacteria can use OMVs to manipulate the host immune response. In this Review, we describe the mechanisms through which OMVs induce host pathology or immune tolerance, and we discuss the development of OMVs as innovative nanotechnologies.

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“…or intravenous immunization and high levels of IgA after i.n. immunization (36,83). In this study, we analyzed Ig titers in sera only.…”

Section: Discussionmentioning

confidence: 99%

Immunization with Vibrio cholerae Outer Membrane Vesicles Induces Protective Immunity in Mice

2008

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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.The devastating diarrheal disease cholera is caused by the gram-negative, motile, curved-rod bacterium Vibrio cholerae (56). Over 200 serogroups of V. cholerae have been identified; however, epidemics are caused only by strains of serogroup O1 and the recently emerged serogroup O139 (27). Cholera is transmitted via the fecal-oral route. The infectious dose can vary tremendously, from 10 3 to 10 11 cells, depending on multiple factors, including the specific V. cholerae isolate as well as the diet, age, blood type, and health status of the patient (16,61,79). In addition, it has been recently reported that V. cholerae secreted by the host is more infectious than in vitrocultured V. cholerae (1,12,63). The existence of such a hyperinfectious state is supported by a mathematical model based on epidemiological data (41) and could help to explain the explosive nature of cholera outbreaks.Soon after oral ingestion, V. cholerae reaches the small bowel, its primary site of colonization, and induces virulence factors, such as toxin-coregulated pilus (TCP) and cholera toxin (CT) (17,42,87). A complex regulatory cascade including ToxT as well as the inner membrane proteins ToxR/S and TcpP/H controls the expression of virulence factors (54, 78). With the infant mouse and rabbit ileal loop animal models of infection, several factors of V. cholerae have been demonstrated to be important for colonization. Interestingly, a large number of these factors are associated with the outer membrane (OM), including lipopolysaccharide (LPS), OM porins (OMPs), TCP, and flagella (5,19,68,73,...

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Local and Systemic Antibody Responses in Mice Immunized Intranasally with Native and Detergent-Extracted Outer Membrane Vesicles fromNeisseria meningitidis

Cited by 25 publications

References 52 publications

Immunization with Escherichia coli Outer Membrane Vesicles Protects Bacteria-Induced Lethality via Th1 and Th17 Cell Responses

Immunization with Escherichia coli Outer Membrane Vesicles Protects Bacteria-Induced Lethality via Th1 and Th17 Cell Responses

Immune modulation by bacterial outer membrane vesicles

Immunization with Vibrio cholerae Outer Membrane Vesicles Induces Protective Immunity in Mice

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