Treatment with the antigranulocyte monoclonal antibody RB6-8C5 impairs resistance of mice to gastrointestinal infection with Listeria monocytogenes

Czuprynski, Charles J.; Theisen, Cara H.; Brown, James F.

doi:10.1128/iai.64.9.3946-3949.1996

Cited by 32 publications

(14 citation statements)

References 26 publications

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“…idly controlled, requiring the use of immunosuppression by polymorphonuclear depletion (Czuprynski et al, 1996) to induce a continuous bacterial growth in the bone marrow and CNS infection (data not shown). Therefore we used the intravenous model of acute listeriosis, allowing the determination of phenotypes of bone marrow and blood infected cells during the induction of a reproducible CNS invasion.…”

Section: Bone Marrow Infection During Listeriosissupporting

confidence: 93%

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Join‐Lambert

Ezine

Monnier

et al. 2004

Cellular Microbiology

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Section: Bone Marrow Infection During Listeriosissupporting

confidence: 93%

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Join‐Lambert

Ezine

Monnier

et al. 2004

Cellular Microbiology

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“…Although L. monocytogenes bacteria can induce systemic infection causing spontaneous abortion, septicemia, and meningitis, anti-L. monocytogenes immunity in humans has not been defined. In murine models of systemic L. monocytogenes infection, mice deficient in neutrophils exhibit increased bacterial burden during early L. monocytogenes infection (14)(15)(16). In addition, murine IFN-g, IL-23, IL-17, and CD8 + T cells have been shown to play a role in protection against L. monocytogenes infection (17)(18)(19)(20)(21).…”

mentioning

confidence: 99%

Multieffector-Functional Immune Responses of HMBPP-Specific Vγ2Vδ2 T Cells in Nonhuman Primates Inoculated with Listeria monocytogenes ΔactA prfA *

Ryan-Payseur

Frencher

Shen

et al. 2012

The Journal of Immunology

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Although Listeria monocytogenes can induce systemic infection causing spontaneous abortion, septicemia, and meningitis, studies have not been performed to investigate human anti-L. monocytogenes immune responses, including those of Ag-specific Vγ2Vδ2 T cells, a dominant human γδ T cell subset. L. monocytogenes is the only pathogen known to possess both the mevalonate and non-mevalonate isoprenoid biosynthesis pathways that produce metabolic phosphates or phosphoantigens activating human Vγ2Vδ2 T cells, making it interesting to explore in vivo anti-L. monocytogenes immune responses of Vγ2Vδ2 T cells. In this study, we demonstrated that subclinical systemic L. monocytogenes infection of rhesus macaques via parenteral inoculation or vaccination with an attenuated Listeria strain induced multieffector-functional immune responses of phosphoantigen-specific Vγ2Vδ2 T cells. Subclinical systemic infection and reinfection with attenuated L. monocytogenes uncovered the ability of Vγ2Vδ2 T cells to mount expansion and adaptive or recall-like expansion. Expanded Vγ2Vδ2 T cells could traffic to and accumulate in the pulmonary compartment and intestinal mucosa. Expanded Vγ2Vδ2 T cells could evolve into effector cells producing IFN-γ, TNF-α, IL-4, IL-17, or perforin after L. monocytogenes infection, and some effector Vγ2Vδ2 T cells could coproduce IL-17 and IFN-γ, IL-4 and IFN-γ, or TNF-α and perforin. Surprisingly, in vivo-expanded Vγ2Vδ2 T effector cells in subclinical L. monocytogenes infection could directly lyse L. monocytogenes-infected target cells and inhibit intracellular L. monocytogenes bacteria. Thus, we present the first demonstration, to our knowledge, of multieffector-functional Vγ2Vδ2 T cell responses against L. monocytogenes.

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“…Other studies suggested that preventing gastric acidity or emulsifying the L, monocytogenes inoculum in a food product can enhance the severity of infection (19)(20). Usually there is httle sign of local invasion or multiplication of L, monocytogenes in the intestinal mucosa (21)(22). Bacteriological and histopathological analyses have documented invasion via Peyer's patches or intestinal epithelial cells (16,21).…”

Section: Experimental Gastrointestinal Infection With L Monocytogenesmentioning

confidence: 99%

“…Even when high challenge doses are used successfully to initiate systemic infection, there are usually few or no lesions in the intestinal mucosa (21,22,103). In addition, L. monocytogenes is rapidly diluted in the intestinal tract and is difficult to recover from intestinal contents more than a few days after g.i.…”

Section: Fig I a Simphbed Illustration Ofthe Hopelessly Complex Intmentioning

confidence: 99%

“…Our results demonstrated that neutrophil depletion, by administration of ihe aniigranulocyte MAb RB6-8C5, dramatically impaired resistance to an i.g. challenge with L. monocytogenes (22), As a result of such treatment, 60% ofthe mice died after l,g. inoculation with as few as 4 x 10* CFU L, monocytogenes, whereas inoculation with 4x10* CFU resulted in the death of only 20% of the control mice (22).…”

Section: Fig I a Simphbed Illustration Ofthe Hopelessly Complex Intmentioning

confidence: 99%

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Non‐specific resistance mechanisms to listeriosis: implications for experimental and naturally occurring infection

Czuprynski

Haak‐Frendscho

1997

Immunological Reviews

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Use of murine listeriosis as an experimental model has greatly increased our understanding of the complex interplay of cells and mediators in non-specific antibacterial resistance (innate immunity). Important contributions made with this experimental model include demonstrating the ability of inflammatory cytokines (i.e. IFN-gamma, IL-1 alpha, TNF-alpha) to protect against bacterial infection, and illustrating the rapidity of the host cytokine response (detectable within 1 h of challenge) during bacterial infection. Most experimental studies of host defense against Listeria monocytogenes (L. monocytogenes) have used a parenteral challenge (i.v. or i.p.). This ignores the pathogenesis of naturally occurring listeriosis, which usually results from ingestion of Listeria-contaminated food products. In this review, we will include consideration of the host-pathogen interactions that occur when L. monocytogenes invades through its natural portal of entry, the gastrointestinal tract. Although resistance to facultative intracellular pathogens, such as L. monocytogenes, was formerly thought to revolve exclusively around the T helper cell/macrophage axis, more recent evidence indicates that neutrophils are able to ingest and kill L. monocytogenes and prevent the unrestricted multiplication of listeriae in parenchymal cells. Exploring the mechanisms involved in this process will provide new insights into the communication between leukocytes and tissue cells in host defense.

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Treatment with the antigranulocyte monoclonal antibody RB6-8C5 impairs resistance of mice to gastrointestinal infection with Listeria monocytogenes

Cited by 32 publications

References 26 publications

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Listeria monocytogenes-infected bone marrow myeloid cells promote bacterial invasion of the central nervous system

Multieffector-Functional Immune Responses of HMBPP-Specific Vγ2Vδ2 T Cells in Nonhuman Primates Inoculated with Listeria monocytogenes ΔactA prfA *

Non‐specific resistance mechanisms to listeriosis: implications for experimental and naturally occurring infection

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