Reduced Transendothelial Migration of Monocytes Infected by<i>Coxiella burnetii</i>

Dellacasagrande, Jérôme; Moulin, Pierre A.; Guilianelli, Catherine; Capo, Christian; Raoult, Didier; Grau, Georges E.; Mège, Jean‐Louis

doi:10.1128/iai.68.6.3784-3786.2000

Cited by 11 publications

(5 citation statements)

References 15 publications

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“…In response to chemoattractants, only monocytes from patients with Wiskott-Aldrich syndrome poorly migrate across EC monolayers [10]. Deficient TM was found to be specific to C. burnetii infection: C. burnetii decreased TM of PBMCs, which is consistent with the effect that C. burnetii has been reported to have on TM of THP-1 monocytic cells [11], whereas stimulation with PHA resulted in substantial TM of PBMCs from patients with Q fever endocarditis. However, any direct effect that C. burnetii infection has on PBMCs is unlikely to account for deficient TM in patients with Q fever endocarditis; therefore, one could infer that C. burnetii instead acts through indirect means.…”

supporting

confidence: 81%

Deficient Transendothelial Migration of Leukocytes in Q Fever: The Role Played by Interleukin‐10

et al. 2006

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Chronic Q fever is characterized by deficient cell-mediated immune response, lack of granulomas, and dysregulation of the cytokine network. Altered transendothelial migration (TM) of peripheral-blood mononuclear cells might account for impaired immune response. TM of lymphocytes and monocytes was decreased in patients with Q fever endocarditis, compared with that in patients recovering from acute Q fever and in control subjects. This defect is related to interleukin (IL)-10, a cytokine involved in the chronic evolution of the disease; neutralizing anti-IL-10 antibodies corrected TM of mononuclear cells from patients with Q fever endocarditis. IL-10 may account for deficient protective immunity in patients with Q fever endocarditis by impairing TM.

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supporting

confidence: 81%

Deficient Transendothelial Migration of Leukocytes in Q Fever: The Role Played by Interleukin‐10

et al. 2006

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“…The presence of such apoptotic macrophages in lung granulomas of mice infected with Mycobacterium tuberculosis supports this hypothesis (38). The overproduction of inflammatory cytokines observed in the context of chronic Q fever (39) could result, in vivo, in increased adherence of C. burnetii-infected monocytes to the endothelium, as shown in vitro (40). Thus, in patients with chronic Q fever, infected monocytes might escape cell contact-dependent apoptosis induced by IFN-␥ by promoting heterotypic interactions with endothelial cells rather than proapoptotic homotypic contacts.…”

Section: Discussionmentioning

confidence: 61%

IFN-γ-Induced Apoptosis and Microbicidal Activity in Monocytes Harboring the Intracellular Bacterium Coxiella burnetii Require Membrane TNF and Homotypic Cell Adherence

Dellacasagrande

Ghigo

Raoult

et al. 2002

The Journal of Immunology

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IFN-gamma is critical for the protection against intracellular bacteria through activation of the antimicrobial machinery of phagocytes. Coxiella burnetii, the etiological agent of Q fever, is a strictly intracellular bacterium that inhabits monocytes/macrophages. We previously showed that IFN-gamma induced C. burnetii killing by promoting the apoptosis of infected monocytes. We show in this study that IFN-gamma-induced apoptosis of infected monocytes was characterized by a time- and dose-dependent activation of caspase-3. IFN-gamma-mediated caspase-3 activation and C. burnetii killing depend on the expression of membrane TNF. Indeed, TNF was transiently expressed on the cell surface of infected monocytes a few hours after IFN-gamma treatment. In addition, anti-TNF Abs inhibited IFN-gamma-mediated caspase-3 activation whereas soluble TNF had no effect on infected cells. Concomitantly, IFN-gamma induced homotypic adherence of C. burnetii-infected monocytes. The latter required the interaction of beta(2) integrins with CD54. When adherence was disrupted by pipetting, by a combination of Abs specific for CD11b, CD18, and CD54, or by an antisense oligonucleotide targeting CD18 mRNA, both cell apoptosis and bacterial killing induced by IFN-gamma were inhibited. Thus, adherence via CD54/beta(2) integrins together with membrane TNF are required to eliminate C. burnetii-infected cells through cell contact-dependent apoptosis. Our results reveal a new component of the antimicrobial arsenal mobilized by IFN-gamma against infection by intracellular bacteria.

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“…Interestingly, C. burnetii is one of the few organisms studied from the perspective of the way in which intracellular infection of monocytes alters their interactions with endothelial cells. Dellacasagrande et al reported that infection of THP-1 cells with a virulent strain of C. burnetii increased cellular adhesion to a TNF-␣-stimulated human microvascular cell line but transmigration across the cell monolayers was significantly inhibited (81). The authors suggested that decreased transmigration might interfere with localization of the bacterium to target tissues and/or may contribute to the formation of poorly formed granulomas that are found in chronic Q fever.…”

Section: Rickettsiaceaementioning

confidence: 99%

Invasion of the Central Nervous System by Intracellular Bacteria

2004

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Infection of the central nervous system (CNS) is a severe and frequently fatal event during the course of many diseases caused by microbes with predominantly intracellular life cycles. Examples of these include the facultative intracellular bacteria Listeria monocytogenes, Mycobacterium tuberculosis, and Brucella and Salmonella spp. and obligate intracellular microbes of the Rickettsiaceae family and Tropheryma whipplei. Unfortunately, the mechanisms used by intracellular bacterial pathogens to enter the CNS are less well known than those used by bacterial pathogens with an extracellular life cycle. The goal of this review is to elaborate on the means by which intracellular bacterial pathogens establish infection within the CNS. This review encompasses the clinical and pathological findings that pertain to the CNS infection in humans and includes experimental data from animal models that illuminate how these microbes enter the CNS. Recent experimental data showing that L. monocytogenes can invade the CNS by more than one mechanism make it a useful model for discussing the various routes for neuroinvasion used by intracellular bacterial pathogens

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Reduced Transendothelial Migration of Monocytes Infected byCoxiella burnetii

Cited by 11 publications

References 15 publications

Deficient Transendothelial Migration of Leukocytes in Q Fever: The Role Played by Interleukin‐10

Deficient Transendothelial Migration of Leukocytes in Q Fever: The Role Played by Interleukin‐10

IFN-γ-Induced Apoptosis and Microbicidal Activity in Monocytes Harboring the Intracellular Bacterium Coxiella burnetii Require Membrane TNF and Homotypic Cell Adherence

Invasion of the Central Nervous System by Intracellular Bacteria

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