The 75-kD tumour necrosis factor (TNF) receptor is specificallyup-regulated in monocytes during Q fever endocarditis

Ghigo, Éric; Capo, Christian; Amirayan, Nathalie; Raoult, Didier; Mège, Jean‐Louis

doi:10.1046/j.1365-2249.2000.01311.x

Cited by 14 publications

(9 citation statements)

References 31 publications

(42 reference statements)

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“…This finding agrees with previous reports that IL-10 increases the release of TNF-RII (24). It may be related to recent reports that chronic Q fever is associated with IL-10 overproduction (6), a defect in C. burnetii killing (10), and an increase in TNF-RII release (16). As soluble TNF-RII is known to antagonize the activity of TNF, it is likely that its upregulation amplifies the monocyte deactivation mediated by IL-10.…”

Section: Discussionsupporting

confidence: 93%

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Interleukin-10 StimulatesCoxiella burnetiiReplication in Human Monocytes through Tumor Necrosis Factor Down-Modulation: Role in Microbicidal Defect of Q Fever

et al. 2001

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Coxiella burnetii, an obligate intracellular bacterium, is the agent of Q fever. The chronic form of the disease is associated with the overproduction of interleukin-10 and deficient C. burnetii killing by monocytes. We hypothesized that the replication of C. burnetii inside monocytes requires a macrophage-deactivating cytokine such as interleukin-10. In the absence of interleukin-10, C. burnetii survived but did not replicate in monocytes. C. burnetii replication (measured 15 days) was induced in interleukin-10-treated monocytes. This effect of interleukin-10 is specific since transforming growth factor ␤1 had no effect on bacterial replication. C. burnetii replication involves the down-modulation of tumor necrosis factor (TNF) release. First, interleukin-10 suppressed C. burnetii-stimulated production of TNF. Second, the addition of recombinant TNF to interleukin-10-treated monocytes inhibited bacterial replication. Third, the incubation of infected monocytes with neutralizing anti-TNF antibodies favored C. burnetii replication. On the other hand, deficient C. burnetii killing by monocytes from patients with chronic Q fever involves interleukin-10. Indeed, C. burnetii replication was observed in monocytes from patients with Q fever endocarditis, but not in those from patients with acute Q fever. Bacterial replication was inhibited by neutralizing anti-interleukin-10 antibodies. As monocytes from patients with endocarditis overproduced interleukin-10, the defective bacterial killing is likely related to endogenous interleukin-10. These results suggest that interleukin-10 enables monocytes to support C. burnetii replication and to favor the development of chronic Q fever.

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Section: Discussionsupporting

confidence: 93%

“…In the absence of regulatory cytokines, C. burnetii elicited a steady increase in TNF-RII release within 48 h of incubation (Fig. 4B), confirming recent results (16). IL-10 amplified C. burnetii-stimulated release of TNF-RII at 0 and 8 h postinfection (P Ͻ 0.05).…”

Section: Il-10 Induces the Replication Of C Burnetii In Monocytessupporting

confidence: 88%

Interleukin-10 StimulatesCoxiella burnetiiReplication in Human Monocytes through Tumor Necrosis Factor Down-Modulation: Role in Microbicidal Defect of Q Fever

et al. 2001

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“…Chronic persistence of C. burnetii within human monocytes is well described and is associated with increased cellular secretion of TNF-␣ (80), IL-10, and transforming growth factor ␤1 (53). Overproduction of IL-10 may play a role in inhibiting the bactericidal activity of the host cell by altering cellular responses to TNF-␣ (130,132). 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.…”

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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“…The coxiellas in valves are readily detected by animal inoculation, cell culture or PCR gene amplification. Studies by French workers 7,8 of cytokine response or release patterns from monocytes or PBMC from endocarditis patients have shown upregulated IL-10 and TNFa production, downregulated IFNg responses with increased TNF-R 75 production.…”

mentioning

confidence: 99%

Variation in immune response genes and chronic Q fever. Concepts: preliminary test with post-Q fever fatigue syndrome

Helbig¹,

Heatley

Harris³

et al. 2003

Genes Immun

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Acute primary Q fever is followed by various chronic sequelae. These include subacute Q fever endocarditis, granulomatous reactions in various organs or a prolonged debilitating post-infection fatigue syndrome (QFS). The causative organism, Coxiella burnetii, persists after an initial infection. The differing chronic outcomes may reflect variations within cytokine and accessory immune control genes which affect regulation of the level of persistence. As a preliminary test of the concept we have genotyped QFS patients and controls for gene variants spanning 15 genes and also examined HLA-B and DR frequencies. QFS patients exhibited a significantly increased frequency of HLA-DR-11 compared with controls and also significant differences in allelic variant frequencies within the NRAMP, and IFNg genes. These results indicate a possible genetic role in the expression of overt chronic Q fever. Further studies will be undertaken to increase sample sizes, to survey other forms of chronic Q fever and to examine Q fever patients who have recovered without sequelae.

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The 75-kD tumour necrosis factor (TNF) receptor is specificallyup-regulated in monocytes during Q fever endocarditis

Cited by 14 publications

References 31 publications

Interleukin-10 StimulatesCoxiella burnetiiReplication in Human Monocytes through Tumor Necrosis Factor Down-Modulation: Role in Microbicidal Defect of Q Fever

Interleukin-10 StimulatesCoxiella burnetiiReplication in Human Monocytes through Tumor Necrosis Factor Down-Modulation: Role in Microbicidal Defect of Q Fever

Invasion of the Central Nervous System by Intracellular Bacteria

Variation in immune response genes and chronic Q fever. Concepts: preliminary test with post-Q fever fatigue syndrome

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