Upregulation of tumor necrosis factor alpha and interleukin-1 beta in Q fever endocarditis

Capo, Christian; Zugun, F; Stein, Andréas; Țârdei, Grațiela; Lépidi, Hubert; Raoult, Didier; Mège, Jean‐Louis

doi:10.1128/iai.64.5.1638-1642.1996

Cited by 50 publications

(33 citation statements)

References 29 publications

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“…TNF and IL-6, but not IL-1b, were upregulated in Q fever. These results extend previous ®ndings showing that the production of TNF by monocytes is markedly enhanced in patients with Q fever endocarditis [6]. The in¯ammatory response to infection is often associated with the production of cytokine antagonists such as soluble receptors for cytokines.…”

Section: Discussionsupporting

confidence: 89%

“…In contrast, chronic Q fever seems to result from an inef®cient response to C. burnetii, as demonstrated by the lack of granulomas, the failure of C. burnetii to induce lymphoproliferation and interferon-gamma (IFN-g) production and the detection of high levels of antibodies to C. burnetii [1,5]. In addition, in¯ammatory cytokines, tumour necrosis factor (TNF) and IL-1b, are produced in excess by patient monocytes [6]. The signi®cance of in¯ammatory response in the two forms of Q fever, as well as the contribution of immune cell activation, are still ignored.…”

Section: Introductionmentioning

confidence: 99%

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Circulating cytokine balance and activation markers of leucocytes in Q fever

Capo

Amirayan

Ghigo

et al. 1999

Clinical and Experimental Immunology

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SUMMARYAs Q fever is associated with an in¯ammatory syndrome, we determined circulating levels of in¯ammatory cytokines, cytokine antagonists, and activation markers of leucocytes in patients with acute Q fever and Q fever endocarditis. Tumour necrosis factor (TNF) and IL-6, but not IL-1b, were markedly increased compared with controls. Cytokine antagonists and activation markers of leucocytes were profoundly different in acute and chronic Q fever. IL-1 receptor antagonist and TNF receptor type II were signi®cantly increased in patients with acute Q fever, suggesting a shift of cytokine balance towards cytokine antagonists. The activation marker of B cells, sCD23, was signi®cantly increased in Q fever endocarditis compared with controls and patients with acute Q fever. In a 2-year follow-up study of patients with Q fever endocarditis, sCD23 and speci®c IgG levels slowly decreased in patients whose symptoms resolved, but remained high in those who required prolonged treatment.

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Section: Discussionsupporting

confidence: 89%

Section: Introductionmentioning

confidence: 99%

Circulating cytokine balance and activation markers of leucocytes in Q fever

Capo

Amirayan

Ghigo

et al. 1999

Clinical and Experimental Immunology

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“…However, C. burnetii does not induce the release of reactive oxygen intermediates by monocytes and macrophages in vitro (233). Surprisingly, virulent phase I C. burnetii strongly stimulates the synthesis of tumor necrosis factor (TNF) by human monocytes (50). This usually increases the microbicidal potential of infected monocytes and thus may restrict the intracellular growth of C. burnetii.…”

Section: Immune System Modulationmentioning

confidence: 99%

Q Fever

1999

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SUMMARY Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of ≥1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.

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“…Non-adherent cells were removed by washing; the remaining cells were considered monocytes because . 95% of them were CD14 1 and had phagocytic characteristics [5].…”

Section: Monocytes and Bacteriamentioning

confidence: 99%

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

Ghigo

Capo

Amirayan

et al. 2000

Clinical and Experimental Immunology

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SUMMARYQ fever is an infectious disease caused by Coxiella burnetii, an obligate intracellular microorganism that inhabits monocytes/macrophages. The dysregulated production of TNF-a in Q fever endocarditis has been associated with defective killing of C. burnetii by patient monocytes. As soluble receptors for TNF-a (TNF-R55 and TNF-R75) regulate TNF-a activity, we investigated their release by monocytes in Q fever. Spontaneous and C. burnetii-stimulated release of TNF-R75, but not of TNF-R55, was upregulated in patients with ongoing endocarditis compared with controls. The increase in TNF-R75 release was related to the activity of Q fever endocarditis, since TNF-R75 release was similar in patients with cured endocarditis and controls. While spontaneous release of TNF-R75 by monocytes from patients with ongoing Q fever endocarditis occurred without changes in its membrane expression, C. burnetii increased the surface expression of TNF-R75. In addition, TNF-R75 transcripts were increased in resting and C. burnetii-stimulated monocytes from patients with ongoing endocarditis. On the other hand, TNF-R75 release was not related to TNF-a secretion. These results indicate that the modulation of TNF-R75 is a critical feature of the pathophysiology of Q fever endocarditis.

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Upregulation of tumor necrosis factor alpha and interleukin-1 beta in Q fever endocarditis

Cited by 50 publications

References 29 publications

Circulating cytokine balance and activation markers of leucocytes in Q fever

Circulating cytokine balance and activation markers of leucocytes in Q fever

Q Fever

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

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