Dysregulation of cytokines in acute Q fever: Role of interleukin-10 and tumor necrosis factor in chronic evolution of Q fever

被引：79

作者：

Honstettre, AL ^{[1
]}

Imbert, GV ^{[1
]}

Ghigo, E ^{[1
]}

Gouriet, FR ^{[1
]}

Capo, C ^{[1
]}

Raoult, D ^{[1
]}

Mege, JL ^{[1
]}

机构：

[1] Univ Mediterranee, Unite Rickettsies, CNRS UMR 6020, Fac Med, F-13385 Marseille, France

来源：

JOURNAL OF INFECTIOUS DISEASES | 2003年 / 187卷 / 06期

关键词：

D O I：

10.1086/368129

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Q fever manifests as primary infection or acute Q fever and may become chronic in patients with underlying valvulopathy. Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever. Compared with control subjects, patients with uncomplicated acute Q fever exhibited increased release of the 4 cytokines. Their amounts were higher in patients with hepatitis than in patients with fever or pneumonia. In patients with valvulopathy, who exhibited the highest risk of chronic evolution, the amounts of TNF and IL-10 were higher than in patients without valvulopathy. TNF production was specifically enhanced in patients who developed Q fever endocarditis. These results show that acute Q fever is associated with cytokine overproduction. Persistent TNF amounts were associated with the occurrence of endocarditis in patients with valvulopathy, and that may be a marker of chronic evolution of Q fever.

引用

页码：956 / 962

页数：7

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