gp130 on macrophages/granulocytes modulates inflammation during experimental tuberculosis

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• 作者：Jan Sodenkamp^a ; Jochen Behrends^a ; Irmgard F&#xf6 ; rster^b ; Werner Mü ; ller^c ; Stefan Ehlers^d ; ^e ; ^f ; Christoph H&#xf6 ; lscher^a ; ^f ; ^{choelscher@fz-borstel.de"" rel=""nofollow}
• 关键词：Bacterial infection ; Rodent ; Cytokines ; Macrophages/monocytes ; T cells
• 刊名：European Journal of Cell Biology
• 出版年：2011
• 出版时间：June-July 2011
• 年：2011
• 卷：90
• 期：6-7
• 页码：505-514
• 全文大小：1468 K

文摘

gp130 is a common receptor chain for cytokines such as interleukin (IL)-27 and IL-6. During experimental tuberculosis (TB), IL-27 prevents optimal antimycobacterial protection and limits the pathological sequelae of chronic inflammation. The anti-inflammatory properties of IL-27 have been attributed mainly to its suppressive effect on T helper (TH) cells. However, because gp130 cytokines also suppress the inflammatory immune response of macrophages, IL-27 may also regulate inflammation by limiting the secretion of pro-inflammatory cytokines. To specifically address the role of gp130 cytokines on macrophages, the outcome of experimental TB was analysed in macrophage/neutrophil-specific gp130-deficient (LysM^cre gp130^loxP/loxP) mice. In these mice, the enhanced induction of inflammatory cytokines and increased expression of the inducible nitric oxide synthase (NOS2) and LRG47 was linked to a greatly augmented TH17 immune response and matrix metalloproteinase (MMP)-9 expression. However, this amplified inflammatory immune response in Mtb-infected LysM^cre gp130^loxP/loxP mice was not associated with reduced bacterial loads and/or accelerated pathology. Our study revealed an immunoregulatory function of gp130 cytokines on macrophages/granulocytes, which is, however, not critical for modulating the outcome of TB.