Effect of fetal calf serum on cytokine release by bone marrow-derived macrophages during infection w

骨髓來(lái)源的巨噬細(xì)胞（BMM）包括人口的靜態(tài)細(xì)胞可以通過(guò)定義信號(hào)激活。在這里，我們直接比較趨化因子和單核因子的釋放由BMM復(fù)活了在無(wú)血清培養(yǎng)基或在無(wú)血清培養(yǎng)基中單核細(xì)胞增生李斯特菌EGD或卡介苗感染。我們專注于這個(gè)問(wèn)題，因?yàn)橐呀?jīng)出現(xiàn)了由BMM由于不同的體外培養(yǎng)條件下，細(xì)胞因子的產(chǎn)生的一些有爭(zhēng)議的報(bào)告。培養(yǎng)在無(wú)血清培養(yǎng)基中引物BMM為單核細(xì)胞趨化蛋白（MCP）釋放1，白細(xì)胞介素（IL）- 6，和IL-12，但對(duì)巨噬細(xì)胞炎性蛋白沒(méi)有影響（MIP）-1和腫瘤壞死因子（TNF）-針對(duì)單增李斯特菌感染α生產(chǎn)。與結(jié)核分枝桿菌感染后，BMM提高和刺激在無(wú)血清培養(yǎng)基中分泌更高水平的MCP-1、MIP-1α、IL-6和TNF-α，但不是IL-12與BMM在無(wú)血清培養(yǎng)基中培養(yǎng)和感染。血清的作用可能部分模仿干擾素γ。因?yàn)樨?fù)責(zé)BMM啟動(dòng)的血清成分不明確，BMM培養(yǎng)在無(wú)血清的條件下提供確定巨噬細(xì)胞活化信號(hào)的適當(dāng)?shù)募?xì)胞。

英文原文：

Bone marrow-derived macrophages (BMM) comprise a population of quiescent cells which can be activated by defined signals. Here, we directly compare the release of chemokines and monokines by BMM raised either in serum-supplemented or in serum-free medium in response to Listeria monocytogenes EGD or Mycobacterium bovis BCG infection. We focused on this issue because there have been several controversial reports on the production of cytokines by BMM due to different in vitro culture conditions. Culture in serum-supplemented medium primed BMM for release of monocyte chemoattractant protein (MCP)-1, interleukin (IL)-6, and IL-12, but had no effect on macrophage inflammatory protein (MIP)-1alpha and tumor necrosis factor (TNF)-alpha production in response to L. monocytogenes infection. After challenge infection with M. bovis, BMM raised and stimulated in serum-supplemented medium secreted higher levels of MCP-1, MIP-1alpha, IL-6, and TNF-alpha but not of IL-12 as compared to BMM cultured and infected in a serum-free medium. The effects of serum could be partially mimicked by interferon-gamma. Because the serum components responsible for BMM priming are undefined, BMM cultured under serum-free conditions provide an appropriate cell population for defining macrophage activating signals.