Qiu B, Frait K A, Reich F, Komuniecki E, Chensue S W
Departments of Pathology and Laboratory Medicine, Veterans Affairs Medical Center, 2215 Fuller Rd., Ann Arbor, MI 48105, USA.
Am J Pathol. 2001 Apr;158(4):1503-15. doi: 10.1016/S0002-9440(10)64101-6.
Transcript expression of 24 chemokines (CKs) was examined throughout 8 days in mouse lungs with type-1 (Th1) or type-2 (Th2) cytokine-mediated granulomas induced by bead-immobilized mycobacterial purified protein derivative or Schistosoma mansoni egg antigens. Where possible, CK protein levels were also measured. In addition, we examined effects of in vivo cytokine depletions. Findings were as follows: 1) bead challenge induced increases in 18 of 24 CK transcripts with type-1 and type-2 responses displaying different patterns. CKs fell into four categories: a) type-1-dominant (gamma-interferon-inducible protein (IP-10), monokine induced by INF-gamma (MIG), macrophage inflammatory protein-2 (MIP-2), lipopolysaccharide-induced chemokine (LIX), rodent growth-related oncogene homologue (KP), macrophage inflammatory protein-1alpha (MIP-1alpha) and -1beta (MIP-1beta), lymphotactin), b) type-2-dominant (eotaxin, monocyte chemotactic protein-2 (MCP-2) and -3 (MCP-3), liver and activation-regulated chemokine (LARC), T cell activation protein-3 (TCA-3), c) type-1 and type-2 co-dominant (MCP-1, MCP-5, monocyte-derived chemokine (MDC), thymus and activation-related chemokine (TARC), C10), and d) constitutive (lungkine, secondary lymphoid-tissue chemokine (SLC), EBI1-ligand chemokine (ELC), fractalkine, macrophage inflammatory protein-1gamma (MIP1-gamma), and stromal cell derived factor-1alpha (SDF1-alpha). 2) CKs displayed characteristic temporal patterns. CXC (IP-10, MIG, MIP-2, LIX, KC) and certain CC (MCP-1, MCP-5, MIP-1alpha, MIP-1beta) CKs were produced maximally within 1 to 2 days. Others (MCP-2, MCP-3, eotaxin, lymphotactin, LARC, TCA-3) displayed peak expression later. 3) Interferon-gamma neutralization profoundly abrogated MIG, but had little effect on other CKs. Tumor necrosis factor-alpha neutralization caused up to 50% reduction in a range of CKs. These findings indicate that type-1 and type-2 granulomas display characteristic CK profiles with coordinated expression that is under cytokine-mediated regulation.
在由包被珠子的分枝杆菌纯化蛋白衍生物或曼氏血吸虫卵抗原诱导的1型(Th1)或2型(Th2)细胞因子介导的小鼠肺部肉芽肿中,对24种趋化因子(CKs)的转录表达进行了为期8天的检测。在可能的情况下,还测量了CK蛋白水平。此外,我们检测了体内细胞因子耗竭的影响。结果如下:1)珠子攻击诱导24种CK转录本中的18种增加,1型和2型反应呈现不同模式。CKs分为四类:a)1型主导(γ-干扰素诱导蛋白(IP-10)、INF-γ诱导的单核因子(MIG)、巨噬细胞炎性蛋白-2(MIP-2)、脂多糖诱导趋化因子(LIX)、啮齿动物生长相关癌基因同源物(KP)、巨噬细胞炎性蛋白-1α(MIP-1α)和-1β(MIP-1β)、淋巴细胞趋化因子),b)2型主导(嗜酸性粒细胞趋化因子、单核细胞趋化蛋白-2(MCP-2)和-3(MCP-3)、肝脏和激活调节趋化因子(LARC)、T细胞激活蛋白-3(TCA-3)),c)1型和2型共同主导(MCP-1、MCP-5、单核细胞衍生趋化因子(MDC)、胸腺和激活相关趋化因子(TARC)、C10),以及d)组成型(肺趋化因子、二级淋巴组织趋化因子(SLC)、EBI1配体趋化因子(ELC)、fractalkine、巨噬细胞炎性蛋白-1γ(MIP1-γ)和基质细胞衍生因子-1α(SDF1-α)。2)CKs呈现出特征性的时间模式。CXC(IP-10、MIG)、MIP-2、LIX、KC)和某些CC(MCP-1、MCP-5、MIP-1α、MIP-1β)CKs在1至2天内产生最大值。其他(MCP-2、MCP-3、嗜酸性粒细胞趋化因子、淋巴细胞趋化因子、LARC、TCA-3)则在稍后显示出峰值表达。3)γ-干扰素中和显著消除了MIG,但对其他CKs影响很小。肿瘤坏死因子-α中和导致一系列CKs降低多达50%。这些发现表明,1型和2型肉芽肿显示出具有协调表达的特征性CK谱,且该表达受细胞因子介导的调节。