Neutrophils are required for 3-methylcholanthrene-initiated, butylated hydroxytoluene-promoted lung carcinogenesis.
Neutrophils are required for 3-methylcholanthrene-initiated, butylated hydroxytoluene-promoted lung carcinogenesis.
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中性粒细胞是 3-甲基胆蒽引发、丁基羟基甲苯促进的肺癌发生所必需的。
DOI:
10.1002/mc.20870
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发表时间:
2012-12
影响因子:
4.6
通讯作者:
You, Ming
中科院分区:
文献类型:
--
作者:
Vikis, Haris G.;Gelman, Andrew E.;Franklin, Andrew;Stein, Lauren;Rymaszewski, Amy;Zhu, Jihong;Liu, Pengyuan;Tichelaar, Jay W.;Krupnick, Alexander S.;You, Ming
Multiple studies have shown a link between chronic inflammation and lung tumorigenesis. Inbred mouse strains vary in their susceptibility to methylcholanthrene (MCA)-initiated butylated hydroxytoluene (BHT)-promoted lung carcinogenesis. In the present study we investigated whether neutrophils play a role in strain dependent differences in susceptibility to lung tumor promotion. We observed a significant elevation in homeostatic levels of neutrophils in the lungs of tumor-susceptible BALB/cByJ (BALB) mice compared to tumor-resistant C57BL/6J (B6) mice. Additionally, BHT treatment further elevated neutrophil numbers as well as neutrophil chemoattractant keratinocyte-derived cytokine (KC)/chemokine (C-X-C motif) ligand 1 (Cxcl1) levels in BALB lung airways. Lung CD11c+ cells were a major source of KC expression and depletion of neutrophils in BALB mice resulted in a 71% decrease in tumor multiplicity. However, tumor multiplicity did not depend on the presence of T cells, despite the accumulation of T cells following BHT treatment. These data demonstrate that neutrophils are essential to promote tumor growth in the MCA/BHT two-step lung carcinogenesis model.
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影响因子:
4.4
作者:
Keane, MP;Belperio, JA;Strieter, RM
通讯作者:
Strieter, RM
影响因子:
2.7
作者:
Gungor, Nejla;Haegens, Astrid;van Schooten, Frederik J.
通讯作者:
van Schooten, Frederik J.
影响因子:
8
作者:
Ji, H;Houghton, AM;Wong, KK
通讯作者:
Wong, KK
影响因子:
4.5
作者:
Bauer, AK;Dwyer-Nield, LD;Malkinson, AM
通讯作者:
Malkinson, AM
影响因子:
4.8
作者:
Gungor, Nejla;Godschalk, Roger W. L.;Knaapen, Ad M.
通讯作者:
Knaapen, Ad M.