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Mediators of Inflammation
Volume 2009, Article ID 817498, 13 pages
Research Article

Tumour Cell Lines HT-29 and FaDu Produce Proinflammatory Cytokines and Activate Neutrophils In Vitro: Possible Applications for Neutrophil-Based Antitumour Treatment

1Applied Mathematics Department, Universidad Complutense de Madrid, 28040 Madrid, Spain
2Haematology Department, Institute of Research of Hospital Santa Creu i Sant Pau, 08025 Barcelona, Spain
3Laboratory of Angiology, Vascular Biology and Inflammation, Institute of Research of Hospital Santa Creu i Sant Pau, 08025 Barcelona, Spain
4Haematology Department, Complejo Hospitalario Virgen de la Salud, 45004 Toledo, Spain
5Centro de Salud La Estación, Talavera de la Reina, 45600 Toledo, Spain
6Research Laboratory, Fundación Jiménez Díaz, 28040 Madrid, Spain

Received 1 July 2009; Accepted 1 November 2009

Academic Editor: Eeva Moilanen

Copyright © 2009 Antonio Brú et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


There is evidence that polymorphonuclear neutrophils (PMNs) can exert severe antineoplastic effects. Cross-talk between tumour cells and endothelial cells (ECs) is necessary for the accumulation of PMN around a tumour. This work reports the ability of two PMN-sensitive, human, permanent cell lines—colorectal adenocarcinoma (HT-29) and pharyngeal squamous-cell carcinoma (FaDu) cells—to act as inflammatory foci. PMNs were cytotoxic to both lines, the adhesion of the PMNs to the tumour cells being important in this effect. The tumour cells released appreciable amounts of IL-8 and GRO , and induced the transmigration of PMN through human microvascular-EC monolayers. Conditioning media associated with both lines induced the adhesion of PMN and the surface expression of ICAM-1 in microvascular-EC. In addition, FaDu-conditioning-medium strongly induced the production of proinflammatory cytokines by microvascular-EC. These results support the idea that tumour cells might normally induce a potent acute inflammatory response, leading to their own destruction.