Abstract
Objective and design: The presence of increased numbers of tumor-infiltrating neutrophils is associated with poorer outcome in patients with adenocarcinoma of the bronchioloalveolar (BAC) subtype. We evaluated the role of inflammatory environment on C-X-C chemokine tumor production.
Materials: Bronchoalveolar lavage from 31 consecutive patients with adenocarcinoma of the BAC subtype as well as tumor and normal pulmonary tissue samples. A549 BAC cell line. Peripheral blood mononuclear cells (PBMC), polymorphonuclear neutrophils (PMN) and alveolar macrophages (AM).
Methods: Elisa measurements and immunohistochemical studies of ENA-78, IL-8, IL-1β and TNF-α. RNA isolation, reverse transcription, and PCR amplification of ENA-78 and IL-8.
Results: C-X-C peptides were expressed by tumor cells of all the tumor specimens tested. ENA-78 and IL-8 were also expressed by AM. To better understand the regulation of the C-X-C production, BAC cell line was cultured alone or with inflammatory cells. PBMC upregulated both tumor ENA-78 and IL-8 mRNA expression and protein release whereas AM only upregulated ENA-78 mRNA expression and protein release; PMN had no effect. Anti-human IL-1β antibodies (ab) inhibited the A549 ENA-78 and IL-8 production stimulated by PBMC-CM. Anti-human TNF-α ab inhibited A549 ENA-78 production stimulated by AM-CM. IL-1β and TNF-α were expressed in vivo by inflammatory cells, although TNF-α was also expressed by tumor cells.
Conclusions: This work emphasizes the role of the host inflammatory response in promoting tumor growth in vivo.
Similar content being viewed by others
Author information
Authors and Affiliations
Corresponding author
Additional information
Received 20 November 2003; returned for revision 28 May 2003; accepted by G. Letts 19 August 2003
Rights and permissions
About this article
Cite this article
Wislez, M., Philippe, C., Antoine, M. et al. Upregulation of bronchioloalveolar carcinoma-derived C-X-C chemokines by tumor infiltrating inflammatory cells. Inflamm. res. 53, 4–12 (2004). https://doi.org/10.1007/s00011-003-1215-3
Received:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00011-003-1215-3