Original Articles

Virchows Archiv

, Volume 428, Issue 2, pp 107-111

First online:

Macrophage inflammatory protein-1 alpha expression in non-neoplastic and neoplastic lung tissue

  • T. KonishiAffiliated withSecond Department of Surgery, Shiga University of Medical Science
  • , H. KatonAffiliated withSecond Department of Surgery, Shiga University of Medical Science
  • , A. MoriAffiliated withSecond Department of Surgery, Shiga University of Medical Science
  • , H. OkabeAffiliated withDepartment of Clinical Laboratory Medicine, Shiga University of Medical Science, Seta
  • , Y. FujiyamaAffiliated withDepartment of Internal Medicine, Shiga University of Medical Science, Seta

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Abstract

The chemokines are members of a bipartite superfamily of soluble proteins that have been implicated in a wide range of acute and chronic inflammatory processes, as well as other immunoregulatory functions. Macrophage inflammatory protein-1 alpha (MIP-1α) belongs to the C-C subfamily of these chemokines and is primarily a potent chemoattractant and activator of monocytes. MIP-1α is also thought to play a role in host defence. We examined the expression of MIP-1α in normal lung, inflammatory lung tissue and lung cancer cells by the immunoperoxidase method using a MIP-1α monoclonal antibody. MIP-1α protein was found to be expressed not only by alveolar macrophages, but also by bronchial ciliated cells, hyperplastic alveolar type II cells and activated fibroblasts surrounding malignant tissue. Of 33 cases of lung cancer, 23 (70%) expressed MIP-1α. These observations suggest that lung cancer cells, non-neoplastic alveolar type II cells and fibroblasts can participate in inflammatory cell recruitment via the production of MIP-1α. Tumour derived MIP-α may also affect the interaction between lung cancer and host inflammatory cells.

Key words

Macrophage inflammatory protein-1 alpha Monoclonal antibody Alveolar type II cell Fibroblast Lung cancer