The Journal of Immunology, Vol 140, Issue 11 3822-3829, Copyright © 1988 by American Association of Immunologists

ARTICLES

Demonstration by in situ hybridization of dissimilar IL-1 beta gene expression in human alveolar macrophages and blood monocytes in response to lipopolysaccharide

JF Bernaudin, K Yamauchi, MD Wewers, MJ Tocci, VJ Ferrans and RG Crystal
Pathology Branch, National Heart, Lung, and Blood Institute, Bethesda, MD 20892.

IL-1 beta is the major form of IL-1 produced by mononuclear phagocytes. To evaluate the possible mechanisms underlying the observation that mature populations of human mononuclear phagocytes as alveolar macrophages are relatively poor IL-1 producers compared with blood monocytes, the expression of the IL-1 beta gene mRNA transcripts was evaluated in LPS-stimulated normal autologous blood monocytes and alveolar macrophages by using a IL-1 beta cDNA probe. Although Northern analysis demonstrated that stimulated monocytes and alveolar macrophages both express 1.8-kb IL-1 beta mRNA transcripts, cytoplasmic dot blot analysis showed that the total IL-1 beta mRNA content in alveolar macrophages was only 38 +/- 5% of that in blood monocytes. In situ hybridization with antisense and sense IL-1 beta RNA probes demonstrated that whereas most of stimulated blood monocytes contained IL-1 beta mRNA transcripts, a significant proportion of autologous alveolar macrophages stimulated in an identical fashion did not express the IL-1 beta gene. Within 4 h after LPS stimulation, IL-1 beta mRNA transcripts were detected in 81 +/- 6% monocytes, whereas only 16 +/- 9% of alveolar macrophages were positive, and by 18 h this had increased only to 43 +/- 15%. Quantification of the size distribution of the IL-1 beta mRNA expressing mononuclear phagocytes demonstrated that, among the population of alveolar macrophages, the cells expressing this gene were not confined to those that were "monocyte- like." These observations demonstrate that there is a heterogeneity among population of mononuclear phagocytes in their ability to express the gene for IL-1 beta, which could explain the differences observed in IL-1 production.

This article has been cited by other articles:

				L. A. Tephly and A. B. Carter Asbestos-Induced MKP-3 Expression Augments TNF-{alpha} Gene Expression in Human Monocytes Am. J. Respir. Cell Mol. Biol., July 1, 2008; 39(1): 113 - 123. [Abstract] [Full Text] [PDF]

				A. B. Carter, L. A. Tephly, S. Venkataraman, L. W. Oberley, Y. Zhang, G. R. Buettner, D. R. Spitz, and G. W. Hunninghake High Levels of Catalase and Glutathione Peroxidase Activity Dampen H2O2 Signaling in Human Alveolar Macrophages Am. J. Respir. Cell Mol. Biol., July 1, 2004; 31(1): 43 - 53. [Abstract] [Full Text] [PDF]

				B Panterne, A Hatzfeld, P Sansilvestri, A Cardoso, M. Monier, P Batard, and J Hatzfeld IL-3, GM-CSF and CSF-1 modulate c-fms mRNA more rapidly in human early monocytic progenitors than in mature or transformed monocytic cells J. Cell Sci., January 7, 1996; 109(7): 1795 - 1801. [Abstract] [PDF]

				M. Rosenfeld, W Siegfried, K Yoshimura, K Yoneyama, M Fukayama, L. Stier, P. Paakko, P Gilardi, L. Stratford-Perricaudet, M Perricaudet, et al. Adenovirus-mediated transfer of a recombinant alpha 1-antitrypsin gene to the lung epithelium in vivo Science, April 19, 1991; 252(5004): 431 - 434. [Abstract] [PDF]