Abstract
It is well known that comparisons of populations or compartments of mononuclear phagocytes show considerable diversity of cellular function. In the case of resident-type macrophages (M⌽), such differences are widely believed to result from influences characteristic of individual compartments exerted on less specialized immigrant monocytes following their ongoing influx from the blood into tissues and tissue spaces. In this connection, data supporting the compartmental regulation of M⌽ arachidonic acid metabolism, at least in the pleural and the peritoneal cavities, were recently reported (1). The data we present show that in the spleen, M⌽ arachidonic acid metabolism is in part an expression of regulatory mechanisms at a distant site, the bone marrow. This demonstration required a model of bone marrow ablation and monocyte depletion, the principles of which are described below.
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Volkman, A., Shibata, Y., Dempsey, W., Morahan, P.S. (1988). Effects of Bone Marrow Ablation on Compartmental Prostaglandin Synthesis by Mononuclear Phagocytes. In: Eisenstein, T.K., Bullock, W.E., Hanna, N. (eds) Host Defenses and Immunomodulation to Intracellular Pathogens. Advances in Experimental Medicine and Biology, vol 239. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-5421-6_4
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DOI: https://doi.org/10.1007/978-1-4757-5421-6_4
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