Macrophages in proliferative vitreoretinopathy and proliferative diabetic retinopathy: differentiation of subpopulations.

Abstract

Macrophages have long been known to play a major role in the pathogenesis of proliferative vitreoretinal disorders. Using the monoclonal antibodies EBMIl (pan macrophage), 27E10 (early inflammatory stage marker), and RM3/1 (healing phase marker), different subpopulations of macrophages were differentiated in surgically removed membranes from patients with macular pucker (n=6), proliferative vitreoretinopathy (PVR) following rhegmatogenous retinal detachment (n=1l), traumatic PVR (n=19), and proliferative diabetic retinopathy (PDR) (n=11). Macrophages were predominantly found in traumatic PVR and PDR. Some healing phase (RM3/1) macrophages were detected in all disease entities. Inflammatory stage macrophages (positive staining for 27E10) could not be detected in PVR following rhegmatogenous retinal detachment and idiopathic macular pucker. In traumatic PVR inflammatory stage macrophages were associated with a short history of disease whereas in PDR all types of macrophages could be detected regardless of clinical history and duration of the disease. (BrJ Ophthalmol 1993; 77: 731-733)

Hypoxia-Induced Pulmonary Vascular Remodeling Requires Recruitment of Circulating Mesenchymal Precursors of a Monocyte/Macrophage Lineage

“…Increased numbers of macrophages have also been documented under various pathological conditions associated with hypoxia, such as in ischemic areas of dermal wounds, in atherosclerotic plaques, malignant tumors, and in eyes with proliferative retinopathy. [35][36][37] MNC/macrophage influx and accumulation has also been reported in primary pulmonary hypertension as well as in secondary forms of pulmonary hypertension, including high-flow congenital heart disease, scleroderma, and pulmonary hypertension-associated acute respiratory distress syndrome. 38,39 However, in none of the aforementioned studies was the potential for the MNCs to give rise to mesenchymal-like cells described.…”

Mechanisms regulating the recruitment of macrophages into hypoxic areas of tumors and other ischemic tissues

“…23 These hypoxic responses of macrophages are unlikely to be confined to tumors, because increased numbers of macrophages have also been reported in ischemic areas of dermal wounds, 24 atherosclerotic plaques, 25 synovia of joints with rheumatoid arthritis, 26 and eyes with proliferative retinopathy. 27 It is therefore possible that macrophages may exhibit a similar phenotype in the hypoxic areas of these diseased tissues.…”

“…23 These hypoxic responses of macrophages are unlikely to be confined to tumors, because increased numbers of macrophages have also been reported in ischemic areas of dermal wounds, 24 atherosclerotic plaques, 25 synovia of joints with rheumatoid arthritis, 26 and eyes with proliferative retinopathy. 27 It is therefore possible that macrophages may exhibit a similar phenotype in the hypoxic areas of these diseased tissues.Here, we outline the various ways in which monocytes are recruited into tumors and then the potential mechanisms used by these tissues to attract and entrap TAMs in hypoxic areas. We also discuss the likely relevance of these mechanisms to macrophage behavior in hypoxic areas of other diseased tissues.…”

Chemokines in proliferative diabetic retinopathy and proliferative vitreoretinopathy

“…The pathogenesis of epiretinal membranes is still not well understood, but inflammatory and immunological processes are known to be implicated. Several studies of epiretinal membranes showed the presence of activated T lymphocytes, B lymphocytes, and macrophages [1][2][3]. The specific mediators that orchestrate the recruitment of leukocytes leading to proliferative vitreoretinal disorders have not been fully elucidated, although several studies demonstrated elevated levels of several chemokines in vitreous humour removed from patients with proliferative vitreoretinal disorders [4][5][6][7][8].…”