Increased Macrophage Division in the Synovial Fluid of Goats Infected with Caprine Arthritis-Encephalitis Virus

Abstract

Macrophages are a major component of the arthritic lesions induced by the lentivirus caprine arthritis-encephalitis virus (CAEV). Using autoradiography and the appearance of mitotic figures to detect dividing macrophages, we found that 2.1% +/- 0.2% of synovial fluid macrophages from uninfected goats are dividing and that after infection with CAEV the percentage increases three- to sixfold. The enhanced macrophage division was not associated with increased dividing of blood monoblasts. The amount of macrophage division correlated with two measures of arthritis: joint swelling and the number of synovial fluid macrophages. Induction of an immune response in the joints of CAEV-infected goats increased the number of dividing macrophages. The synovial fluid of infected animals was mitogenic for macrophages from infected animals in amounts that correlated with the amount of macrophage division occurring in the joints. Activated lymphocytes produced nondialyzable lymphokines mitogenic for macrophages from CAEV-infected goats but not from uninfected goats. These results suggest that in situ macrophage division contributes to the lesions induced by CAEV and that infection leads to greater responsiveness of macrophages to mitogenic factors produced by lymphocytes.

Proviral sequences detected by polymerase chain reaction in peripheral blood cells of horses with equine infectious anemia lentivirus

“…(c) Transit time of immature circulating macrophages to the tissues may be increased. Lentivirus infection of monocytes and macrophages results in activation of the cells, as indicated by increased phagocytosis, adherence, motility, production of superoxide anion, esterase staining [3] and migration inhibition [2] in vitro, increased macrophage division in vivo [16], increased interferon production by lymphocytes cocultured with infected macrophages [31] and increased expression of Class II major histocompatibility antigens [45]. Alteration in the rate of maturation and migration to tissue may be affected as well.…”

Monocyte‐mediated entry of pathogens into the central nervous system

“…Whilst resident macrophages in normal tissue are relatively stable and long-lived cells, there is in fact a slow, constant rate of turnover as senescent cells are replaced by monocytes from the blood or by local proliferation (Oehmichen & Gruninger, 1974;Oehmichen, 1978;Ling, 1979a; Blusse van oud Alblas & van Furth, 1979;van Furth et al, 1980;Jutila & Banks, 1988). The turnover rates of macrophage populations in various tissues are low.…”

Detection and properties of the human proliferative monocyte subpopulation

“…However, we and others have shown that a small percentage of human monocytes can enter the cell cycle in vitro in response to agents such as M-CSF and granulocyte M-CSF (GM-CSF) [20 -22]. We have termed this pre-sumably immature subpopulation proliferative monocytes (PM) [21][22][23][24] and have proposed they could enter sites of inflammation and contribute to the local macrophage proliferation, which has been observed clinically and in animal models of inflammation [25][26][27][28]. Surface marker analysis has been carried out following in vitro culture of PM [23], but their characteristics upon isolation and relationship to other subpopulations have not been examined.…”