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Altered antigen-presenting capacity of human monocytes after phagocytosis of bacteria.

By J Pryjma, J Baran, M Ernst, M Woloszyn and H D Flad

Abstract

The antigen-presenting and accessory functions of monocytes were studied after phagocytosis of bacteria. Peripheral blood monocytes isolated from mononuclear cells by counterflow elutriation were incubated with suspensions of opsonized bacteria (Staphylococcus aureus, Escherichia coli, Pseudomonas aeruginosa, or Salmonella enteritidis) under conditions in which at least 80% of the monocytes engulfed microorganisms. Either the cells were pulsed with antigen (purified derivative of tuberculin or tetanus toxoid) and used as antigen-presenting cells for autologous T lymphocytes or the accessory function of the cells was examined in pokeweed mitogen-activated cultures of T cells. It has been found that phagocytosis of bacteria by monocytes reduces their ability to trigger antigen- and mitogen-induced proliferation. The reduced proliferative response of T lymphocytes was not due to a change of the kinetics of the response or triggering of suppressor mechanisms. Furthermore, antigen processing was not affected much after phagocytosis of bacteria since antigen-pulsed and paraformaldehyde-fixed cells containing bacteria were comparable to control cells in their antigen-presenting capacity. This phenomenon was observed after phagocytosis of both living and dead bacteria and was not correlated to the viability of monocytes, which were more affected after phagocytosis of living bacteria than of dead ones. As a result of phagocytosis of bacteria, reduced expression of CD54, CD14, and HLA-DQ, variable reduction of HLA-DP, CD58, and CD64, and reduced viability of monocytes were observed. In conclusion, phagocytosis of bacteria by monocytes affects their antigen-presenting and accessory functions presumably because of changes in the expression of molecules essential for monocyte-T-cell interactions and reduction of their viability

Topics: Research Article
Year: 1994
OAI identifier: oai:pubmedcentral.nih.gov:186454
Provided by: PubMed Central
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