Decreased Fc Receptor Expression on Macrophages Following Simple Hemorrhage as Observed by Scanning Immunoelectron Microscopy

Abstract

Although it is known that macrophage (M phi) functions such as phagocytosis and antigen presentation are depressed following hemorrhage and resuscitation, the mechanism remains unknown. The aim of this study was to determine, using scanning immunoelectron microscopic techniques, whether there is any alteration in the Fc receptors on the M phi after hemorrhage. To study this, male C3H/HeN mice were bled to a mean blood pressure (BP) of 35 mm Hg and maintained at that pressure for 1 hr, then resuscitated with their own blood and adequate fluids. Twenty-four hrs later, Kupffer cells from livers and splenic adherent cells were isolated, incubated for 16 hr, and then exposed to polysterene beads conjugated with antimouse IgG that specifically binds to Fc receptors. The cells were then prepared for observation by scanning electron microscopy. At least 100 cells from each animal were examined. The number of Kupffer cells from posthemorrhage mice that exhibited specific receptor labeling was significantly decreased (41.0 +/- 2.6, P less than 0.05) compared with control (64.2 +/- 7.5). The number of splenic adherent cells from posthemorrhage mice exhibiting specific receptor labeling was also significantly decreased (35.7 +/- 2.5, P less than 0.01) compared with control (61.2 +/- 3.9). The internalization of markers was also seen in some cells. The cause of the decrease in receptor labeling following hemorrhage may be the loss, inactivation, and/or internalization of receptors. Thus the decreased number of functional macrophages may contribute to the depression of antigen presentation and to the enhanced susceptibility to sepsis following hemorrhage.

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Downregulation of TLR4‐dependent ATP production is critical for estrogen‐mediated immunoprotection in Kupffer cells following trauma‐hemorrhage

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B LYMPHOCYTES UNDERGO APOPTOSIS BECAUSE OF FcγRIIb stress response to infection: A novel mechanism of cell death in sepsis

“…It is noteworthy that the loss of FcRs was also observed in hemorrhagic shock, suggesting that it is a common phenomenon in critical illness (37). Whether this was because of aggregation by immune complexes, apoptosis-secondary effects, or shock-related cell dysfunctions remains unclear.…”