Aberrations in post-trauma monocyte (MO) subpopulation: role in septic shock syndrome
Miller-Graziano, C.L.; Szabo, G.; Kodys, K.; Griffey, K.
Journal of Trauma 30(12 Suppl): S86-S96
1990
ISSN/ISBN: 0022-5282 PMID: 2254998 Document Number: 363789
Appearance of increased proportions of monocytes bearing the 72kd(FcRI) receptor for IgG correlated to aberrant monocyte (MO) functions, depressed immune functions, and poor clinical outcome. The trauma patients' FcRI+ MO subpopulation produced the majority of their elevated IL-6, TNF alpha, TGF beta, and PGE2. IgG stimulation of patients' MO through FcRI not only stimulated TNF alpha, IL-6, and PGE2 levels, but also greatly augmented the levels of these monokines produced after subsequent bacterial challenge. Post-trauma increased IL-6 levels can lead to polyclonal B-cell activation and high levels of circulating, nonspecific IgG as seen in trauma patients. This nonspecific IgG triggers the FcRI on the increased numbers of FcRI+ MO leading to ever-increasing monokine levels. IL-4 was found to downregulate patients' FcRI+ MO production of mediators. The cycle of altered cytokine levels, increased FcRI+ MO numbers, elevated IgG, and augmented triggering of FcRI+ MO may be broken by addition of IL-4.