muramidase and Transfusion-Reaction

In a study designed to determine the preventive effect of lysozyme on post-transfusion hepatitis, 260 patients with orthopedic diseases, who received blood by transfusion during a period of 5 years from June 1970 to May 1975, were divided at random into a group of 123 patients treated with lysozyme is doses of 60 to 170 mg/day for 4 to 24 weeks, and a control group of 137 patients. The incidence of post-transfusion hepatitis was 10 (8.1%) out of 123 patients for the treated group, and 28 (20.4%) out of 137 patients for the control group. Icteric hepatitis occurred in 1 (0.8%) patient in the treated group, while its incidence in the control group was 8 (5.8%) out of 137 patients.

Topics: Adult; Aged; Clinical Trials as Topic; Female; Hepatitis B; Humans; Male; Middle Aged; Muramidase; Random Allocation; Transfusion Reaction

Despite the significant adverse clinical consequences of RBC alloimmunization, our understanding of the signals that induce immune responses to transfused RBCs remains incomplete. Though RBC storage has been shown to enhance alloimmunization in the hen egg lysozyme, ovalbumin, and human Duffy (HOD) RBC alloantigen mouse model, the molecular signals leading to immune activation in this system remain unclear. Given that the nonclassical major histocompatibility complex (MHC) Class I molecule CD1D can bind to multiple different lysophospholipids and direct immune activation, we hypothesized that storage of RBCs increases lysophospholipids known to bind CD1D, and further that recipient CD1D recognition of these altered lipids mediates storage-induced alloimmunization responses.. We used a mass spectrometry-based approach to analyze the changes in lysophospholipids that are induced during storage of mouse RBCs. CD1D knockout (CD1D-KO) and wild-type (WT) control mice were transfused with stored HOD RBCs to measure the impact of CD1D deficiency on RBC alloimmunization.. RBC storage results in alterations in multiple lysophospholipid species known to bind to CD1D and activate the immune system. Prior to transfusion, CD1D-deficient mice had lower baseline levels of polyclonal immunoglobulin (IgG) relative to WT mice. In response to stored RBC transfusion, CD1D-deficient mice generated similar levels of anti-HOD IgM and anti-HOD IgG.. Although storage of RBCs leads to alteration of several lysophospholipids known to be capable of binding CD1D, storage-induced RBC alloimmunization responses are not impacted by recipient CD1D deficiency.

Topics: Alarmins; Animals; Antibody Specificity; Antigens, CD1d; Blood Preservation; Blood Transfusion; Duffy Blood-Group System; Erythrocytes; Female; Immunization; Immunoglobulin G; Immunoglobulin M; Isoantibodies; Isoantigens; Lysophospholipids; Male; Mass Spectrometry; Mice; Mice, Inbred Strains; Mice, Knockout; Mice, Transgenic; Muramidase; Ovalbumin; Receptors, Cell Surface; Transfusion Reaction

Transfusion of red blood cells (RBCs) into patients with anti-donor RBC antibodies (crossmatch-incompatible transfusion) can result in lethal antibody-mediated hemolysis. Less well appreciated is the ability of anti-RBC antibodies to specifically remove their target antigen from donor RBCs without compromising cell survival or adversely affecting the transfusion recipient. In an effort to elucidate the mechanistic details of this process, we describe the first animal model of nonhemolytic antibody-induced RBC antigen loss. RBCs from transgenic mHEL mice express surface hen egg lysozyme (HEL) as a transmembrane protein. Transfusion of mHEL RBCs into mice immunized with HEL results in selective loss of HEL antigen from donor RBCs without affecting other blood group antigens or reducing the circulatory life span of the transfused RBCs. While this process does not require the presence of a spleen, it requires both anti-RBC immunoglobulin G (IgG) antibodies and the FcgammaIII receptor. These studies provide mechanistic insight into the phenomenon of antigen loss during incompatible transfusion in humans.

Topics: Animals; Antigen-Antibody Reactions; Antigens, Surface; Erythrocytes; Immunization; Immunoglobulin G; Isoantibodies; Mice; Mice, Inbred C57BL; Mice, Knockout; Mice, Transgenic; Models, Animal; Muramidase; Receptors, IgG; Transfusion Reaction