Hemoglobin vesicles (HbVs) could serve as a substitute for red blood cells (RBCs) in
resuscitation from massive
hemorrhage. A massive transfusion of RBCs can increase the risk of
infection, which is not caused by contaminating micro-organisms in the transfused RBCs but by a breakdown of the host defense system. We previously found that
complement activity was increased after
resuscitation with HbVs at a putative dose in a rat model of
hemorrhagic shock. It is known that
complement system plays a key role in host defense in the embryonic stage. Therefore, the objective of this study was to address whether the suppression of
bacterial infections in
hemorrhagic shock rats was a result of increased
complement activity after massive HbV transfusion. For this purpose, Escherichia coli were incubated with plasma samples obtained from a rat model of
hemorrhagic shock resuscitated by HbVs or RBCs, and bacterial growth was determined under ex vivo conditions. As a result, E. coli growth was found to be suppressed by increased
complement activity, mediated by the production of
IgM from spleen. However, this antibacterial activity disappeared when the E. coli were treated with
complement-inactivated plasma obtained from splenoctomized rats. In addition, the
resuscitation of HbVs from
hemorrhagic shock increased the survival rate and viable bacterial counts in blood in cecum
ligation and
puncture rats, a
sepsis model. In conclusion, the
resuscitation of HbVs in the rat model of
hemorrhagic shock suppresses bacterial growth via complement activation induced by
IgM.