Rapid drop in serum iron concentration as a host defense mechanism. A review of experimental and clinical evidence.
Serum iron levels drop during stress and infection in all orders of vertebrates. These alterations constitute a physiologic response that benefits the host by depriving the invading pathogens of nutritionally required iron. Within an iron-poor environment, multiplication rates of pathogens are significantly diminished. The coordinated alteration of fever and serum iron concentration works synergistically in slowing the pathogens' growth rate. Attempts by bacteria to tear iron from serum transferrin with siderophores, iron binding compounds may be blocked with host lactoferrins that have an even higher affinity for the iron. When these attempts to block acquisition of iron by pathogens are compromised by hematomas, hemolysis, or parenteral administration of iron, mortality from infections dramatically increase. This article reviews the experimental and clinical evidence which supports the importance of iron metabolism in host immunity.
D001419:Bacteria / Q000254:growth & development / Q000378:metabolism*; D001424:Bacterial Infections / Q000097:blood / Q000503:physiopathology*; D001831:Body Temperature; D002570:Ceruloplasmin / Q000378:metabolism; D006801:Humans; D007501:Iron / Q000097:blood* / Q000502:physiology; D007781:Lactoferrin / Q000097:blood; D014168:Transferrin / Q000378:metabolism
D014168:Transferrin; D007501:Iron; D002570:Ceruloplasmin; D007781:Lactoferrin