Myocardial Protection by Monophosphoryl Lipid A: Potential Mechanisms

Monophosphoryl lipid A is a derivative of the lipopolysaccharide (LPS) from gramnegative bacteria (52,53). This drug has had several different abbreviations in the literature, including MPL, MPLA, and the most commonly used—MLA. It was extracted to reduce the associated toxicity while retaining the immunomodulatory properties of the parent endotoxin molecule. MLA has been shown to induce certain beneficial immunostimulatory effects such as macrophage stimulation, cytokine release, and a variety of other effects upon both humoral and cell-mediated immunological host defense response (3,17,21,27,36,61). The beneficial effects of MLA have been used in 1) inducing tolerance to endotoxemia in both laboratory animals and humans, 2) immunotherapy or immunoprophylaxis, 3) adjuvant for a number of vaccines, 4) inducing delayed protection against cerebral vasospasm caused by subarachnoid hemorrhage, and 5) delayed cardioprotection through complex mechanisms. This paper provides a detailed review of the current state of knowledge of the role of this drug in myocardial protection.