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. 2015 Feb 3;6:11. doi: 10.3389/fphys.2015.00011

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Copyright © 2015 Cederlund, Deronic, Pallon, Sørensen and Åkerström.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Tentative function of A1M in protection against bystander oxidative damage caused by neutrophils. The figure summarizes the findings of this paper in a physiological context. Recruitment and activation of neutrophils during inflammation involves MPO-mediated bacterial killing but may also yield LDL-oxidation as a side-effect. (1) Neutrophil culture medium or purified MPO induces heme-binding of A1M, and proteolytic cleavage of the protein which was previously shown to activate a heme-degradation activity of A1M (Allhorn et al., 2002). (2) The induced heme-degradation mechanism of A1M is tentatively “disarming” the peroxidase, preventing oxidative burst. (3) LDL-oxidation by MPO is inhibited by A1M, and pre-formed oxidation products on LDL are reduced.