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Mannose-Binding Lectin Is a Regulator of Inflammation That Accompanies Myocardial Ischemia and Reperfusion Injury

2005; American Association of Immunologists; Volume: 175; Issue: 1 Linguagem: Inglês

10.4049/jimmunol.175.1.541

1550-6606

Mary C. Walsh, Todd Bourcier, Kazue Takahashi, Lei Shi, Marc Busche, Russell P. Rother, Scott D. Solomon, R. Alan B. Ezekowitz, Gregory L. Stahl,

Adenosine and Purinergic Signaling

Abstract The mannose-binding lectin (MBL), a circulating pattern recognition molecule, recognizes a wide range of infectious agents with resultant initiation of the complement cascade in an Ab-independent manner. MBL recognizes infectious non-self and altered self in the guise of apoptotic and necrotic cells. In this study, we demonstrate that mice lacking MBL, and hence are devoid of MBL-dependent lectin pathway activation but have fully active alternative and classical complement pathways, are protected from cardiac reperfusion injury with resultant preservation of cardiac function. Significantly, mice that lack a major component of the classical complement pathway initiation complex (C1q) but have an intact MBL complement pathway, are not protected from injury. These results suggest that the MBL-dependent pathway of complement activation is a key regulator of myocardial reperfusion ischemic injury. MBL is an example of a pattern recognition molecule that plays a dual role in modifying inflammatory responses to sterile and infectious injury.