Allograft Inflammatory Factor-1 in Cardiac Ischemia Re-perfusion Injury: Release of Molecular Markers in an in Vitro Setting

D. Olga McDaniel, Xinchun Zhou, Debbie A. Rigney, Larry S. McDaniel, Giorgio Aru, Curtis Tribble, Lawrence Creswell, Walter H. Merrill

Department of Microbiology, University of Mississippi Medical Center, Jackson, USA.
Department of Pathology, University of Mississippi Medical Center, Jackson, USA.
Department of Surgery, University of Mississippi Medical Center, Jackson, USA.

DOI: 10.4236/ojots.2013.31002                

Abstract

Initial ischemia/reperfusion injury (IRI) may have an impact on recipient immune responses after transplantation. Allograft inflammatory factor-1 (AIF-1) has been implicated in the regulation of inflammation associated with organ rejection. We hypothesized that it is either passively released from injured tissues during organ procurement, or actively secreted by allograft infiltrating cells contributing to allograft dysfunction. We investigated the impact of IRI in an in vitro study of human heart tissue during the process of transplantation. The mRNA expression levels for both isoforms of the AIF-1, I2 and I3 were significantly increased after 30 minutes reperfusion (AIF-1 I2: p < 0.01 vs. AIF-1 I3: p < 0.005). Expression levels for IL-18 and the TLRs were increased after 30 minutes of reperfusion. Only IL-18 and TLR-2 were statistically significant (IL-18: p < 0.0001 vs. TLR-2: p < 0.01). The mRNA expression levels for AIF-1 I2 and IL-18 were decreased from the original levels of ischemia after 60 and 90 minutes reperfusion. The TLR-2 and -4 were presented with minimal levels of reduction after 60 minutes. However, mRNA expression levels for all were decreased to the original levels of ischemia after 90 minutes, except for AIF-1 I3, but the difference was not statistically significant. AIF-1 and IL-18 were specifically detected in myocytes and interstitial tissues by immunohistochemistry (IHC) stain after IRI. TLR-4 was non-specific, and TLR2 was minimally expressed. The study discusses the evidence supporting that the AIF-1 may have therapeutic potential for strategies in the control of innate immune responses early on, after transplantation.

Keywords

Allograft Inflammatory Factor-1; Cardiac Myocytes; Innate Immunity; Ischemia/Reperfusion; Rejection; Toll-Like Receptors

Conflicts of Interest

The authors declare no conflicts of interest.

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