| BACKGROUND AND AIM:Understanding the mechanism of atherosclerosis has and still is the major pathwayto help prevent and cure coronary heart diseases. We now know that both innateand adaptive immunity help in the development of inflammation, which is the basis ofatherosclerosis. In this context, Thymic Stromal Lymphopoietin (TSLP) has sincerecently been found to be a major precursor of inflammation, having both pro-andanti-inflammatory properties. Though no research has yet been conducted on theeffect of TSLP in coronary heart diseases, we will show that TSLP, via a pro-inflammatory Th17-cytokine secreting mechanism, contribute to the development ofatherosclerotic plaques in mice in ApoE/TSLPR deficient mice.METHODS:9TSLPR-/-(TSLP-Receptor Knock-out) transgenic mice were bred with10ApoE-/-(Apolipoprotein Knock-out) over a duration of6months till F3or third generationmice were obtained, a total of100. After PCR was carried out on their tails togenotype pure breeds, only ApoE-/-TSLPR-/-Double KO (DKO), a total of41, wereselected for the study. These mice, aged8-16weeks, were fed with a Western Dietwith a protein to fat ratio of2:5for12weeks. After the High Fat Diet, the mice wereeuthanized, dissected and their aorta (root,thoracic and abdominal) were collected.These were dissected, cross-and transectioned, and stained with Haemotoxylin/Eosin and Oil Red respectively to identify atherosclerotic plaques.10ApoE-/-mice also fed both on High Fat Diet, were used as control.RESULTS:The aorta of ApoE-/-TSLPR-/-mice fed on High Fat Diet showed very little or noatherosclerotic plaque at week12. However, those of ApoE-/-mice, also of High FatDiet showed moderately to severely atherosclerotic plaques, specially at the aorticroot, trunk and abdominal segments. This correlated with our experiment objectives.CONCLUSION:From the results obtained in this study, we deduced that TSLP can promoteatherosclerosis as a pro-inflammatory marker, and thus TSLPR deficiencysuppresses atherosclerosis. |
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