Low mitochondrial DNA copy number in resected cecum appendix correlates with high severity of acute appendicitis.

Acute appendicitis (AA) is one of the most common abdominal emergencies, and appendectomy remains the best treatment of choice in the current clinical practice. Approximately 15–30% patients with clinically suspected acute appendicitis (CSAA) were found to have a normal appendix during appendectomy, which also was known as negative acute appendicitis (NAA). 1 As a result, several clinical parameters, scoring systems or decision trees have been advocated to differentiate true acute appendicitis (TAA) from NAA before appendectomy. 123 However, few studies investigated the underlying biological or immunological pathogenesis of acute appendicitis. The main pathogenesis of acute appendicitis is believed to be obstruction of the lumen caused by bacterial overgrowth and invasion. 4 Luminal mucosa would not only act as a frontier barrier to block the bacterial attack but also trigger innate immunity through the recognition of microbial molecular patterns, secreting chemokine/or cytokine, attracting activated leukocytes, increasing vascular permeability and blood flow to destroy the invaded bacteria. 5 A recent study demonstrated that a decrease in mitochondrial DNA (mtDNA) of the damaged tissue may participate in the triggering of innate immunity during viral infection. 6 Other studies also demonstrated that low mtDNA copy numbers of the leukocytes or peripheral blood mononuclear cells (PBMCs) were associated with high severity of HIV infection, 7 generalized inflammation process 8 or advanced SLE disease activity. 910 The role of mtDNA alteration in the pathogenesis of tissue inflammation or infection deserves further study. 111213 Recently, it was demonstrated that mtDNA molecules could be released from the damaged tissue as a result of reactive oxygen species (ROS)-triggered oxidative damages. 14 Among these oxidative DNA damages, the formation of 8-hydroxyl-2′-deoxyguanosine (8-OHdG), an oxidative damage on guanine (G), is the most common one. 1516 Because mtDNA is much more susceptible to oxidative damage than did the nuclear DNA (nDNA), the amount of 8-OHdG accumulated in mtDNA may be an index to reflect cellular oxidative damage. Generally, the 8-OHdG can be repaired by human 8-oxoguanine DNA glycosylase 1 (hOGG1) through the mechanism of base excision repair during the recovery process. 1516 In this study, we investigated the mtDNA alterations, including the copy number and the degree of oxidative damage, of resected cecum appendix of CSAA patients. The experimental data were further analyzed with the consideration of pathological data and clinical parameters.