From our findings, we conclude that exercise training exerts remarkable antiproliferative and antiinflammatory effects in the rat colonic mucosa, suggesting that this may be an important mechanism to explain how exercise protects against colonic cancer.

Cathepsin G (CatG), a serine protease present in mast cells and neutrophils, can produce angiotensin-II (Ang-II) and degrade elastin. Here we demonstrate increased CatG expression in smooth muscle cells (SMCs), endothelial cells (ECs), macrophages, and T cells from human atherosclerotic lesions. In low-density lipoprotein (LDL) receptor-deficient (Ldlr−/−) mice, the absence of CatG reduces arterial wall elastin degradation and attenuates early atherosclerosis when mice consume a Western diet for 3 months. When mice consume this diet for 6 months, however, CatG deficiency exacerbates atherosclerosis in aortic arch without affecting lesion inflammatory cell content or extracellular matrix accumulation, but raises plasma total cholesterol and LDL levels without affecting high-density lipoprotein (HDL) or triglyceride levels. Patients with atherosclerosis also have significantly reduced plasma CatG levels that correlate inversely with total cholesterol (r= −0.535, P<0.0001) and LDL cholesterol (r= −0.559, P<0.0001), but not with HDL cholesterol (P=0.901) or triglycerides (P=0.186). Such inverse correlations with total cholesterol (r= −0.504, P<0.0001) and LDL cholesterol (r= −0.502, P<0.0001) remain significant after adjusting for lipid lowering treatments among this patient population. Human CatG degrades purified human LDL, but not HDL. This study suggests that CatG promotes early atherogenesis through its elastinolytic activity, but suppresses late progression of atherosclerosis by degrading LDL without affecting HDL or triglycerides.

Infiltration of surgical wounds with long-acting local anaesthetics (LA) is used to reduce postoperative incisional pain. We hypothesised that infiltration with LA interferes with wound healing in rats. Seventy-two rats were allocated into nine groups. After intraperitoneal anaesthesia, the interscapular dorsal region was infiltrated with equivolumes of saline, 0·5% bupivacaine or ropivacaine, in a randomised double-blind fashion. A standardised incision was performed in the infiltrated area and sutured closed. The rats were euthanised on the 3rd or 14th day after the operation and tissue from the incision site was subjected to histochemical analyses and mechanical testing (MT). Compared with the control group, bupivacaine displayed a significant increase in the macrophage number on day 3 (+63% versus +27% for ropivacaine). The transforming growth factor β-1 expression had a significant increase in the LA (versus saline) groups, +63% in ropivacaine group and +115% in bupivacaine group on day 3 (P < 0·05). The collagen fibres as measured by dyed area were significantly higher in the bupivacaine group on day 3 (+56%, P < 0·01 versus +15% for ropivacaine). CD34 was reduced in bupivacaine group (-51%, P < 0·05 versus +3% for ropivacaine). On day 14, no statistical differences were observed in either LA group (versus saline) with respect to histopathologic or inflammatory mediators. MT on day 14 showed no differences between the LA and saline groups. The LA-induced increases in histological markers did not extend beyond the third day, suggesting that wound infiltration with long-acting LA does not impair the wound healing process in rats.

Objective Asthma and abdominal aortic aneurysms (AAA) both involve inflammation. Patients with asthma have an increased risk of developing AAA or experiencing aortic rupture. This study tests the development of one disease on the progression of the other. Approach and Results Ovalbumin sensitization and challenge in mice led to the development of allergic lung inflammation (ALI). Subcutaneous infusion of angiotensin II (Ang-II) into mice produced AAA. Simultaneous production of ALI in AAA mice doubled abdominal aortic diameter and increased macrophage and mast cell content, arterial media smooth muscle cell (SMC) loss, cell proliferation, and angiogenesis in AAA lesions. ALI also increased plasma IgE, reduced plasma IL5, and increased bronchioalveolar total inflammatory cell and eosinophil accumulation. Intraperitoneal administration of an anti-IgE antibody suppressed AAA lesion formation and reduced lesion inflammation, plasma IgE, and bronchioalveolar inflammation. Pre-establishment of ALI also increased AAA lesion size and lesion accumulation of macrophage, mast cell, and media SMC loss, increased plasma IgE, reduced plasma IL5, IL13, and TGF-β, and increased bronchioalveolar inflammation. Consequent production of ALI also doubled lesion size of pre-established AAA and increased lesion mast cell and T cell accumulation, media SMC loss, lesion cell proliferation and apoptosis, plasma IgE, and bronchioalveolar inflammation. In peri-aortic CaCl2 injury-induced AAA in mice, production of ALI also increased AAA formation, lesion inflammation, plasma IgE, and bronchioalveolar inflammatory cell accumulation. Conclusion This study suggests a pathologic link between airway allergic disease and AAA. Production of one disease aggravates the progression of the other.