Angiotensin converting enzyme and angiotensin receptor inhibitors could not be evaluated. In conclusion, aPLs occurring in AAA patients are associated with increased serological markers of inflammation and predicted progressive disease. These findings further Sipeimine support the concept of possibly underlying immune-mechanisms in AAA development. No association was observed between aPLs and the presence or size of an intra-aneurysmal thrombus. There is increasing interest in the role of nucleotides in immune and inflammatory responses, and in particular their role in lung diseases. There are currently known to be eight subtypes of G protein coupled P2Y receptorsand seven subtypes of ionotropic P2X receptorswhich respond to purine and pyrimidine nucleotides, and nearly all of these subtypes can be found on cells in the airways. It has been suggested that ATP may play a role in the pathogenesis of asthma, and allergen challenge has been shown to result in an increase in ATP in bronchoalveolar lavage fluid from asthmatic patients. In a mouse model of asthma, allergen challenge also resulted in an increase in ATP concentrations in bronchoalveolar lavage fluidand caused asthma-like symptoms which could be inhibited by administration of apyraseor by non-selective ATP antagonists such as suramin. These findings were interpreted as indicating recruitment and activation of lung dendritic cells by ATP, resulting in induction of asthmalike responses. The P2X7 receptor has been suggested to be involved in this process, and P2X7 knockout mice display reduced airway reactivity and leukocyte recruitment. The P2X7 receptor is known to play a key role in the processing and release of the proinflammatory cytokine IL-1b, and in patients with asthma P2X7 receptors are upregulated on eosinophils and on macrophages in bronchoalveolar lavage fluid, which secreted larger amounts of IL-1b in response to a P2X7 agonist. Reduced P2X7 function was associated with a lower incidence of asthma in children at high risk of the disease. Emphysema and chronic obstructive pulmonary diseaseare smoking-related lung diseases in which ATP has been suggested to play a role. In studies in mice, exposure to cigarette smoke increased the amount of ATP in BALF, and this was associated with inflammation and emphysema. Cigarette smoke caused the release of ATP from neutrophils, an increase in ATP in BALF and upregulation of P2 receptors on neutrophils, macrophages and lung tissue. Both cigarette smoke and ATP caused the release of the chemokine CXCL8 and elastasewhich could be prevented by suramin or apyrase. Suramin also reduced the smoke-induced lung inflammation and emphysema, and genetic deletion of the P2Y2 receptor reduced the smokeinduced production of cytokines including IFN-c and IL-1b and was also protective against smoke-induced inflammation. In a human study comparing non-smokers, healthy smokers and patients with COPD, there was a progressive increase in these groups in ATP levels in BALF, acute smoke exposure led to a further increase in the smokers and ATP levels were negatively correlated with lung function in the COPD patients. Tubeimoside-I Exhaled breath condensates from patients with COPD contained higher levels of purines than those from healthy subjects, and the levels correlated with the severity of the disease. In addition, enhanced responses to ATP were found in blood neutrophils and airway macrophages taken from patients with COPD, and there was upregulation of P2Y2 and P2X7.