Several species of scavenger receptors have so far been identified. However, it remains unclear which receptors are more crucial for the foam cell formation and progression. In the present study, we compared five major scavenger receptors (SR-A, CD36, CLA-1, CD68, and LOX-1) in their levels of expression at the different stages of foam cells derived from THP-1 cells. The expression of all scavenger receptors examined was up-regulated by the stimulation with TPA for 48 hours, despite the expressions of SR-A, CD36 and LOX-1 being very low before the treatment with TPA. Four to 7 days after the removal of TPA, the levels of CD36, CLA-1 and CD68 were increased significantly. In contrast, the expression of SR-A was suppressed significantly, and no change was observed in that of LOX-1. Furthermore, when the transformed macrophages were incubated with oxidized LDL, in which the uptake of [3H] cholesteryl oleoyl ether-labeled OxLDL was linear up to 7 days after the addition of OxLDL, the expression of CD36, CLA-1 and CD68 were greatly enhanced. This enhancement was more prominent than that without oxidized LDL, and the enhancement was sustained throughout the experimental period. On the other hand, SR-A was not up-regulated, and LOX-1 was down-regulated. We thus propose that CD36, CLA-1 and CD68, but not SR-A and LOX-1, may play crucial roles in the progression of macrophages to foam cells, which is a key step for the initiation of atherosclerosis.
In the coronavirus disease-2019 (COVID-19) era, point-of-care lung ultrasound (LUS) has attracted increased attention. Prospective studies on LUS for the assessment of pneumonia in adult patients were extensively carried out for more than 10 years before this era. None of these prospective studies attempted to differentiate bacterial and viral pneumonia in adult patients using LUS. The majority of studies considered the LUS examination to be positive if sonographic consolidations or multiple B-lines were observed. Significant differences existed in the accuracy of these studies. Some studies revealed that LUS showed superior sensitivity to chest X-ray. These results indicate that point-of-care LUS has the potential to be an initial imaging modality for the diagnosis of pneumonia. The LUS diagnosis of ventilator-associated pneumonia in intensive care units is more challenging in comparison with the diagnosis of community-acquired pneumonia in emergency departments due to the limited access to the mechanically ventilated patients and the high prevalence of atelectasis. However, several studies have demonstrated that the combination of LUS findings with other clinical markers improved the diagnostic accuracy. In the COVID-19 era, many case reports and small observational studies on COVID-19 pneumonia have been published in a short period. Multiple B-lines were the most common and consistent finding in COVID-19 pneumonia. Serial LUS showed the deterioration of the disease. The knowledge and ideas on the application of LUS in the management of pneumonia that are expected to accumulate in the COVID-19 era may provide us with clues regarding more appropriate management.
A patient with congenitally deficient apolipoprotein (apo) E showed numerous tuberoerutive, tendon xanthomas and severe atherosclerosis, despite a low LDL concentration.In order to study the mechanism of xanthoma formation observed in apo E-deficient patients, we evaluated the effect of VLDL and HDL from the patient on cholesterol ester (CE) accumulation in macrophages.The results showed that there was no difference in CE formation in macrophages among normal VLDL, the patient's VLDL and apo E containing VLDL, which was prepared by incubation of the patient's VLDL with recombinant apo E. On the other hand, apo E containing HDL, which was prepared by incubation of the patient's HDL with recombinant apo E, accelerated cholesterol efflux more effectively than did the patient's HDL and decreased intracellular CE content. Moreover, free apo E accelerated cholesterol efflux from lipid loaded macrophages.These results suggest that macrophages are prevented from transforming into foam cells by their secretion of apo E. This may also explain the marked atherosclerosis and xanthomatosis observed in the patient with apo Edeficiency.
Cerebrotendinous xanthomatosis (CTX) is a rare familial sterol storage disease, causing multiple xanthomas in tendons and the brain. The underlying biochemical defect is a lack of the hepatic mitochondrial cholesterol 27-hydroxylase involved in the normal biosynthesis of bile acid, resulting in reduced biosynthesis of chenodeoxycholic acid (CDCA). It has been reported that administration of CDCA to CTX patients improves neurological disorders and xanthomas of the Achilles tendon. The present study investigated the effect of CDCA on the mechanism of cholesterol accumulation in macrophages, the major cells in xanthoma. The LDL from the patients in this study was significantly more susceptible to oxidative modification than normal LDL, and supplement therapy with CDCA resulted in an improvement in the susceptibility to oxidative modification. In the incubation of CDCA with plasma, 13% of the CDCA added to serum was recovered in the LDL fraction. In addition, supplementation with CDCA enhanced cholesteryl ester transfer protein (CETP) activity and reduced high-densitylipoprotein cholesterol levels in the plasma. This evidence suggests that the multiple xanthomas observed in CTX may be induced by increased oxidized LDL and the low activity of CETP, both of which are caused by a lack of CDCA. J Atheroscler Thromb, 2004; 11: 167-172.
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