At the time when patients with lupus or lupus erythematosus (SLE) are diagnosed, about 15% to 30% will already have inflammation in which it is nervous, which violates the function of the kidneys and can lead to kidney failure. From 30% to 50% of SLE patients will ultimately develop initis, and half of them will eventually develop the final kidney disease.
Research team of the Medical University of Southern Medicals led by Jim Oatses, MD, Director of the Faculty of Rheumatology and Immunology, and the Vice -President for Research in the Department of Medicine, develops a new approach to preventing carcinomas – improving the health and functioning of cells that come out of the blood vessels Rental endothelium to prevent the immune of cashews.
The team reports in the field of lupus science and medicine that the exposure of serum endothelial renal cells from patients with lupus kidney inflammation, who experience the explosion, caused cell failure, which leads to this inflammation. In contrast, when the same cells were simultaneously exposed to serum with renal inflammation and the studied L-sekterin drugs, the inflammation was reduced, and the genes associated with the production of nitric oxide, which is known to be protected against inflammation. The serum was obtained from Biobank with samples from patients with lupus, and South Carolina Clinical & Translational Research Institute supported samples in processing and banking.
In patients with SLE, autoimmune diseaseThe body collects immune defense not against the attacking embryo, but against the body itself, causing inflammation, tissue damage, and sometimes organs. In the case of lupus kidney inflammation, it is a kidney aimed at the immune system.
“I compare this aiming through the immune system to what is happening after a transplant,” said Oaters. “Thus, patients who had a transplanted kidney require drugs suppressing the immune system to prevent rejection. In the case of patients with kidney inflammation, the lupus reject their own kidney.”
Immunological suppression was also a therapy in patients with lupus kidney inflammation, but carries the costs-applicants become much more exposed to infection.
The approach to treatment developed by Oatses Lab does not suppress natural body functions, such as immunity, but uses pharmaceuticals to withdraw inflammation and establish a more protective environment of endothelial cells, enabling proper functioning.
“When the endothelial cells that come out of blood vessels are handicapped, exposes people to the risk of heart attacks and strokes, but also inflammatory or scar events in the kidney. Risk people to damage to the organs,” said Oatses. “This is the main goal of my laboratory – restoring the protective actions of properly functioning endothelial cells.”
Oatses Laboratory Manager Dayvia Russell, the first author of the latest publication, sums up a new approach.
“The dishes are a gateway to your organs,” she said. “The concept of our studies consists in protecting kidneys in patients with lupus kidney inflammation by preventing vascular damage.”
The key to maintaining healthy endothelial cells is the production of nitric oxide molecule, which can protect against inflammation and oxidative stress, as well as help in maintaining healthy blood flow and prevent immune cell leaks into the tissue. However, oxidative stress, such as the one produced by risk factors of chronic disease, such as obesity, burning and diabetes, can cause endothelial cell failure, increasing the likelihood of inflammation.
In particular, oxidative stress interrupts the production of nitric oxide by turning off the endothelical enzyme of nitric oxide synthase (ENOS), causing the production of peroxide, a strong free radical. SuperTleside has an unpaired electron, thanks to which it is highly reactive and destroys for other molecules.
“Enos is a Yin and Yang molecule,” said Oatses. “When it works properly, it can produce nitric oxide that protects against inflammation, but when it is not, it can have the opposite effect, causing peroxide that causes oxidative stress.”
In their study, Mous scientists for the first time showed the influence of lupus renal inflammation on the genetic profile of renal endothelial cells and the ways in which L-seketerina, which increases the ENOS function, changes these genetic profiles. The team showed that the exposure to serum endothelial cells from patients with the development of kidney inflammation led to a higher expression of genes associated with inflammation. In contrast, the simultaneous exposure of renal endothelium cells to both serum with kidney inflammation and L-sectine L-Sumipterin caused a decrease in the expression of genes associated with oxidative stress and increased expression of genes associated with the production of nitric oxide, which suggests the protective effect.
This research line is new because it aims to control the inflammatory environment, which can cause tissue and organs damage, and not by suppressing the immune system, which can make people susceptible to infection, but by using pharmaceuticals to adapt natural cellular processes to restore the function of endothelial cells, and thus protection against inflammation.
If these findings are confirmed in animal studies of mice susceptible to lupus, the team would then like to conduct a small scale evidence test in people after obtaining the necessary financing.
Discoveries can also affect the use of L-seketerin in diseases other than lupus kidney, said Russell. It is known that one of the genes has increased with L-Sekterin L, is reduced in kidneys in type 2 diabetes.
“He suggests that L-sekterina has the potential not only in the treatment of lupus kidney inflammation, but also other vascular diseases, and maybe even type 2 diabetes,” she said.