Sepsis-Fighting off the Underlying Infection

The treatment uses an unconventional antibody that converts abnormally harmful protein into protective one. Sepsis is a serious medical condition that caused by an overwhelming immune response to the infection; it eventually damages the body’s organs by depriving them nutrients and oxygen. In the worst cases, the patients spiral toward septic shock and multiple organs – lungs, kidneys, liver – may quickly fail and cause of death.

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The condition – which is more common than the heart attacks – is a leading cause of deaths, and a higher number of deaths from prostate cancer, breast cancer and AIDS combined.

Sepsis does not arise on its own but stems from other medical conditions, such as an infection in urinary tract, skin, lungs, abdomen (such as appendicitis) or other part of the body. Invasive medical procedures that are accidentally introduce bacteria into the bloodstream can also bring on sepsis.

Strengthen blood vessels:

One of the first thing that happens in sepsis – when the immune system overreacts and attacks the body – is that the blood vessels become weak and leaky. This results in a cascade of life-threatening effects, ranging from severe inflammation and organ damage, to the pulmonary edema (fluid in the lungs) and the death itself.

There is currently no cure for this sepsis; doctors are only able to target underlying infection and hope that patients can find strength to fight the sepsis on their own.

To prevent and protect the blood vessels from its worse effects and thus to improve the odds that the body can deal with the sepsis.

Antibody simultaneously block ANG2 and activation of TIE2:

Earlier attempts boost the effect of TIE2, or reduce the effect of ANG2 – the protein that blocks TIE2 – have either not been very effective or are impractical for clinical use. Antibody called ABTAA (short for ANG2-binding and TIE2-activating antibody) that works by simultaneously blocking the ANG2 and activating TIE2. “Upon binding to ANG2, ABTAA triggers clustering of ANG2, assembling an ABTAA/ANG2 complex that can subsequently bind and activate TIE2.”Thus, by binding to it, ABTAA converts normally harmful ANG2 into the protein complex that boosts a protective effect.

Journal of Emergency Medicine & Critical Care

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