Antibody Treatment For Influenza

An antibody targeting the molecule ANGPTL4 could help influenza patients recover faster, study suggests.

AsianScientist (Feb. 20, 2015) – Nanyang Technological University (NTU) scientists have developed an antibody which has the potential to help patients suffering from pneumonia and influenza to recover faster. Their results have been published in Cell Reports.

Proven effective in lab tests, more research needs to be done before the antibody can be safely tested in humans. The scientists are now using the new antibody to develop a diagnostic kit which can help doctors accurately track the recovery progress of flu and pneumonia patients.

Two biotech multi-national corporations, Abcam and Adipogen International, have won the rights to license the antibody. The two multinational companies will produce the antibody for sale to global organisations doing research in vaccine and drug development.

This new antibody was developed by Associate Professor Andrew Tan, who led an interdisciplinary team of scientists from NTU’s School of Biological Sciences, Institute of Molecular and Cell Biology, National University of Singapore (NUS) and doctors from National University Health System.

“While it will take up to eight years to develop the antibody into a useable treatment for human patients, we are currently developing a diagnostic kit which should be commercialized in about three years,” said Tan.

“The kit will be able to help doctors diagnose the severity of pneumonia and the efficacy of the prescribed treatment. This is done by detecting the concentration of a particular protein called ANGPTL4, which is present in samples taken from patients suffering from upper respiratory tract infections.”

Pneumonia is now the second cause of deaths in Singapore at about 18 percent, just after cancer. It is also the leading cause of death in children worldwide accounting for 15 percent of all deaths for children under five years old.

Influenza epidemics, such as the deadly 1918 Spanish Flu which killed over 50 million people or the severe acute respiratory syndrome (SARS) outbreak in 2002, are also of concern to governments and to the general populace worldwide.

The new antibody works by blocking ANGPTL4 which was found to be in high concentration in the tissue samples taken from patients suffering from pneumonia.

“When the antibody we developed was given to mice suffering from pneumonia and influenza which had high levels of ANGPTL4, these mice recovered much faster than the other mice who didn’t receive the antibodies,” Tan said.

“We know that ANGPTL4 usually helps to regulate blood vessel leakiness. But this is the first time we have shown that by blocking this protein, we are able to control the natural response of inflammation, which in turn reduces the damage that inflammation does to the lungs.”

“The concentration of ANGPTL4 correlates to the amount of inflammation the patient is having,” Assoc Prof Tan explained. “With our diagnostic kit, doctors will be able to see if a particular treatment is working for a patient. This is done by observing whether the concentration of ANGPTL4 is decreasing or not.”

Assoc Prof Vincent Chow from NUS Yong Loo Lin School of Medicine, a co-author of the paper, said, “This study reveals the potential diagnostic and therapeutic value of targeting ANGPTL4 in pneumonia, and warrants further detailed clinical investigation in pneumonia patients.”

NTU researcher Li Liang, the first author of the paper, said they have proved that ANGPTL4 causes the blood vessels in the lungs to be leakier, allowing more white blood cells and other antibodies to enter the lungs to combat the infection. By blocking ANGPTL4, the ‘leakiness’ of the blood vessels is lessened, thus reducing the inflammation process.

The article can be found at: Li et al. (2015) Angiopoietin-like 4 Increases Pulmonary Tissue Leakiness and Damage during Influenza Pneumonia.

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Source: Nanyang Technological University.
Disclaimer: This article does not necessarily reflect the views of AsianScientist or its staff.

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