When a foreign body or a disease-causing microbe enters our body, specific Y-shaped proteins called antibodies identify and set off the processes leading to their elimination.
However, in some bronchectiasis patients, antibodies actually make things worse. A paper published in The Journal of Experimental Medicine this week has confirmed and offered a possible mechanism that would explain this phenomenon.
Accelerate lung damage Bronchiectasis makes the lungs prone to colonisation by bacteria. Pseudomonas aeruginosa bacteria are found in up to 30 per cent of adult patients and have been associated with reduced quality of life and accelerated lung damage. P.aeruginosa infection has also known to be resistant to many kinds of antibiotics and is therefore difficult to get rid of.
Scientists from University of Birmingham set out to explain why some bronchectiasis patients with the normal amount of antibodies in their blood were unable to fight P. aeruginosa infection.
They found out that this was because of the presence of a blocking factor which, upon further experimentation, was confirmed to be the antibodies themselves
SignalP. aeruginosa has extra-long sugar molecule chains on their surface. It appeared that a type of antibody called IgG2 was binding to these sugars.
Usually antibody-binding serves as a signal for other immune cells to arrive at the destination and destroy the trouble-maker, but in this case the IgG2 was somehow protecting the bacteria.
To confirm this, the scientists tested the blood of bronchectiasis patients with P. aeruginosa infections and found that those with impaired immunity had increased levels of IgG2. Moreover, when IgG2 was removed from the blood stream, the bacteria-killing capacity returned. “We believe the IgG binds to the sugar molecule at such high density that it creates a physical barrier between the bacterial cell surface and the antibacterial components of the blood which in normal patients would mediate killing of the bacterium,” wrote one of the authors Ian R. Henderson, Professor of Microbial Biology at University of Birmingham, in an email to this correspondent.
Failed attempts These findings could have implications in on-going vaccine research, especially if the strategy involves the sugar coating of the bacteria. Indeed, Henderson believes that three attempts at creating a vaccine failed because of this.
By immunising the patient with doses of this sugar, the body will generate more of the blocking IgG2 antibodies which will protect the bacterium from killing instead of making them immune to infection.
