Staphylococcus aureus is a bacterial pathogen that is
largely responsible for human infections that impact the skin and soft
tissue. These kinds of infections can
be serious enough to lead to life threatening conditions such as sepsis (blood
poisoning as a result of microorganisms or the toxins they produce),
endocarditis (inflammation of the interior lining of the chambers of the heart)
and bacteremia (bacteria in the blood). A
distinctive characteristic of a staphylococcal infection is the formation of
abscesses that are comprised of bacterial colonies surrounded by fibrin – a
structural protein. The severity of
infections with this organism has been attributed to its ability to evade and
undermine the immune response. It is,
therefore, essential to understand the nature of its mechanism of action in
regard to defending itself from the immune system.
Human immunity can be delineated into two distinct
responses. The first if referred to as
the “innate” response and the second as the “adaptive” response. The former is designed to respond immediately
to an invasion by deleterious organisms such as bacteria. The adaptive response is typically secondary
and engages the T and B lymphocyte populations that are in constant circulation
within the blood and lymph systems. This
response affords more enduring and long term immunity to the insulting microorganism(s).
As part of the innate response to Staphylococcus aureus
infection, neutrophils – white blood cells that move to the site of infection –
release their DNA in the a form that is referred to as neutrophil extracellular
traps (NETs). The intrinsic purpose of
these NETs is to immobilize the pathogen and enhance the activity of peptides –
small proteins – that possess anti-bacterial activity. However, Staphylococcus aureus effectively
undermines this immune response.
The mechanism of action that the pathogen employs to
counteract the role of neutrophils has been characterized through the efforts
of Dr. Vilasack Thammavongsa and his colleagues at the Department of
Microbiology of the University of Chicago.
As a result of their research efforts, they discovered that
staphylococcus aureus sidesteps the innate immune response by effectively
converting NETs to deoxyadenosine. This
modification is a product of two enzymes – nuclease and adenosine synthase –
secreted by the pathogen. This action
triggers the destruction of immune cells and also prevents macrophages – white
cells whose role is to ingest invading organisms - from entering the
staphylococcal abscesses.
This finding is of great value; for, it helps elucidates the
mechanism through which staphylococcus successfully evades the human immune
system.
