Anyway back to
GBS, which is mostly harmless – until it isn’t. It can colonise people without
causing an infection. It mainly lives in the gastro-intestinal (GI) and
genito-urinary (GU) tracts. Unfortunately, it can have major and severe impacts
during pregnancy. It is the leading cause of neonatal infection, having severe
consequences for the newborn baby. It passes from the mother, who has some
level of immune protection, to the baby (who doesn’t) during, or shortly after,
birth. Whilst antibiotics can reduce the burden of disease, they are not
completely effective and alternative preventative approaches are needed. One of
which is vaccination, but one of the challenges is that the mechanism by which
women are protected against disease is not well understood. More work is needed
to understand the interplay between the immune system and the colonising
bacteria.
In our latest
study, Group B Streptococcus (GBS) colonisation
is dynamic over time, whilst GBS capsular polysaccharides-specific antibody
remains stable we worked
with Professor Kirsty le Doare and her group at St George’s University in
London to look at the interplay of GBS colonisation and the immune response.
Women were recruited and had samples taken from their GI-GU tracts every 2
weeks for 12 weeks. We then measured whether GBS was present, which strain of
GBS it was and whether colonisation led to an increase in the amount of
antibody the women made.
We observed that
colonisation with GBS was dynamic – there were volunteers that were colonised
initially that subsequently cleared the colonisation, there were others that
acquired bacterial colonisation, there were some that were never colonised and
others that had multiple different strains. However, whilst the bacterial
colonisation was variable, the levels of antibody were fairly constant implying
that acquisition of bacteria may not be directly affecting whether the women
make more antibody – or that they have previously been exposed to the same
strains and therefore don’t make new responses. Alternatively, there may be
something special about the guts that mean that bacteria that live there (but
are not necessarily causing disease) don’t trigger the immune response.
This study was
performed during the COVID lockdowns which significantly disrupted the
collection of samples. However, thanks to innovations by the study leads – such
as home sampling, it was possible to continue. These kinds of approaches may
mean larger studies can be performed as they are less intensive on the
researchers and participants.
This study
demonstrated the complex interplay between host and bacteria. Further
investigation is needed to understand how best to utilise a vaccine to protect
against this devastating disease.
