Azharul Islam, Suraj Abraham and Anthony P Moran
Guillain-Barre syndrome (GBS) is an autoimmune disease in which body’s immune system attacks the nervous system that leads to nerve inflammation causing muscle weakness. This syndrome affects people of both sexes between ages 25 and 50 years. It is not clear what exactly triggers GBS. However, Campylobacter jejuni is found to be the most common pathogenic factor that is found to trigger GBS and this is widely reported. Several of these studies have shown that surface lipopolysaccharide (LPS) present in C. jejuni may act as an antigenic factor that induces GBS. In addition, some of these reports have also suggested that in addition to the host cell and bacterial antigenic factor interactions, the molecular mimicry between C. jejuni LPS and peripheral nerve gangliosides may play a significant role in the development of GBS. Although LPS was recognized as a potent antigen by different studies, nevertheless, the antigenic diversity and the lack of clearly defined protective epitopes are major constraints in developing vaccines against C. jejuni. In this review, we will briefly overview the molecular mimicry mechanism, potential vaccine development strategies, the current successes and pitfalls in developing vaccines against C. jejuni-induced GBS.
