Taken together, hSiglec-9-hIg2 provides an antibacterial benefit against GBS serotype III infection in the transgenic mice mediated by interfering with the down-regulation of the immune responsiveness of neutrophils, rescuing host complement system functionality, thereby removing the survival advantage to the GBS, and also possibly by enhanced bacterial clearance through the innate immune mechanism utilizing the Fc portion of human IgG2 constituting hSiglec-9-hIg2. This evidence concerns the gene HILPDA and Guillain-Barre syndrome.