Immune Mediated Development of Guillain-Barré Syndrome
Guillain-Barré syndrome is an acute inflammatory demyelinating polyneuropathy that presents with ascending motor weakness, sensory abnormalities, and loss of reflexes. Guillain-Barré syndrome can be divided into 4 major clinically distinct forms: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the Miller Fisher syndrome (MFS), acute motor axonal neuropathy (AMAN), and acute sensorimotor axonal neuropathy (AMSAN). There are a number of potential triggers that in genetically susceptible individuals can cause this disease such as surgery, vaccinations, or infections with Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, or Mycoplasma pneumoniae1. The mechanism underlying the development of this autoimmune response is not completely understood and is the topic of this discussion. The case described is a man recently diagnosed with the AIDP variant of Guillain-Barré …show more content…
TLRs function through promoting production of pro-inflammatory cytokines, via MyD88 and NF-kB signaling. To assess whether there is a difference in expression of TLR2 and TLR4 in GBS, Du and collegues extracted RNA from peripheral blood mononuclear cells collected from either patients with GBS or healthy controls4. Relative expression of TLR2, TLR4, MyD88 and NF-kB were all increased significantly (p<0.05) for patients with GBS compared to healthy controls. Additionally proinflammatory cytokines TNF-alpha and IL-1 beta were secreted at a higher rate in the GBS patients compared to healthy controls. The study group also found that patients with severe GBS were more likely to have both a positive IgG and IgM anti-ganglioside antibody compared to those with mild GBS4. This study suggests that TLR2 and TLR4 may be involved in the pathogenesis of
Guillain-Barré syndrome is an acute inflammatory demyelinating polyneuropathy that presents with ascending motor weakness, sensory abnormalities, and loss of reflexes. Guillain-Barré syndrome can be divided into 4 major clinically distinct forms: acute inflammatory demyelinating polyradiculoneuropathy (AIDP), the Miller Fisher syndrome (MFS), acute motor axonal neuropathy (AMAN), and acute sensorimotor axonal neuropathy (AMSAN). There are a number of potential triggers that in genetically susceptible individuals can cause this disease such as surgery, vaccinations, or infections with Campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, or Mycoplasma pneumoniae1. The mechanism underlying the development of this autoimmune response is not completely understood and is the topic of this discussion. The case described is a man recently diagnosed with the AIDP variant of Guillain-Barré …show more content…
TLRs function through promoting production of pro-inflammatory cytokines, via MyD88 and NF-kB signaling. To assess whether there is a difference in expression of TLR2 and TLR4 in GBS, Du and collegues extracted RNA from peripheral blood mononuclear cells collected from either patients with GBS or healthy controls4. Relative expression of TLR2, TLR4, MyD88 and NF-kB were all increased significantly (p<0.05) for patients with GBS compared to healthy controls. Additionally proinflammatory cytokines TNF-alpha and IL-1 beta were secreted at a higher rate in the GBS patients compared to healthy controls. The study group also found that patients with severe GBS were more likely to have both a positive IgG and IgM anti-ganglioside antibody compared to those with mild GBS4. This study suggests that TLR2 and TLR4 may be involved in the pathogenesis of