<i>FAS</i> and <i>FASL</i> gene polymorphisms in patients with GBS and healthy controls.

<p><i>FAS</i> and <i>FASL</i> gene polymorphisms in patients with GBS and healthy controls.</p

<i>FAS</i> and <i>FASL</i> promoter polymorphisms in patients with GBS stratified by clinical and immunological features.

<p><i>FAS</i> and <i>FASL</i> promoter polymorphisms in patients with GBS stratified by clinical and immunological features.</p

Demographic, clinical and electrophysiological characteristics of the 300 patients with GBS and 300 healthy controls.

<p>Demographic, clinical and electrophysiological characteristics of the 300 patients with GBS and 300 healthy controls.</p

Serum levels of sFas and sFasL in severely and mildly affected patients with GBS.

<p>Severity of disease was assessed using the GBS disability score, a GDS ≥ 3 was defined as severely affected and ≤ 2, as mildly affected. The Whisker-box plots indicate the minimum, maximum and median values; *<i>P</i> < 0.05, Mann–Whitney <i>U</i>-test.</p

<i>FAS</i> promoter polymorphisms and serum sFas level are associated with increased risk of nerve damage in Bangladeshi patients with Guillain-Barré syndrome

<div><p>Guillain-Barré syndrome (GBS) is an autoimmune disorder of the peripheral nervous system triggered by molecular mimicry between pathogen lipopolysaccharides and host nerve gangliosides. Polymorphisms in the Fas receptor (<i>FAS</i>) and Fas ligand (<i>FASL</i>) genes may potentially alter the elimination of autoreactive immune cells and affect disease susceptibility or disease severity in GBS. We detected single nucleotide polymorphisms (SNPs) in <i>FAS</i> (-1377G/A and -670A/G) and <i>FASL</i> (-843C/T) in a prospective cohort of 300 patients with GBS and 300 healthy controls from the Bangladeshi population. Genotype distributions were not significantly different between patients with GBS and healthy controls. The <i>FAS</i> -670 AG heterozygous (<i>P</i> = 0.0005, OR = 2.5, 95% CI = 1.5–4.2) and GG homozygous (<i>P</i> = 0.0048, OR = 2.6, 95% CI = 1.3–5.0) genotypes were more common in patients with anti-GM1 antibodies than patients without anti-GM1 antibodies. The <i>FAS</i> -670 G allele was more prevalent in anti-GM1 antibody-positive than -negative patients (<i>P</i> = 0.0002, OR = 1.9, 95% CI = 1.4–2.7) and also in patients with the axonal subtype than demyelinating subtype (<i>P</i> < 0.0001, OR = 4.8, 95% CI = 2.3–10.1). The 1377G/-670G GG haplotype was significantly associated with the axonal subtype (<i>P</i> < 0.0001) and anti-ganglioside antibody-positivity (<i>P</i> = 0.0008) in GBS. Serum sFas (237.5 pg/mL vs. 159.5 pg/mL; <i>P</i> < 0.0001) and sFasL (225.1 pg/mL vs. 183.4 pg/mL; <i>P</i> = 0.0069) were elevated in patients with GBS compared to healthy controls, and among patients with high serum sFas was associated with severe GBS (<i>P</i> = 0.0406). In conclusion, this study indicates <i>FAS-FASL</i> promoter SNPs may promote the production of cross-reactive anti-ganglioside antibodies in GBS.</p></div

Associations between <i>FAS</i> -1377/-670 haplotypes and GBS.

<p>Associations between <i>FAS</i> -1377/-670 haplotypes and GBS.</p

Moving average of yearly estimated to total patients and under-5 years children, proportion of rotavirus, underweight, stunting, wasting, mean temperature, rainfall, sea level pressure and humidity (1993–2012).

<p>Moving average of yearly estimated to total patients and under-5 years children, proportion of rotavirus, underweight, stunting, wasting, mean temperature, rainfall, sea level pressure and humidity (1993–2012).</p