Abstract
Complement activation plays a critical role in the pathogenesis of Guillain-Barré syndrome (GBS), a debilitating immune-mediated neuropathy. Mannose-binding lectin (MBL) is a complement activation factor of lectin pathway which as genetic host factor may influence the susceptibility or severity of GBS. We investigated the frequency of MBL2 promoter (− 550H/L and − 221X/Y) and functional region (exon 1 A/O) polymorphisms and their association with disease susceptibility, clinical features and serum MBL among GBS patients (n = 300) and healthy controls (n = 300) in Bangladesh. The median patient age was 30 years (IQR: 18–42; males, 68%). MBL2 polymorphisms were not significantly associated with GBS susceptibility compared to healthy controls. HL heterozygosity in GBS patients was significantly associated with mild functional disability at enrolment (P = 0.0145, OR, 95% CI 2.1, 1.17–3.82). The HY, YA, HA and HYA heterozygous haplotypes were more common among mildly affected (P = 0.0067, P = 0.0086, P = 0.0075, P = 0.0032, respectively) than severely affected patients with GBS. Reduced serum MBL was significantly associated with the LL, OO and no HYA variants and GBS disease severity. No significant association was observed between MBL2 polymorphisms and electrophysiological variants, recent Campylobacter jejuni infection or anti-ganglioside (GM1) antibody responses in GBS. In conclusion, MBL2 gene polymorphisms are related to reduced serum MBL and associated with the severity of GBS.
| Original language | English |
|---|---|
| Article number | 5791 |
| Journal | Scientific Reports |
| Volume | 12 |
| Issue number | 1 |
| DOIs | |
| Publication status | Published - 6 Apr 2022 |
Bibliographical note
Funding Information:This research activity was funded by the icddr,b, Dhaka, Bangladesh. ZI has received grant support from the Fogarty International Center, National Institute of Neurological Disorders and Stroke of the National Institutes of Health, USA, under Award Number K43TW011447. SH has received grant support from “Global Health Equity Scholars NIH FIC TW010540”, USA. icddr,b acknowledges with gratitude the commitment of the Government of Bangladesh to its research efforts, and also gratefully acknowledges all donors who provide unrestricted support, including the icddr,b is grateful to the governments of Bangladesh, Canada, Sweden and the UK for providing core/unrestricted support. The authors are indebted to the neurologists who encouraged their patients to take part in this study.
Funding Information:
This research activity was funded by the icddr,b, Dhaka, Bangladesh. ZI has received grant support from the Fogarty International Center, National Institute of Neurological Disorders and Stroke of the National Institutes of Health, USA, under Award Number K43TW011447. SH has received grant support from “Global Health Equity Scholars NIH FIC TW010540”, USA. icddr,b acknowledges with gratitude the commitment of the Government of Bangladesh to its research efforts, and also gratefully acknowledges all donors who provide unrestricted support, including the icddr,b is grateful to the governments of Bangladesh, Canada, Sweden and the UK for providing core/unrestricted support. The authors are indebted to the neurologists who encouraged their patients to take part in this study.
Publisher Copyright:
© 2022, The Author(s).