Guillain–Barré syndrome, transverse myelitis and infectious diseases

Yhojan Rodríguez, Manuel Rojas, Yovana Pacheco, Yeny Acosta-Ampudia, Carolina Ramírez-Santana, Diana M. Monsalve, M. Eric Gershwin, Juan Manuel Anaya

Research output: Contribution to journalReview article

14 Citations (Scopus)

Abstract

Guillain–Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.

Original languageEnglish (US)
Pages (from-to)547-562
Number of pages16
JournalCellular and Molecular Immunology
Volume15
Issue number6
DOIs
StatePublished - Jun 1 2018

Fingerprint

Transverse Myelitis
Communicable Diseases
Molecular Mimicry
Spinal Cord
Polyradiculoneuropathy
Campylobacter Infections
Campylobacter jejuni
Genetic Loci
Guillain-Barre Syndrome
Polyneuropathies
Gangliosides
Schwann Cells
Disease Susceptibility
Wounds and Injuries
Cellular Structures
Genetic Predisposition to Disease
Myelin Sheath
Natural History
Peripheral Nerves
Disease Outbreaks

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Infectious Diseases

Cite this

Rodríguez, Y., Rojas, M., Pacheco, Y., Acosta-Ampudia, Y., Ramírez-Santana, C., Monsalve, D. M., ... Anaya, J. M. (2018). Guillain–Barré syndrome, transverse myelitis and infectious diseases. Cellular and Molecular Immunology, 15(6), 547-562. https://doi.org/10.1038/cmi.2017.142

Guillain–Barré syndrome, transverse myelitis and infectious diseases. / Rodríguez, Yhojan; Rojas, Manuel; Pacheco, Yovana; Acosta-Ampudia, Yeny; Ramírez-Santana, Carolina; Monsalve, Diana M.; Gershwin, M. Eric; Anaya, Juan Manuel.

In: Cellular and Molecular Immunology, Vol. 15, No. 6, 01.06.2018, p. 547-562.

Research output: Contribution to journalReview article

Rodríguez, Y, Rojas, M, Pacheco, Y, Acosta-Ampudia, Y, Ramírez-Santana, C, Monsalve, DM, Gershwin, ME & Anaya, JM 2018, 'Guillain–Barré syndrome, transverse myelitis and infectious diseases', Cellular and Molecular Immunology, vol. 15, no. 6, pp. 547-562. https://doi.org/10.1038/cmi.2017.142
Rodríguez Y, Rojas M, Pacheco Y, Acosta-Ampudia Y, Ramírez-Santana C, Monsalve DM et al. Guillain–Barré syndrome, transverse myelitis and infectious diseases. Cellular and Molecular Immunology. 2018 Jun 1;15(6):547-562. https://doi.org/10.1038/cmi.2017.142
Rodríguez, Yhojan ; Rojas, Manuel ; Pacheco, Yovana ; Acosta-Ampudia, Yeny ; Ramírez-Santana, Carolina ; Monsalve, Diana M. ; Gershwin, M. Eric ; Anaya, Juan Manuel. / Guillain–Barré syndrome, transverse myelitis and infectious diseases. In: Cellular and Molecular Immunology. 2018 ; Vol. 15, No. 6. pp. 547-562.
@article{49927501087a43c1afd36ce6a1f69545,
title = "Guillain–Barr{\'e} syndrome, transverse myelitis and infectious diseases",
abstract = "Guillain–Barr{\'e} syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.",
author = "Yhojan Rodr{\'i}guez and Manuel Rojas and Yovana Pacheco and Yeny Acosta-Ampudia and Carolina Ram{\'i}rez-Santana and Monsalve, {Diana M.} and Gershwin, {M. Eric} and Anaya, {Juan Manuel}",
year = "2018",
month = "6",
day = "1",
doi = "10.1038/cmi.2017.142",
language = "English (US)",
volume = "15",
pages = "547--562",
journal = "Cellular and Molecular Immunology",
issn = "1672-7681",
publisher = "Nature Publishing Group",
number = "6",

}

TY - JOUR

T1 - Guillain–Barré syndrome, transverse myelitis and infectious diseases

AU - Rodríguez, Yhojan

AU - Rojas, Manuel

AU - Pacheco, Yovana

AU - Acosta-Ampudia, Yeny

AU - Ramírez-Santana, Carolina

AU - Monsalve, Diana M.

AU - Gershwin, M. Eric

AU - Anaya, Juan Manuel

PY - 2018/6/1

Y1 - 2018/6/1

N2 - Guillain–Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.

AB - Guillain–Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.

UR - http://www.scopus.com/inward/record.url?scp=85044178113&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85044178113&partnerID=8YFLogxK

U2 - 10.1038/cmi.2017.142

DO - 10.1038/cmi.2017.142

M3 - Review article

C2 - 29375121

AN - SCOPUS:85044178113

VL - 15

SP - 547

EP - 562

JO - Cellular and Molecular Immunology

JF - Cellular and Molecular Immunology

SN - 1672-7681

IS - 6

ER -