Abstract

Multiple sclerosis (MS) is caused by a complex interaction of genetic and environmental factors. Numerous causative factors have been identified that play a role in MS, including exposure to bacteria. Mycobacteria, Chlamydia pneumoniae, Helicobacter pylori, and other bacteria have been proposed as risk factors for MS with different mechanisms of action. Conversely, some pathogens may have a protective effect on its etiology. In terms of acquired immunity, molecular mimicry has been hypothesized as the mechanism by which bacterial structures such as DNA, the cell wall, and intracytoplasmic components can activate autoreactive T cells or produce autoantibodies in certain host genetic backgrounds of susceptible individuals. In innate immunity, Toll-like receptors play an essential role in combating invading bacteria, and their activation leads to the release of cytokines or chemokines that mediate effective adaptive immune responses. These receptors may also be involved in central nervous system autoimmunity, and their contribution depends on the infection site and on the pathogen. We have reviewed the current knowledge of the influence of bacteria on MS development, emphasizing the potential mechanisms of action by which bacteria affect MS initiation and/or progression.

Highlights

  • Multiple sclerosis (MS) has a complex pathophysiology that results from multiple and unclear interactions between genetic and environmental factors

  • There are several examples of virus–bacteria interactions (Almand et al, 2017), which mainly occur when the pathogens colonize the same site during infection, sometimes viruses can act at different locations within the host (Steed and Stappenbeck, 2014)

  • It has been demonstrated that some pathogens including Mycobacterium tuberculosis, Streptococcus pneumoniae, and others can penetrate the blood–brain barrier (BBB) or the blood– cerebrospinal fluid barrier and enter into the central nervous system (CNS), altering its permeability by releasing toxic cell wall components (Dando et al, 2014)

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Summary

INTRODUCTION

Multiple sclerosis (MS) has a complex pathophysiology that results from multiple and unclear interactions between genetic and environmental factors. Epstein–Barr virus (EBV) seems to be the strongest candidate as a risk factor (Olsson et al, 2017). Subclinical EBV infection is present in over 95% of all individuals, including those with MS; the MS incidence and prevalence differ in each country. Coinfection with another pathogen, including bacteria, could explain the difference between high- and low-risk areas for MS. There are several examples of virus–bacteria interactions (Almand et al, 2017), which mainly occur when the pathogens colonize the same site during infection, sometimes viruses can act at different locations within the host (Steed and Stappenbeck, 2014). The human immunodeficiency virus targets a wide variety of immune cells, causing depletion of CD4+ T cells and up-regulation of CD14+ cells, which likely contributes to the susceptibility of co-infection with Mycobacterium tuberculosis (Pawlowski et al, 2012)

Role of Bacteria in Multiple Sclerosis
MECHANISMS OF AUTOIMMUNE DISEASE INDUCTION
Suspected mechanism of action
Chlamydia pneumoniae Mycoplasma pneumoniae
Mycobacterium bovis BCG
GUT MICROBIOTA
CONCLUSION
Findings
AUTHOR CONTRIBUTIONS
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