Role of Bacterial Infection in Exacerbation of Multiple Sclerosis

Ns, Rapp; Gilroy, John; Am, Lerner

doi:10.1097/00002060-199511000-00004

Cited by 58 publications

(39 citation statements)

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“…Microbial infection is the environmental factor most strongly associated with exacerbations of MS as well as other autoimmune diseases (26,(61)(62)(63). Furthermore, mice that are transgenic for a myelin-specific TCR develop spontaneous EAE when housed in a nonsterile facility, but not in a sterile, specific pathogen-free facility (64).…”

Section: Discussionmentioning

confidence: 99%

Activation of APCs Through CD40 or Toll-Like Receptor 9 Overcomes Tolerance and Precipitates Autoimmune Disease

Ichikawa

Williams

Segal

2002

The Journal of Immunology

131

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Some autoreactive T cells normally escape thymic selection and persist in the periphery. This is true of myelin-reactive CD4+ T cells, the effectors of experimental autoimmune encephalomyelitis (EAE) in laboratory animals and the presumed mediators of multiple sclerosis in humans. Nonetheless, most individuals do not succumb to autoimmune disease. There is growing evidence that while peripheral APCs stimulate immune responses against foreign Ags in the setting of tissue destruction and “danger,” they actually maintain tolerance against self Ags under steady state conditions. We hypothesized that tolerance against candidate autoantigens could be reversed by activation of APCs via CD40 or Toll-like receptor 9 signaling. Adult SJL mice injected i.p. with a peptide fragment of proteolipid protein (a candidate autoantigen in multiple sclerosis) emulsified in IFA fail to mount lymphoproliferative or cytokine responses and are protected from EAE upon subsequent challenge with the Ag combined with adjuvants. Here we report that tolerized proteolipid protein-specific lymph node cells regain the ability to divide, differentiate along a Th1 lineage, and transfer EAE when reactivated in the presence of agonistic Abs against CD40 or CpG oligonucleotides. The effects of both anti-CD40 and CpG oligonucleotides are dependent upon induction of IL-12. Our findings suggest two mechanisms to explain the well-documented association between infectious illnesses and flare-ups of multiple sclerosis. Microbial pathogens could 1) release molecules that bind Toll-like receptors, and/or 2) stimulate microbe-specific T cells to express CD40 ligand, thereby licensing APCs that bear both microbial and autoantigens to break tolerance.

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Section: Discussionmentioning

confidence: 99%

Activation of APCs Through CD40 or Toll-Like Receptor 9 Overcomes Tolerance and Precipitates Autoimmune Disease

Ichikawa

Williams

Segal

2002

The Journal of Immunology

131

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“…Acute pyelonephritis presents with costovertebral angle pain or tenderness, often with fever, and variable lower tract symptoms. Some patients with neurological illnesses may be more difficult to assess because of atypical presentations (8,25,26). Patients with spinal cord injuries may present with symptoms such as increased bladder and leg spasms (8) or autonomic dysreflexia (25), and patients with multiple sclerosis may experience increased fatigue and deterioration in neurological function (26).…”

Section: Clinical Assessmentmentioning

confidence: 99%

Complicated Urinary Tract Infection in Adults

Nicolle¹

2005

Canadian Journal of Infectious Diseases and Medical Microbiolog

216

156

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OBJECTIVE: To review current knowledge relevant to complicated urinary tract infection, and to provide evidence-based recommendations for management. METHODS: The literature was reviewed through a PubMed search, and additional articles were identified by journal reference review. A draft guideline was prepared and critically reviewed by members of the Association of Medical Microbiology and Infectious Disease Canada Guidelines Committee, with modifications incorporated following the review. RESULTS: Many urological abnormalities may be associated with complicated urinary infection. There is a wide spectrum of potential infecting organisms, and isolated bacteria tend to be more resistant to antimicrobial therapy. Morbidity and infection outcomes in subjects with complicated urinary infection are principally determined by the underlying abnormality rather than the infection. Principles of management include uniform collection of a urine specimen for culture before antimicrobial therapy, characterization of the underlying genitourinary abnormality, and nontreatment of asymptomatic bacteriuria except before an invasive genitourinary procedure. The antimicrobial regimen is determined by clinical presentation, patient tolerance, renal function and known or anticipated infecting organisms. If the underlying abnormality contributing to the urinary infection cannot be corrected, then early post-treatment recurrence of infection is anticipated. CONCLUSIONS: The management of complicated urinary infection is individualized depending on patient variables and the infecting organism. Further clinical investigations are necessary to assist in determining optimal antimicrobial regimens.

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“…A number of studies have shown that approximately one-third of MS relapses are preceded by a viral infection (Sibley et al, 1985;Andersen et al, 1993;Panitch, 1994;Edwards et al, 1998;Buljevac et al, 2002). Relapse in individuals with MS has also been associated with bacterial infections, such as those of the urinary tract, which appear to trigger relapse in as many as 30% of MS patients (Rapp et al, 1995). Chlamydia pneumoniae infection is known to be associated with exacerbation of clinical signs in individuals with MS (Buljevac et al, 2003) and worsening of clinical score in a murine EAE model (Du et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Systemic Inflammatory Response Reactivates Immune-Mediated Lesions in Rat Brain

Serres¹,

Anthony²,

Jiang³

et al. 2009

J. Neurosci.

107

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The potential association between microbial infection and reactivation of a multiple sclerosis (MS) lesion is an important issue that remains unresolved, primarily because of the absence of suitable animal models and imaging techniques. Here, we have evaluated this question in an empirical manner using immunohistochemistry and magnetic resonance imaging (MRI), before and after the induction of a systemic inflammatory response in two distinct models of MS. In a pattern-II-type focal myelin oligodendrocyte glycoproteinexperimental autoimmune encephalomyelitis model, systemic endotoxin injection caused an increase in regional cerebral blood volume (rCBV) around the lesion site after 6 h, together with a reduction in the magnetization transfer ratio of the lesioned corpus callosum. These changes were followed by an increase in the diffusion of tissue water within the lesion 24 h after endotoxin challenge and new leukocyte recruitment as revealed both immunohistochemically and by MRI tracking of ultrasmall superparamagnetic iron oxidelabeled macrophages. Importantly, we detected in vivo expression of E-and P-selectin in quiescent lesions by MRI-detectable glyconanoparticles conjugated to sialyl Lewis X . This finding may explain, at least in part, the ability of quiescent MS lesions to rapidly reinitiate the cell recruitment processes. In a pattern-I-type delayed-type hypersensitivity response model, a similar effect of endotoxin challenge on rCBV was observed, together with delayed breakdown of the blood-brain barrier, showing that systemic infection can alter the pathogenesis of MS-like lesions regardless of lesion etiology. These findings will have important implications for the management and monitoring of individuals with MS.

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Role of Bacterial Infection in Exacerbation of Multiple Sclerosis

Cited by 58 publications

References 0 publications

Activation of APCs Through CD40 or Toll-Like Receptor 9 Overcomes Tolerance and Precipitates Autoimmune Disease

Activation of APCs Through CD40 or Toll-Like Receptor 9 Overcomes Tolerance and Precipitates Autoimmune Disease

Complicated Urinary Tract Infection in Adults

Systemic Inflammatory Response Reactivates Immune-Mediated Lesions in Rat Brain

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