Elevated Levels of IL-23 in a Subset of Patients With Post-Lyme Disease Symptoms Following Erythema Migrans

Strle, Klemen; Stupica, Daša; Drouin, Elise E.; Steere, Allen C.; Strle, Franc

doi:10.1093/cid/cit735

Cited by 98 publications

(90 citation statements)

References 29 publications

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“…These symptoms might be a part of a central sensitization syndrome 179 or be attributable to immune system abnormalities, for example, increased levels of IL-23 (REF. 180) or heightened levels of anti-neuronal antibodies 181 . This area is further confused as PTLDS, or what has been referred to as ‘chronic Lyme disease’, has become a diagnosis for medically unexplained symptoms, even when patients have no evidence of past or present Lyme borreliosis 182,183 .…”

Section: Quality Of Lifementioning

confidence: 99%

Lyme borreliosis

Steere

Strle

Wormser

et al. 2016

Nat Rev Dis Primers

648

697

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Lyme borreliosis is a tick-borne disease that predominantly occurs in temperate regions of the northern hemisphere and is primarily caused by the bacterium Borrelia burgdorferi in North America and Borrelia afzelii or Borrelia garinii in Europe and Asia. Infection usually begins with an expanding skin lesion, known as erythema migrans (referred to as stage 1), which, if untreated, can be followed by early disseminated infection, particularly neurological abnormalities (stage 2), and by late infection, especially arthritis in North America or acrodermatitis chronica atrophicans in Europe (stage 3). However, the disease can present with any of these manifestations. During infection, the bacteria migrate through the host tissues, adhere to certain cells and can evade immune clearance. Yet, these organisms are eventually killed by both innate and adaptive immune responses and most inflammatory manifestations of the infection resolve. Except for patients with erythema migrans, Lyme borreliosis is diagnosed based on a characteristic clinical constellation of signs and symptoms with serological confirmation of infection. All manifestations of the infection can usually be treated with appropriate antibiotic regimens, but the disease can be followed by post-infectious sequelae in some patients. Prevention of Lyme borreliosis primarily involves the avoidance of tick bites by personal protective measures.

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Section: Quality Of Lifementioning

confidence: 99%

Lyme borreliosis

Steere

Strle

Wormser

et al. 2016

Nat Rev Dis Primers

648

697

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show abstract

“…In our experiments, both cytokines were present to induce the development of IL-17. Apparently, the presence of IL-23 is important for promoting the development of Th17 cells, but IL-1b was the key driver of the amount of IL-17 produced A previous study by Strle et al [28] showed elevated levels of IL-23 in patients with post-Lyme disease symptoms, and elevated levels of IL-17 have been found in cerebrospinal fluid of patients with neuroborreliosis [23]. It has been suggested that Th17 cells and their associated cytokines are involved in the pathogenesis of Lyme arthritis [11,29,30].…”

Section: Discussionmentioning

confidence: 94%

Autophagy suppresses host adaptive immune responses toward Borrelia burgdorferi

Buffen

Oosting

et al. 2016

Journal of Leukocyte Biology

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We have previously demonstrated that inhibition of autophagy increased the Borrelia burgdorferi induced innate cytokine production in vitro, but little is known regarding the effect of autophagy on in vivo models of Borrelia infection. Here, we showed that ATG7-deficient mice that were intra-articular injected with Borrelia spirochetes displayed increased joint swelling, cell influx, and enhanced interleukin-1β and interleukin-6 production by inflamed synovial tissue. Because both interleukin-1β and interleukin-6 are linked to the development of adaptive immune responses, we examine the function of autophagy on Borrelia induced adaptive immunity. Human peripheral blood mononuclear cells treated with autophagy inhibitors showed an increase in interleukin-17, interleukin-22, and interferon-γ production in response to exposure to Borrelia burgdorferi. Increased IL-17 production was dependent on IL-1β release but, interestingly, not on interleukin-23 production. In addition, cytokine quantitative trait loci in ATG9B modulate the Borrelia induced interleukin-17 production. Because high levels of IL-17 have been found in patients with confirmed, severe, chronic borreliosis, we propose that the modulation of autophagy may be a potential target for anti-inflammatory therapy in patients with persistent Lyme disease.

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“…33 Some have suggested that patients with elevated interleukin 23 during infection may be more likely to have persistent symptoms after treatment. 34 Other work suggests that active infection results in elevated serum concentrations of CXCL9 and CXCL10. 35 The implications, or even the reproducibility, of these observations remain to be determined.…”

Section: Lyme Pathophysiologymentioning

confidence: 99%

Nervous System Lyme Disease

Halperin

2015

Clinics in Laboratory Medicine

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Elevated Levels of IL-23 in a Subset of Patients With Post-Lyme Disease Symptoms Following Erythema Migrans

Cited by 98 publications

References 29 publications

Lyme borreliosis

Lyme borreliosis

Autophagy suppresses host adaptive immune responses toward Borrelia burgdorferi

Nervous System Lyme Disease

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