https://www.ncbi.nlm.nih.gov/pubmed/31930745/

2020 Jan 13. doi: 10.1111/imr.12837. [Epub ahead of print]

A joint effort: The interplay between the innate and the adaptive immune system in Lyme arthritis.

Abstract

Articular joints are a major target of Borrelia burgdorferi, the causative agent of Lyme arthritis. Despite antibiotic treatment, recurrent or persistent Lyme arthritis is observed in a significant number of patients. The host immune response plays a crucial role in this chronic arthritic joint complication of Borrelia infections. During the early stages of B. burgdorferi infection, a major hinder in generating a proper host immune response is the lack of induction of a strong adaptive immune response. This may lead to a delayed hyperinflammatory reaction later in the disease. Several mechanisms have been suggested that might be pivotal for the development of Lyme arthritis and will be highlighted in this review, from molecular mimicry of matrix metallopeptidases and glycosaminoglycans, to autoimmune responses to live bacteria, or remnants of Borrelia spirochetes in joints. Murine studies have suggested that the inflammatory responses are initiated by innate immune cells, but this does not exclude the involvement of the adaptive immune system in this dysregulated immune profile. Genetic predisposition, via human leukocyte antigen-DR isotype and microRNA expression, has been associated with the development of antibiotic-refractory Lyme arthritis. Yet the ultimate cause for (antibiotic-refractory) Lyme arthritis remains unknown. Complex processes of different immune cells and signaling cascades are involved in the development of Lyme arthritis. When these various mechanisms are fully been unraveled, new treatment strategies can be developed to target (antibiotic-refractory) Lyme arthritis more effectively.

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For more: Peer-Reviewed Evidence of Persistence of Lyme:MSIDS copy

https://madisonarealymesupportgroup.com/2019/02/22/why-mainstream-lyme-msids-research-remains-in-the-dark-ages/

Excerpt:

By combining the PTLDS group with the third group, there are 60% of patients ending up with chronic symptoms, a number that more closely matches my experience as a patient advocate (9).

THIS IS AN IMPORTANT POINT AS RESEARCHERS CONTINUE TO DOWNPLAY THE ASPECT OF PERSISTENT SYMPTOMS BY USING THE FALSELY SKEWED LOW PERCENTAGES.
  • Burrascano found Lyme disease has a 4-week cycle, where every 4 weeks patients experience a symptom flair. Burgdorfer found this in mice studies, and IGeneX found the same thing in urine antigen studies.Borrelia grow and are active, then become inactive.Four weeks later they activate.This has been shown recently in vitro. Think of Bb as a slow relapsing fever.This nuance is important because antibiotics only kill during the active phase.You need a minimum of a month to bracket a whole generation cycle.

 

  • When patients reach a plateau, he recommends cycling therapy where you discontinue antibiotics until symptoms return.Then, return to full treatment until symptoms are gone. He states that many patients become symptom free after 4 of these cycles.He also used this on himself with success.

In brief, all the research to date has used faulty study parameters.  Typically you must test positive on the 2-tiered testing and have the EM rash to even enter the study – leaving out a large patient population.  When you study the organism for any length of time at all you realize this is not your average bacteria.  Treatment must address this complexity.  The idea that 3 weeks of the mono therapy of doxycycline “curing” this is asinine. Also, little research has been done on concurrent infection.  Many researchers feel this is a rare event, yet in the real world many, many patients have far more than Lyme.  What little we know shows that concurrent infection is more severe and of a longer duration, yet these studies don’t ever touch this.

Current testing uses one species of borrelia when researchers are discovering a new species every year – which testing will never pick up.