Lyme Arthritis is a markedly debilitating symptom of stage three Borrelia Burgdorferi infection. With the picc line in place and an assortment of potent antibiotics and herbal protocols I'm still unable to lessen the inflammation and arthritic symptoms in my small joints. Stopping antibiotics merely potentiates the symptoms.
The controversy becomes apparent when we try to identify the causative agent of these symptoms. One viewpoint deduces that the causative agent is an overactive immune response, where three weeks of antibiotic treatment is all that is needed to eradicate the infection. This auto-immune response is partly due to dead Borrelia Burgdorferi proteins. On the contrary, another faction deduces that an active infection is the causative agent of the auto-immune response and that suppressing the immune system with steroids will further spread an already disseminated infection. This view additionally supports the bleb theory, where Borrelia Burgdorferi spirochetes shed their outer-surface OPSA 31 protein, which in many cases mutates to B-cells causing an auto-immune response.
I know plenty of people that walk around with Borrelia Burgdorferi asymptomatically, they probably do not have many spirochetes shedding blebs. They may have cystic forms and their immune system is keeping them in dormancy or is an asymptomatic state merely a TH2 dominant TH1/TH2 differentiation and a favoring environment for the reproduction of bacteria and the dissemination of infection?
In my understanding, Borrelia Burgdorferi bacteria like to manipulate cytokines. In joint fluid they purposely elevate IL-10 anti-inflammatory cytokine, which would help to RELIEVE arthritis symptoms but would increase spirochete load. However, low IL-10 levels in joint fluid would lead to arthritic symptoms but a markedly less spirochete load. IL-10 is noted to suppress immune system response if elevated. Outer-surface OPSA 31 protein is able to augment NK cells, which can lead to induction of TNF-a, IL-8, inflammatory Protein 1, RANTES protein. Hence, in the presences of an active infection the stimulation of a pathogenic response to Borrelia Burgdorferi infection induces Lyme Arthritis.
"Neutrophils can kill B. burgdorferi in the absence of antibody (96, 118) and release specific granules that also augment killing of spirochetes and local tissue damage (57, 96). Therefore, it seems apparent that a strong influx of neutrophils upon infection would assist in the clearance of spirochetes, greatly limiting their dissemination and ability to induce arthritis. However, the bacteria tricks the immune system into releasing immune mediators that prevent infiltration of neutrophils. Therefore, neutrophils release enzymes that degrade host tissue while killing B. burgdorferi. In addition, antigen-presenting cells such as macrophages and dendritic cells, which work diligently (but inadequately) to clear initial borrelial infection, activate T cells to specifically kill B. burgdorferi and, in doing so, initiate significant inflammatory events that may result in destructive arthritis. These shortcomings in the innate immune response to B. burgdorferi infection are magnified when factors such as differential surface antigen expression in the host (87, 88, 128) elicits additional, potentially damaging immune responses against an organism that escaped innate immune surveillance."
So feeling better symptom wise might not indicate an eradication of the infection and very well could indicate a dissemination of the infection if treatment was not done appropriately. Hence, B. Burgdorferi likes to elevate anti-inflammatory cytokines and manipulate the TH1/TH2 differentiation to a TH2 dominance in the most general sentience.
So, a lot of the later debilitating symptoms involving arthritis are just that. T-cell cytokines, natural killer cells and the immune system fighting the bacteria, So in my case, the administration of steroid drugs and immune suppressant drugs might not be a good thing?
I was asked by my neurologist to try cannabis and see if it helped my joint pain. In my understanding, THC suppresses the immune system and potentiates TH1, in regards to TH1/TH2 differentiation, which presents a potential risk of decreased resistance to infections such as Borrelia Burgdorferi. THC impairs HEL processing as well as suppresses fixation-resistant co-stimulatory signal to helper T cells by diminishing expression of macrophage heat-stable antigen.
It also increases TH2 differentiation by increasing levels of IL-4, IL-10; which would help symptoms of Lyme arthritis and decreases IFN-a, IL-12; associated with TH1 response.
CBD was able to block collagen induced arthritis after oral ingestion but is also said to suppress the immune system. What I'm looking for is something that can help relieve Arthritic symptoms without suppressing my immune system.
Edited by birthdaysuit, 07 October 2016 - 08:45 PM.
