Primary Human Microglia Are Phagocytically Active and Respond to Borrelia burgdorferi With Upregulation of Chemokines and Cytokines.
The Lyme disease causing bacterium Borrelia burgdorferi has an affinity for the central nervous system (CNS) and has been isolated from human cerebral spinal fluid by 18 days following Ixodes scapularis tick bite. Signaling from resident immune cells of the CNS could enhance CNS penetration by B. burgdorferi and activated immune cells through the blood brain barrier resulting in multiple neurological complications, collectively termed neuroborreliosis. The ensuing symptoms of neurological impairment likely arise from a glial-driven, host inflammatory response to B. burgdorferi.
To date, however, the mechanism by which the bacterium initiates neuroinflammation leading to neural dysfunction remains unclear. We hypothesized that dead B. burgdorferi and bacterial debris persist in the CNS in spite of antibiotic treatment and contribute to the continuing inflammatory response in the CNS.
To test our hypothesis, cultures of primary human microglia were incubated with live, antibiotic-killed and antibiotic-killed sonicated B. burgdorferi to define the response of microglia to different forms of the bacterium. We demonstrate that primary human microglia treated with B. burgdorferi show increased expression of pattern recognition receptors and genes known to be involved with cytoskeletal rearrangement and phagocytosis including MARCO, SCARB1, PLA2, PLD2, CD14, and TLR3. In addition, we observed increased expression and secretion of pro-inflammatory mediators and neurotrophic factors such as IL-6, IL-8, CXCL-1, and CXCL-10. Our data also indicate that B. burgdorferi interacts with the cell surface of primary human microglia and may be internalized following this initial interaction.
Furthermore, our results indicate that dead and sonicated forms of B. burgdorferi induce a significantly larger inflammatory response than live bacteria. Our results support our hypothesis and provide evidence that microglia contribute to the damaging inflammatory events associated with neuroborreliosis.
The study in the following link corroborates the above study in that it did not find active CNS infection with Lyme encephalopathy: https://www.medscape.com/viewarticle/891992
The following short video shows phagocytosis in action. For those of my vintage, think of Pac Man gobbling up things in its path. This is exactly what our immune cells (macrophages or white blood cells) do. Notice that “special digestive enzymes” shred the bacterium into pieces. This is why enzyme therapy can help Lyme/MSIDS patients – both digestive and systemic enzymes can help in numerous ways – one of which is by shredding the bacteria, and cleaning the blood of debris. According to the above study, this debris is very probably ONE reason we have high inflammation, pain, and symptoms. Anything you can do to clear out that debris is helpful.
Immune Cells Eating Bacteria (Phagocytosis)
This video describes the structure and function of microglia.
By Matt Jensen. Created by Matthew Barry Jensen.
For more on Enzymes: https://madisonarealymesupportgroup.com/2016/04/22/systemic-enzymes/
Lactoferrin, an iron-binding milk glycoprotein has also been found to help due to borrelia’s ability to hijack our plasminogen system allowing it to penetrate tissue barriers: https://madisonarealymesupportgroup.com/2018/05/03/lactoferrin-for-lyme/
DMSO & MSM may also help certain patients due to their anti-inflammatory, anticoagulant, oxygenating, free radical scavenging, detoxifying, and antiparasitic properties. Please read this article to understand both substances better. https://madisonarealymesupportgroup.com/2018/03/02/dmso-msm-for-lyme-msids/
And, as always, please work with your medical practitioner and discuss ALL treatment ideas. There are medical contraindications on nearly every substance and you need to be privy to them.