2 replies to this topic

[bwane]

 33 yr male with chronic e.coli infection of prostate and bladder. CT scan showed normal urogential tract. 

 

Been on numerous rounds of antibiotics, bladder infection always comes back with the same e.coli 

 

infection moved up to the kidneys, was able to clear away symptoms with keflex and bactrim. 

 

Been keeping symptoms of bladder infection under control with D-mannose 2g x4 daily.

 

Recently skipped D-mannose due to busy work schedule, kidney infection came back but was able to clear away symptoms each time with just D-mannose

 

Kidney infection symptoms become more frequent, require more dosing of D-mannose daily. 

 

Strongly suspect that e.coli has established biofilms in my kidney/ureter/renal pelvis. 

 

Is there a combination of supplements and antibiotics that can destroy this fucking biofilm before my I get chronic kidney disease and end up in renal failure?

 

 

[Hip]

A good option, if you can find a willing medical professional, may be to create an autovaccine (aka: autogenous vaccine) which selectively targets the E. coli in your kidneys and urinary tract. 

 

Antibiotics can actually increase biofilm formation and bacterial dysbiosis in the urinary tract and kidneys, whereas an autovaccine precision targets the culprit bacterium, E. coli in this case, and will not promote dysbiosis.

 

An autovaccine is a vaccine made from the patient's own killed bacteria. A doctor or laboratory will take a sample of the culprit bacterium, in your case taking a sample of the E. coli from your urine, culture the bacteria and grow large amount of it, then kill the bacterium, and create an injectable vaccine out of it. That vaccine then trains your immune system to fight that particular bacterium.

 

Unfortunately it is going to be hard to find someone who can make you an autovaccine. Autovaccines are used a lot for veterinary purposes, but not often in human medicine. 

 

 

So a close alternative is to buy a ready-made E. coli vaccine like Uromune (MV140) which will work in the same way, stimulating your immune system to target the  E. coli. Unfortunately Uromune is not easy to obtain. 

[Hebbeh]

Research reveals potential new strategy to combat urinary tract infections -- ScienceDaily

 

 

Identifying the dynamic events occurring during urinary tract infections (UTI) has revealed a new potential strategy to combat this condition, considered the most common type of infection. Researchers at Baylor College of Medicine and Washington University School of Medicine have discovered that the sequence of events taking place during UTI sustains a delicate balance between the responses directed at eliminating the bacteria and those minimizing tissue damage that may occur in the process.

The NRF2 pathway stood out as a key contributor to this balance, by regulating both the potential damage to tissues and the elimination of bacteria. Treating an animal model of UTI with the FDA-approved, anti-inflammatory drug dimethyl fumarate (DMF), a known NRF2 activator, reduced tissue damage and bacterial burden, opening the possibility that DMF could be used to manage this condition in the future. The study appears in the journal Cell Reports.

"Urinary tract infections are not only common, but typically recurrent and tend to give rise to antibiotic-resistant bacteria, a serious medical concern," said corresponding author Dr. Indira Mysorekar, E. L. Wagner Endowed Professor of Medicine- infectious diseases at Baylor, previously at Washington University School of Medicine.

"More than 85% of UTI are caused by uropathogenic E. coli (UPEC), bacteria that can attach to the surface of the epithelial cells lining the inside of the bladder, called urothelial cells," said first author Dr. Chetanchandra S. Joshi, a postdoctoral associate in the Mysorekar lab. "Attached UPEC can then enter the urothelial cells, where they reproduce. In the current study, we looked at how urothelial cells fight back UPEC invasion and proliferation while preserving their integrity, which is essential for proper bladder function."

Understanding the process that follows a UPEC infection revealed a potential new strategy to combat the condition. "We learned that active NRF2 was involved in both neutralizing ROS, which helped protect urothelial cells, and eliminating UPEC," Joshi said. "These findings suggested that a drug that activated NRF2, such as DMF, might help clear UPEC infections."

 

Activators and Inhibitors of NRF2: A Review of Their Potential for Clinical Development (nih.gov)

 

Several natural compounds have been identified as electrophilic NRF2 inducers, including sulforaphane, curcumin, resveratrol, quercetin, genistein, and more recently andrographolide [69]. For instance, sulforaphane (SFN), an isothiocyanate found in cruciferous vegetables, has been successfully used for the treatment of patients with type II diabetes mellitus [70, 71]. Due to the capacity of SFN to cross the blood-brain barrier, it protects against neurodegenerative disorders as demonstrated in murine models of disease. Regarding acute brain damage, SFN was shown to exert protective effects in hypoxic-ischemic injury in rats by reducing the infarct ratio and by upregulating NRF2 and HO-1 [72, 73]. In neurodegenerative disease models, SFN proved protective capacity against the neurotoxic Aβ 1-42 peptide in neuronal cells [74]. In vivo, SFN ameliorated cognitive impairment in an acute mouse model of Alzheimer disease (AD) [75]. In Parkinson disease (PD), SFN protected dopaminergic cells against the cytotoxic effects of 6-hydroxydopamine [76]. In the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of PD, SFN counteracted astrogliosis and microgliosis and reduced the death of dopaminergic neurons [77–79]. To improve the stability of SFN, Evgen Pharma has developed a cyclodextrin formulation, SFX-01, which is under phase II clinical trial for the treatment of subarachnoid haemorrhage. A hybrid molecule of SFN and melatonin (ITH12674) was designed to have a dual “drug-prodrug” mechanism of action for the treatment of brain ischemia [80].

 

Another natural compound that modifies Cys-151 in KEAP1 and has also ROS-scavenging activity is curcumin, a linear diarylheptanoid present in turmeric (Curcuma longa) [81]. It has been used for the treatment of obesity, metabolic syndrome, and prediabetes [82–84]. Furthermore, curcumin has been shown to suppress the deleterious action of carcinogens by activating NRF2 [85, 86].