Microbial endocrinology as a basis for improved L-DOPA bioavailability in Parkinson's patients treated for Helicobacter pylori.

Antibiotic therapy to eradicate Helicobacter pylori, the causative agent of gastric and duodenal ulcers, has been suggested to improve L-DOPA bioavailability in Parkinson's and thereby improve patient symptomology. To date, there has been no proven mechanism to explain the purported benefit of treatment of H. pylori in the management of Parkinson's disease. I propose the hypothesis, and provide initial data, that the mechanism of action is due to direct utilization of L-DOPA by H. pylori to maintain its ecological niche within the gastrointestinal tract. In support of this hypothesis, data is presented which demonstrates for the first time the ability of L-DOPA to influence the in vitro growth of H. pylori in an iron-restricted minimal medium. H. pylori utilization of L-DOPA for its own growth requirement reduces the amount of per orally administered L-DOPA that would be available to the patient for the treatment of Parkinson's disease-related pathology. Neuroendocrine-mediated interactions with bacteria represent the emerging interdisciplinary field of microbial endocrinology. Thus, microbial endocrinology provides for a mechanism between L-DOPA and H. pylori with which to explain the purported benefit of H. pylori-directed antibiotic therapy to improve L-DOPA bioavailability in Parkinson's patients and thereby improve drug therapy management. Further, if other bacterial species within the gastrointestinal tract depend on the availability of L-DOPA or other similar neuroendocrine-based drugs for their survival, then the efficacy of such neuroendocrine-based drugs not restricted solely for the management of parkinsonian symptomology may also be adversely affected and may therefore justify the use of an antibiotic regimen to eradicate them.