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This activity is intended for gastroenterologists, family medicine and primary care clinicians, internists, nurses, physician assistants, and other members of the health care team for patients with inflammatory bowel disease.
The goal of this activity is for learners to be better able to describe a potential treatment targeting inflammation-causing gut bacteria contributing to inflammatory bowel disease by using bacteriophage viruses that may become the basis for developing therapies for inflammatory bowel disease and other types of disorders.
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CME / ABIM MOC / CE Released: 10/21/2022
Valid for credit through: 10/21/2023, 11:59 PM EST
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Inflammatory bowel diseases (IBDs), including ulcerative colitis (UC) and Crohn's disease (CD), are auto-inflammatory disorders in which an uncontrolled innate and adaptive immune response causes sustained tissue damage. Through multiple mechanisms, the gut microbiota contribute to this aberrant immune response in patients genetically vulnerable to IBD.
Bacteriophages are ubiquitous, self-replicating viruses that infect bacteria with high host specificity. Systemic use of phage therapy is promising as a rescue treatment directed against multidrug-resistant (MDR) pathogens but is limited to short-term use, given bacterial resistance and host immunity. Long-term use of oral phage therapy to sustain suppression of pathological gastrointestinal bacteria is still elusive.
New research from the Weizmann Institute of Science has shown that bacteriophages, or viruses that infect bacteria cells, can be used to target gut bacteria that worsen symptoms of UC and CD.
The project, published in Cell, studied 537 volunteers in France, Israel, the United States, and Germany to identify the bacteria strains behind the problem-causing inflammation that patients with IBD have.
From stool samples, the scientists identified Klebsiella pneumoniae (Kp) as "strongly associated with [IBD] exacerbation and severity," and filtered through 41 Kp-fighting viruses (called phages), ultimately selecting 5 phages that best targeted the strain and prevented the rise of mutants that could spread resistance.
The "5-phage cocktail" got rid of Kp in lab dishes and reduced inflammation and tissue damage caused by the strain in mice. The phages also proved stable in a fake human gut and were "well-tolerated" when given by mouth in a first-in-human phase I clinical trial of 18 healthy volunteers. In the trial, the phages multiplied in the intestines and caused no off-target changes, according to the researchers.
"To our knowledge, this constitutes the first 'silver bullet' approach promising a precise suppression of disease-causing gut microbes, without harming the surrounding microbiome," said Eran Elinav, PhD, the lead author and a professor in Weizmann's Systems Immunology Department.
The work shows that it is possible to manage IBD with something other than antibiotics, which are less specific, can cause adverse effects, and likely trigger bacterial resistance, the researchers said. They stressed the resistance-avoiding qualities of phages given by mouth and hope that the phage therapy will one day be used with induction therapy in IBD, according to the study.
"If the phage cocktail is found to be safe and effective in larger clinical trials, it may become the basis for developing therapies for not only inflammatory bowel disease but also other disorders found to be affected by gut microbes, including obesity, diabetes, neurodegenerative disease and perhaps even cancer," the university wrote in a news release.
Although the cause and cure for IBD are unknown, the early-stage study shows that it may be possible to use phage therapy to relieve some painful symptoms of UC and CD.
"Our vision is to eventually develop personalized therapies for a variety of disorders, in which the disease-causing strains of gut bacteria will be identified in each patient, and a phage cocktail will be designed to kill only those strains," Dr Elinav said.
"These exciting prospects merit further studies," the researchers wrote.
Cell. 2022;185(16):2879-2898.[1]