Paper - Immunostimulation in the era of the metagenome

Type: Paper
Authors: Amy D. Proal, Paul J. Albert, Greg P. Blaney M.D., Inge A. Lindseth, Chris Benediktsson and Trevor G Marshall PhD
Publication: Cellular & molecular immunology
Citation: Proal AD, Albert PJ, Blaney GP, Lindseth IA, Benediktsson C, Marshall TG. Immunostimulation in the era of the metagenome. Cell Mol Immunol. 2011 May;8(3):213-25. doi: 10.1038/cmi.2010.77. Epub 2011 Jan 31.
[PMID: 21278764] [PMCID: 4076734] [DOI: 10.1038/cmi.2010.77]

See also: Preprint (full text)

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Microbes are increasingly being implicated in autoimmune disease. This calls for a re-evaluation of how these chronic inflammatory illnesses are routinely treated. The standard of care for autoimmune disease remains the use of medications that slow the immune response, while treatments aimed at eradicating microbes seek the exact opposite—stimulation of the innate immune responseThe body's first line of defense against intracellular and other pathogens. According to the Marshall Pathogenesis the innate immune system becomes disabled as patients develop chronic disease.. Immunostimulation is complicated by a cascade of sequelae, including exacerbated inflammationThe complex biological response of vascular tissues to harmful stimuli such as pathogens or damaged cells. It is a protective attempt by the organism to remove the injurious stimuli as well as initiate the healing process for the tissue., which occurs in response to microbial death. Over the past 8 years, we have collaborated with American and international clinical professionals to research a model-based treatment for inflammatory disease. This intervention, designed to stimulate the innate immune response, has required a reevaluation of disease progression and amelioration. Paramount is the inherent conflict between palliation and microbicidal efficacy. Increased microbicidal activity was experienced as immunopathologyA temporary increase in disease symptoms experienced by Marshall Protocol patients that results from the release of cytokines and endotoxins as disease-causing bacteria are killed.—a temporary worsening of symptoms. Further studies are needed, but they will require careful planning to manage this immunopathology.

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