Some of the organisms that make biotoxins that can cause CIRS include dinoflagellates ( Pfiesteria, Gambierdiscus (ciguatera), Karenia (and other species that produce brevetoxins) cyanobacteria ( Microcystis, Cylindrospermopsis, Lyngbya wollei) fungi ( Wallemia, Stachybotrys, Chaetomium, Trichoderma, Aspergillus versicolor, Aspergillus versicolor and others) actinomycetes ( Streptomyces and others) apicomplexans ( Babesia, Sarcocystis, Eimeria), and spirochetes ( Borrelia spp burgdorferi and (likely) B. An ongoing exposure to the above microbes and/or compounds can result in a recurrent activation of immune responses, leading to exaggerated immune responses and prolonged production of inflammatory mediators, especially in the absence of regulation of inflammation by neuropeptides MSH or VIP. These microbes and compounds include but are not limited to fungi, bacteria, actinomycetes, and mycobacteria and their toxins as well as inflammagens from fragments of fungal structures and beta glucans, mannans, hemolysins, proteinases, spirocyclic drimanes and volatile organic compounds (VOCs). These compounds initiate an innate immune inflammatory response in the human host. When CIRS is acquired because of an exposure to a WDB, it is termed CIRS-WDB (Expert Treating Physicians Consensus, 2010).Īccording to a report released by the World Health Organization in 2009, in a WDB, people are chronically exposed to different microbes and/or compounds of microbial or other origin that are present in the indoor air of a WDB.
Other environmental sources of biotoxins that can lead to CIRS include certain compounds made by dinoflagellates, cyanobacteria, fungi, actinomycetes, bacteria, mycobacteria, etc. The exposure to environmental sources of biotoxins includes a chronic exposure to the interior environment of water-damaged buildings (WDB), or ingestion of fish contaminated with the toxins of marine dinoflagellates, such as ciguatoxins.
CIRS may be acquired through different mechanisms, for example, an exposure to toxins or inflammagens that may include, but are not limited to, environmental biotoxins, and chronic illness from Lyme disease present even after treatment with antibiotics. BACKGROUND OF THE INVENTIONĬIRS is a form of Systemic Inflammatory Response Syndrome (SIRS) and is characterized by (1) lack of regulation of host inflammatory response as evidenced by deficiency of alpha melanocyte stimulating hormone (MSH) and/or vasoactive intestinal polypeptide (VIP) (2) presence of more than one of Th1 responses (pro-inflammatory) Th2 responses (anti-inflammatory) Th17 responses (tied to transforming growth factor beta-1 (TGF-β1)) coagulation abnormalities, especially abnormalities in von Willebrand's profile activation of complement split products activation of elements under regulation of hypoxia inducible factor including vascular endothelial growth factor (VEGF) and erythropoietin abnormal regulation of ACTH responses to cortisol and ADH responses to osmolality. The proteogenomic analysis for the diagnosis, treatment, and monitoring of CIRS is based on identifying proteins and/or genes that are differentially expressed in subjects suffering from CIRS compared to healthy subjects. The invention specifically relates to the diagnosis, treatment and monitoring of CIRS through a comprehensive approach comprising an assessment of a subject for case definition parameters and a proteogenomic analysis. The present invention relates generally to the diagnosis, treatment, and monitoring of Chronic Inflammatory Response Syndrome (CIRS), kits for use in the methods, and pharmaceutical compositions for use in the methods of treatment. 7, 2012, the disclosure of which is hereby incorporated by reference herein in its entirety. This application claims priority to Provisional Application No.
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