E. histolytica invasion may contribute to T-helper-2 bias and antibody production particularly against E. histolytica lectins and their association with tissue antigens such as phospholipids, actin and ANCA. By penetrating the intestinal tissues, E. histolytica is able to disturb tight junction assemblies, thereby opening the intestinal tight junctions and putting the body at risk for autoimmunity. Once in the bloodstream, E. histolytica may trigger autoimmunity against neurological or bone tissues, due to its homology with gangliosides and skeletal actin.
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Increased risk of bone and neurological disorders.
E. histolytica invasion may contribute to T-helper-2 bias and antibody production particularly against E. histolytica lectins and their association with tissue antigens such as phospholipids, actin and ANCA. By penetrating the intestinal tissues, E. histolytica is able to disturb tight junction assemblies, thereby opening the intestinal tight junctions and putting the body at risk for autoimmunity. Once in the bloodstream, E. histolytica may trigger autoimmunity against neurological or bone tissues, due to its homology with gangliosides and skeletal actin.
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Acinetobacter, Aspergillus, Babesia + Ehrlichia + Bartonella, Blastocystis hominis, Borrelia burgdorferi, Campylobacter jejuni, Candida albicans, Chlamydias, Citrullinated EBV, Clostridium difficile, Cryptosporidium, CYP450, mimic Hepatitis C Peptide, Cytomegalovirus, Entamoeba histolytica, Giardia lamblia, Helicobacter pylori, Human + Chlamydia HSP-60, Human Herpesvirus-6, Klebsiella, Mycobacterium avium, Mycoplasmas, Penicillium, Porphyromonas gingivalis, Rotavirus, Stachybotrys chartarum, Streptococcal M Protein, Streptococcus mutans, Streptozymes, Yersinia enterocolitica
