There Are Many Tests Available Today. However, Many Labs Fail to Test These three markers. We Believe unless you have had all three markers done, Lab testing is not sufficient.
1. Actomyosin IgA:
GI microfilaments of the actomyosin network are critical for apical junctional complex biogenesis and function. The apical junctional complex, made up in part by tight junction proteins zonulin and occludin, is responsible for preventing antigen invasion and preservation of the biochemical homeostasis within the GI tract. The actomyosin network can signal tight junction contractions and give structure to their assembly.
Autoimmune liver disorders, Celiac, Chronic hepatitis, Crohns, Myasthenia Gravis
Known Cross Reactions:
Giardia lamblia, Entamoeba histolytica
Many environmental factors, such as bacterial toxins, can affect the stability of the actomyosin network and occludin/zonulin. Antibodies to the actomyosin network are, therefore, biomarkers of intestinal barrier dysfunction, either via bacterial infiltration or by an autoimmune mechanism aimed at the GI tract. for the best clinical value, antibodies against the actomyosin network should be measured in conjunction with lipopolysaccharide (LPS) and occludin/ zonulin proteins.
When antibodies are detected against actomyosin alone, it indicates autoimmunity against the mucosal epithelium and other tissue cell cytoskeleton of the intestinal barrier.
When antibodies are detected against the actomyosin network and LPS, but none are detected for occludin/zonulin, this indicates a breakdown in intestinal barrier integrity by bacterial antigens through the transcellular pathway. The detection of antibodies against actomyosin, LPS, and occludin/zonulin indicates that there has been both transcellular and paracellular penetration of the intestinal barrier.
2. Occludin/Zonulin IgG, IgA, IgM
The GI tract is lined by a protective epithelium. The tightness and stability of this barrier is regulated by a series of intercellular junction, collectively called tight junctions. These junctions allow a regulated entry of selected molecules.
The integrity of the intestinal barrier is vital for the protection of the body against antigen invasion and for the preservation of gut microchemical homeostasis. Occludin/Zonulin proteins constitute the majority of the building blocks of the tight junctions.
Celiac, Inflammatory bowel disease, Type 1 Diabetes, Autoimmunity
The detection of antibodies against Occludin/Zonulin indicates that normal regulation of tight junctions is compromised, and that the tight junctions are breaking down due to an autoimmune mechanism initiated by environmental triggers such as infections, toxic chemicals, and some dietary proteins and peptides. When Occludin/Zonulin antibody levels are measured in conjunction with levels for lipopolysaccharide (LPS) and actomyosin, the resulting information can provide a more accurate diagnosis. The detection of positive Occludin/Zonulin antibody levels alone indicates a paraellular breakdown of the intestinal barrier that is triggered by factors other than bacterial antigen infiltration.
The presence of antibodies against both Occludin/Zonulin and LPS indicates that the integrity of the intestinal barrier has been breached by bacterial antigens through the paracellular pathway. Elevated antibody levels for occulin/zonulin, LPS, and actomyosin indicate that there has been penetration through both the transcellular and paracellular pathways.
In many autoimmune diseases, including Celiac and Type 1 diabetes, the onset of the disease is usually preceded by occulin/zonulin upregulation.
Genetically susceptible people who test positive for occludin/zonulin should be further assessed, monitored, and set on a preventative program for Type I diabetes and autoimmunity.
3. Lipopolysaccharides (LPS) IgG, IgA, IgM
Lipopolysaccharides (LPS) is a molecule made up of a lipid and a polysaccharide. LPS is a component of the surface membrane of gram-negative bacteria found in the GI tract. Gram-negative bacteria include: E coli, Salmonella, Shigella, Pseudomonas, H Pylori, Legionella, Wolbachia. As an endotoxin, LPS increases the negative charge of the bacterial membrane and promotes the upregulation of pro-inflammatory cytokines- which cause further immune system dysregulation.
Chronic fatigue, gram-negative bacterial infection, increased intestinal permeability, major depression, Miller Fisher syndrome, short bowel syndrome
Known Cross Reactions:
LPS is a bacterial endotoxin that elicits a strong immune response. The detection of antibodies against LPS indicated infiltration of macromolecule-sized endotoxins into the intestinal barrier and the systemic circulation. For better clinical evaluation, LPS should be measured in conjunction with antibodies against tight junction proteins, Occludin/Zonulin, and epithelial structure proteins from the actomyosin network. If antibodies to LPS alone are elevated while antibody levels for Occludin/Zonulin and actomyosin are negative, the person may have gut flora dysbiosis.
When both LPS and Occludin/Zonulin antibodies are positive and actomyosin antibody is not detected, there is likely a breakdown in intestinal barrier integrity caused by infiltration of bacterial antigens through the paracellular pathway. Results showing elevations in LPS and actomyosin antibody levels, but not in Occludin/Zonulin, indicate a high possibility of breakdown in the intestinal barrier integrity. by bacterial antigens through the transcellular pathway.