Lipopolysaccharides IgA+IgM

check icon Optimal Result: 0 - 2.6 ELISA Index.

Lipopolysaccharides (LPS) are endotoxins from gram-negative bacteria in the gut. The LPS protects gram-negative bacteria from gram-positive bacteria. When gram-negative bacterium dies it releases its LPS, which travels through the epithelial cells of the intestinal barrier and finds its way into the blood stream. Once LPS reaches the blood stream, it causes inflammation throughout the body and has been implicated in playing a role in multiple disorders.

- When Lipopolysaccharides (LPS) enter the bloodstream, it can contribute to plaque formation in the arteries leading to heart disease and has been implicated in metabolic, liver, thyroid, bone and nervous system disorders.
- LPS can also open the blood-brain barrier and put the brain and nervous system at risk.

Antibodies Appear:

→ Gram-negative bacterial infection

→ Hemolytic uremic syndrome

→ Increase intestinal permeability

→ Typhoid fever

Known Cross-Reactions:

DNA-histone, Ganglioside, Antiphospholipid antibodies

References:

- Ludwig, et al. Saliva IgM and IgA are a sensitive indicator of the humoral immune response to Escherichia coli O157 lipopolysaccharide in children with enteropathic hemolytic uremic syndrome. Pediatr Res, 2002; 52:307–313.

- Chart, et al. Analysis of saliva for antibodies to the LPS of Escherichia coli O157 in patients with serum antibodies to E. coli O157 LPS. J Med Microbiol, 2003, 52:569–572.

- Herath. Early diagnosis of typhoid fever by the detection of salivary IgA. J Clin Pathol, 2003;56:694–648.

- Maes, et al. The gut-brain barrier in major depression: intestinal mucosal dysfunction with an increased translocation of LPS from gram negative enterobacteria (leaky gut) plays a role in the inflammatory pathophysiology of depression. Neuroendocrinol Lett, 2008; 29(1):117-124.

- Neisser, et al. Serum antibodies against gangliosides and Campylobacter jejuni lipopolysaccharides in Miller Fisher Syndrome. Infect Immunity, 1997; 65(10):4038-4042.

- Poxton, et al. Antibodies to lipopolysaccharide.Immunol Methods, 1995; 186:1-15.

- Sumazaki, et al. Monoclonal antibody against bacterial lipopolysaccharide cross-reacts with DNA-histone. Clin exp Immunol, 1986; 66:103-110.

- Zaka-ur-Rab, et al. Evaluation of salivary anti-Salmonella typhi lipopolysaccharide IgA ELISA for serodiagnosis of typhoid fever in children. Arch Dis Child, 2012; 97(3):236-238.

- Cheng, et al. IgA antiphospholipid antibodies in normal human saliva cross-react with bacterial lipopolysaccharide. Int Arch Allergy Immunol, 1993; 101:297-298.

What does it mean if your Lipopolysaccharides IgA+IgM result is too high?

Lipopolysaccharides (LPS) is the compound in the membranes of harmful bacteria that trigger inflammation. Immune cells in the mucosal lining do not interact with LPS unless the walls are breached due to leaky gut. Upon exposure, the immune system produces antibodies to LPS, another marker we can measure to identify leaky gut. LPS antibodies also signify gut flora dysbiosis, or the overgrowth of harmful bacteria in the digestive tract. When we see LPS antibodies in the bloodstream we know it is causing inflammation throughout the body and may have breached the blood-brain barrier, causing inflammation in the brain.

Clinical Significance:

Lipopolysaccharides (LPS) are bacterial endotoxins that elicit a strong immune response. The detection of salivary antibodies against LPS indicates mucosal immune reactivity to LPS. Upregulated antibodies to LPS indicate gut dysbiosis. If the patient is experiencing recent-onset high fever, weakness and stomach pains, or has bloody diarrhea, the elevated salivary LPS may be an indication of Typhoid fever or Escherichia coli infection respectively.

In an S typhi LPS study, researchers found the level of salivary anti-LPS IgA was significantly higher in typhoid cases compared to febrile and healthy control and also revealed that the maximum sensitivity of salivary anti-LPS IgA are in the second and third weeks of illness, with the levels falling thereafter.

Salivary IgA and IgM antibodies were found to decline to their normal levels 45 to 90 days after the acute phase. Studies on Escherichia coli infections showed greater specificity and sensitivity of salivary IgA over serum antibodies during the acute phase of hemolytic uremic syndrome.

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