Cholera Antibodies, Proteins & ELISA Kits

Cholera is a disease caused by the serogroups O1 and O139 of the bacteria Vibrio cholerae (V. cholerae). There are an estimated 1.3-4 million cholera cases reported annually. Cholera leads to severe diarrhea, vomiting, dehydration and it can progress to mortality in extreme cases.

Cholera is spread through water or food which is contaminated with V. cholerae. In particular, cholera is endemic in regions such as Africa and Asia whereby there is poor sanitation and high fecal contamination in drinking water.

There are live-attenuated and inactivated whole cell oral cholera vaccines which are safe and well tolerated. However, due to the vast amount of cholera cases reported annually there is still the need for further cholera research for the enhancement and development of vaccines.

V. Cholerae colonizes the small intestine and produces its main virulence factor which is the cholera toxin. This exotoxin is composed of one A subunit and five B subunits. The B subunit binds to monosialoganglioside (GM1) on host cell surfaces. The A subunit activates adenylate cyclase and elevates intracellular cyclic adenosine monophosphate (cAMP) levels. This in turn leads to fluid loss, inhibition of electroneutral sodium chloride absorption and increased chloride secretion which ultimately results in severe forms of diarrhea.

As aforementioned, the cholera toxin B subunit binds to GM1 on the host cell surface during pathogenesis. As well as this, V. cholerae flagellin is recognized by toll-like receptor 5 (TLR5) and interleukin-8 (IL-8) gets induced. TLR4 has been said to recognize V. cholerae lipopolysaccharide (LPS) and induce the production of cytokines via a MyD88-dependent pathway. Recently, it has also been shown that TLR2 is activated in cholera infections by the outer membrane vesicle (OMV) of V. cholerae.

A key area of research is the immune response against V. cholerae. It has been shown in studies that there is an upregulation of cytokines and chemokines during cholera infections such as interleukin-1alpha (IL-1alpha), IL-1beta, TNF-alpha, IL-6, IL-8, granulocyte–macrophage colony-stimulating factor (GM-CSF) and monocyte chemotactic protein-1 (MCP-1). As well as this, cytokines which are regularly associated with antigen-specific acquired immunity such as IL-2, IL-4, IL-5, IL-10 and IL-12p40 were not detected during cholera infections.

Immunometabolism is an important area of science which encompasses regions of metabolism and immunology. Many of the functional capacities of immune cells are dependent on the metabolic state of the cell and its capability to mount an immune response.

Some studies have shown that V. cholerae generates adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS) and it can use nitrate as an electron acceptor in the respiratory chain. However, at present there is very little research covering how immune cell metabolism is affected by V. cholerae infections, meaning it represents a potential research area for future investigations. Assay Genie provides a wide range of immunometabolism assays such as glycolysis, fatty acid oxidation, the citric acid (TCA) cycle and OXPHOS assays kits.

Animal models are useful research tools which are often used in early stages of therapeutic product development and pathogenesis studies. While humans are the main hosts for V. cholerae, animals can still become infected if they have high quantities of the bacteria present in their body. In particular, mice and rabbits are the most common animal models for cholera infections. Rabbits and mice infected with V. cholerae display similar symptoms observed in human cholera and they are often used for pathophysiology and vaccine studies.