There are two types of staphylococcus aureus derived enterotoxins. In patients with nasal polyposis IgE antibodies to staphylococcus aureus enterotoxins A and B have been demonstrated. Now the definition of nasal polyposis has undergone a subtle change. It is now being referred to as chronic rhinosinusitis with nasal polyposis. This disorder is characterised by an eosinophilic T helper type II inflammation. IL-5 happens to be the driving force of inflammation in these patients. It is important to differentiate this disorder from chronic sinusitis without polyposis in which T1 helper cells mediated inflammation is seen. In this disorder gamma interferon and transforming growth factor beta are considered to tbe driving force of inflammation.
A short note on staphylococcus aureus:
Staphylococcus aureus has recognised as an important pathogen in various human diseases. Infections of this organism ranges from skin infections to enteric infections. This organism has been found inside the nasal cavity. Patients in whom these organisms are found in the nasal cavity can be divided into intermittent and persistent carrier states. Staphyloccous have been known to produce toxins. Staphylococcus aureus are capable of secreting super antigens. These superantigens helps the organims in evading the adaptive immune mechanism of the body. These superantigens can directly activate T cells via its ability to bind to the MHC class II molecule. Hence these super antigens need not be processed by the antigen presenting cells. Only when an antigen is processed by the antigen precenting cell the adaptive immune mechanism of the body can be kick started.
How nasal polyposis is formed due to the presence of staphylococcus superantigens like enterotoxin A and e.
T lymphocytes in response to the superantigens starts to proliferate. This proliferation is confined to the T lymphocytes bearing specific vβ domains. This significant clonal expansion of T cells bearing vβ domains is known as (vβ skewing). These T lymphocytes in turn causes increased production of IL-5. This causes oedema of the mucosal lining of the nasal cavity. Excessive and persistent oedema in turn leads to nasal polyposis. These superantigens also cause aspirin sensitivity due to its ability to upregulate eosinophilic inflammation.
Courtesy otolaryngology e news