Role of Superantigens in Allergic Inflammation: Their Relationship to Allergic Rhinitis, Chronic Rhinosinusitis, Asthma, and Atopic Dermatitis

Abstract

Objectives Our intention was to review all material published to date regarding superantigens (SAgs) and allergy from an otorhinolaryngological viewpoint to understand this association more clearly. Methods We identified all materials published mentioning both SAg and allergic rhinitis (AR), chronic sinusitis, asthma, and atopic dermatitis (AD) that are indexed on PubMed, Google, or the ProQuest Central databases. Results Staphylococcus aureus is a significant bacterial pathogen in humans and has the ability to produce enterotoxins with superantigenic features. The inflammatory response in allergy seen in both B cell and T cell may be attributed to SAgs. Sufferers of both allergic asthma with rhinitis and AR alone produce serological evidence of immunoglobulin E formation to SAgs produced by S. aureus. Perennial AR sufferers carry S. aureus more frequently and the presence of the organism within the nasal cavity may exacerbate perennial AR. SAg produced by S. aureus potentially worsens the asthmatic inflammatory response within the airway and may lead to the airways becoming hyperresponsive, as well as possibly activating T cells if asthmatic control is poor. Staphylococcal SAgs potentially increase the risk of developing chronic rhinosinusitis with nasal polyposis, additionally being a marker for more severe disease. If SAgs bring about chronic inflammatory responses in the nose and sinuses, then T cells excreting interferon-gamma may be a crucial mediator. In allergic dermatitis, S. aureus could be a key player in exacerbation of the condition. Even in younger pediatric patients with allergic dermatitis, allergic hypersensitivity to SAgs is frequent and may be a factor explaining how severe the condition becomes. Conclusion Just as SAgs are known to feature in many allergic conditions, they play their part in AR, chronic rhinosinusitis, asthma, and AD. Further research is required before the relationship between SAgs and allergy can be adequately explained.

Study of the impact of long-duration space missions at the International Space Station on the astronaut microbiome

“…A number of studies have found a higher abundance of Staphylococcal bacteria in the upper respiratory tract of patients with chronic rhinosinusitis 66,67 and a reduction in diversity 68 . Staphylococcus has also been found positively associated with other respiratory diseases, such as allergic rhinitis and asthma 69 . While other factors could be playing a role in the upper respiratory symptoms experienced by the crew at the ISS, an elevated relative abundance of nasal Staphylococcal bacteria is consistent with these symptoms 10 .…”

Evidence linking atopy and staphylococcal superantigens to the pathogenesis of lymphomatoid papulosis, a recurrent CD30+ cutaneous lymphoproliferative disorder

“…[25] Current studies indicate that colonized SSAg-producing S. aureus intensify cutaneous inflammation of atopic dermatitis and Sézary syndrome and promote tumor progression in Sézary syndrome. [26,27] Antibiotics have an ameliorating effect on inflammation in these conditions, [28] [29] Oral antibiotics are also administered as a treatment for LyP. However, because LyP is a chronic condition characterized by intermittent flare ups of lesions, it is difficult to determine the long term effectiveness of anti-Staphylococcal antibiotics for LyP.…”

IL-35 is critical in suppressing superantigenic Staphylococcus aureus-driven inflammatory Th17 responses in human nasopharynx-associated lymphoid tissue

“…6 Further, SAg-Sau colonization has been associated with a range of inflammatory/autoimmune conditions, including asthma, chronic rhinosinusitis, Wegener's granulomatosis (WG) and multiple sclerosis (MS). 3,[7][8][9] Nasopharynx-associated lymphoid tissues (NALT) are mucosal immune organs in the upper respiratory tract and are known induction sites for immunity against a number of respiratory pathogens. The exposure to a large number of microbial antigens results in a substantial number of proinflammatory T cells in NALT which could potentially lead to a highly inflammatory response in the presence of SAg-Sau.…”