World Allergy Forum: Bacterial Infection and Allergy
Staphylococcus Aureus and Nasal Polyposis
Claus Bachert
Bilateral nasal polyposis (NP) represents a chronic disabling inflammatory disease of the sinuses with so far unknown aetiology. Tissue eosinophilia is a hallmark of this disease in most of the cases and is believed to be related to polyp growth, and concomitant asthma is found frequently in patients with severe eosinophilic inflammation in the nasal tissue. Treatment so far consists of surgery and topical/systemic corticosteroids, with numerous recurrences in a subgroup of NP patients.
In recent years, we could demonstrate that interleukin-5 protein is dramatically increased in NP tissue, and that it has a prominent functional role in inhibiting eosinophil apoptosis, representing a key cytokine in the pathogenesis of this disease. Based on several studies, we developed a concept suitable to explain the growth of nasal polyps by a localized eosinophilic inflammation associated with pseudocyst formation and albumin retention. Furthermore, we could show that in about 50% of the polyps, total IgE protein concentrations are highly increased in NP tissue, correlating to the severity of local eosinophilic inflammation and the presence of asthma in those patients. By Elispot analysis of IgE-producing cells and comparisons between local tissue and serum total and specific IgE data, it became obvious that there was a local multiclonal IgE synthesis in those polyps with severely increased IgE protein levels in the tissue. Atopy, defined as skin test positivity to the most common inhalant or food allergens, was not related to local IgE concentrations in NP.
We recently could demonstrate that the local multiclonal IgE synthesis in NP was linked to the presence of specific IgE formation to Staphylococcus aureus enterotoxins (SAE´s), as was shown before for severe atopic dermatitis. Furthermore, in polyps with SAE specific IgE, biolinylated SAE´s stained lymphocytes accumulating in follicle-like structures, including T-cells, B-cells, APC´s and IgE-positive cells.
In summary, these findings indicate that SAE´s may act as superantigens and thus disease modifiers in a subgroup of NP subjects with severe local eosinophilic inflammation and concomitant asthma. This concept implies new treatment possibilities for an important subgroup of NP patients and may help to elucidate another link between upper and lower airways.
References
Bachert B, Wagenmann M, Hauser U, Rudack C. IL-5 is upregulated in human nasal polyp tissue. J Allergy Clin Immunol. 1997;99:837-842.
Simon HU, Yousefi S, Schranz C, Schapowal A, Bachert C, Blaser K. Direct demonstration of delayed eosinophil apoptosis as a mechanism causing tissue eosinophilia. J Immunol. 1997;158:3902-3908.
Bachert C, Wagenmann, Rudack C, Höpken K, Hillebrandt M, Wang D, van Cauwenberge P. The role of cytokines in infectious sinusitis and nasal polyposis. Allergy. 1998;53:2-13.
Bachert C, Gevaert, Holtappels G, Cuvelier C, van Cauwenberge P. Nasal polyposis: from cytokines to growth. Am J Rhinol. 2000;14:279-290.
Bachert C, Gevaert P, Holtappels G, van Cauwenberge P. Nasal
polyposis: is there a link between eosinophils and IgE? Int Arch Allergy Appl
Immunol. 2000: in press.
