[Streptococcus super antigen in polyp tissue of patients with nasal polyposis and chronic rhinosinusitis in comparison to normal population]

Nasal polyp [NP] is a benign mucosal mass located in both sinuses and nares which is mostly seen in association with cystic fibrosis, asthma or oversensitivity to aspirin. The prominent histological feature of NP is inflammatory cell infiltration with eosinophil predominance. Superantigens role in causing NP complications is already proven. Superantigens, which are mostly originated from Streptococci and Staphylococci, activate T cells strongly and increase the process of production and release of cytokines, and secretion of IgE from B cells, which in turn directly affects proinflammatory cells such as eosinophils, both in their tissues infiltration and functions. The samples are collected from patients referring to ENT clinic in Rasoul Akram training Hospital in Tehran after thorough clinical and paraclinical examinations. For control group the samples collected from patients undergoing rhinoplasty. All the samples kept frozen and sent to immunology lab. The DNA of the excised tissues extracted and amplified by using the superantigens specific primers and PCR product detected by gel electrophoresis. The date analyzed by using mean and SD and CHI[2] analytical tools. Fifteen healthy individuals, 25 patients with rhinosinusitis and 24 with polyposis entered this trial. Group A Streptococcus toxin detection was significantly more frequent in those with nasal polyp and rhinosinusitis compared to healthy individuals [P=0.001 and 0.005, respectively], but the results were almost the same for those with nasal polyp and rhinosinusitis [P=0.4]. Streptococci may play an important role in induction or clinical exacerbation of polyposis and group A Streptococcus pyogenes exotoxin [SPEs] with superantigenic effects may have a crucial role in etiology and pathogenesis of polyps with or without rhinosinusitis. It is postulated that, T cells polyclonal activation by SPEs may cause recruitment of inflammatory cells in nasal mucosa. These inflammatory cells include IgE producing B cells leading to allergic and inflammatory reactions in NP.

[Inflammatory cytokine detection in adenotonsill and peripheral blood mononuclear cells-culture in adenotonsillectomy patients: a comparative study]

Tonsils and adenoid hypertrophy is a major respiratory symptom in children which is partly due to recruitment of inflammatory cells in upper airway lymph nodes as a result of the effects of synthesis and release of different inflammatory cytokines. It seems that infections play role in concert with these cytokines leading to tonsilar hypertrophy and other pathologic consequences. It is proposed that cellular infiltrate of tonsils and adenoids may secrete different quantities of these cytokines compared with peripheral blood mononuclear cells [PBMC] cultures. Among patients who were admitted for adenotonsillectomy to the ENT ward, 37 patients, under 1-12 years old patients with fulfill criteria selected to include the study. Excised adenoid and tonsils cultured and inflammatory cytokines Interferon-gamma [INF-gamma], Interlukine-1 [IL-1], IL-6, IL-8 and tumor necrosis factor-alpha [TNF-alpha] measured in cellular culture supernatant. The same cytokines measured in PBMC cultures. The data shows that there is a significant difference between IFN-gamma and IL-8 amounts in adenoid tissue culture supernatant and PBMC culture of our patients. Furthermore, the amounts of IFN-gamma, IL-1 and IL-8 showed considerable difference between tonsilar tissue culture supernatant and PBMC culture of these patients. Although there is a significant correlation between IL-6 amounts in tissue culture supernatant and PBMC culture [P=0.02], the respective data for TNF is only almost significant. Inflammatory cytokines may have significant role in the early provoke of inflammation occurred in hypertrophied tonsils and adenoid. The majority of these cytokines increase the expression of adhesion molecules on epithelial cells and influence the recruitment of leucocytes and inflamed tonsils. On the other hand lack of sufficient cytokine release may lead to persistent infections and may cause chronic inflammation and hypertrophied tissue