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Tehran University Medical Journal [TUMJ]. 2013; 71 (1): 31-36
in Persian | IMEMR | ID: emr-148044

ABSTRACT

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

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