RESUMO
Hearing processing and communication abilities development may be influenced by chronic inflammation of the airways in children, especially in case of otitis media and/or adenotonsillar hypertrophy. The present review summarizes the influence of adenotonsillar hypertrophy on speech abilities as well as the consequences of otitis media, with a particular focus on peripheral and central hearing, on the development of language, attention, and memory skills.
Assuntos
Aptidão/fisiologia , Audição/fisiologia , Inflamação/fisiopatologia , Desenvolvimento da Linguagem , Otorrinolaringopatias/fisiopatologia , Otorrinolaringopatias/psicologia , Criança , Doença Crônica , HumanosRESUMO
It has been hypothesized that the progressive deletion of CD4+ T cells in the course of infection due to human immunodeficiency virus (HIV) may be mediated in part by interaction with a superantigen inherent in an HIV protein. Consequently, selective loss of CD4+ cells with a T cell receptor V beta-chain capable of interaction with superantigen would produce a CD4+ population less or totally unresponsive to superantigen such as staphylococcal enterotoxins B and A (SEB and SEA respectively), but not to other mitogens such as concanavalin A, anti-CD3 (OKT3), or pokeweed mitogen. We tested this hypothesis by comparing the proliferative response of SEB and SEA with the other mitogens for 25 controls, 20 HIV+, and 15 donors with acquired immune deficiency syndrome (AIDS). We found that peripheral blood mononuclear cells, as well as the CD4+ and CD8+ subsets from both HIV+ and AIDS sources, the degree of suppression of mitogenesis for SEB and SEA was approximately equal to or less than that of the other mitogens. Moreover, suppression of HIV+ CD4+ and CD8+ T cell responses to SEB and SEA was equal (26%). If HIV superantigens exist, our data suggest that they are not responsible for the selective depletion of the CD4+ T cell subset as evaluated by SEB and SEA specificity.