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| Author(s): |
Karen Tiago dos Santos
Total Authors: 1
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| Document type: | Doctoral Thesis |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2013-12-02 |
| Examining board members: |
Soraia Kátia Pereira Costa;
Edson Antunes;
Wothan Tavares de Lima;
Joilson de Oliveira Martins;
Paulo Hilario Nascimento Saldiva
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| Advisor: | Soraia Kátia Pereira Costa; Jean Pierre Schatzmann Peron |
| Abstract | |
Air pollution is a public health problem worldwide, related to the worsening of asthma, mainly in susceptible individual. Ours previous data showed that early-life exposure to the 1,2-naphthoquinone (1,2-NQ), one of those air contaminants adsorbed on diesel exhaust particles (DEP), increased the susceptibility to asthma at adulthood. Recent studies have been shown that DEP are able to increase Toll like receptors (TLR) mRNA expression of in the lungs of rodents, suggesting that environmental pollutants can act as TLRs ligands. This study aimed: 1) to investigate the role of TLR4 and the mechanisms involved in increased susceptibility to allergic inflammation; 2) evaluate immune cells population involved in innate/adaptive response. We demonstrate that aggravation of asthma in mice early exposed to 1,2-NQ is modulated by TLR4-MyD88 intracellular signaling pathway. We concluded that the short contact of individuals susceptible with 1,2-NQ interfere with immune cells maturation and function, which affect the adaptive response and thus promoted increase of asthma. (AU) | |