RESUMO
The aim of this study was to detect and characterize Giardia lamblia in animals in the UAE. Eighty-seven fecal samples were tested for G. lamblia using the conserved fragment of small subunit (SSU)-rRNA by nested PCR. Giardia-positive isolates were genotyped for assemblages A and B using assemblage specific primers of the triosephosphate isomerase (tpi) gene. Thirty samples (34.5%) were positive for G. lamblia. Conversely, neither genotype A nor B were detected using tpi genotyping on the studied samples. Further investigations are required using higher number of samples including both human and animals in the country taking into consideration the analysis of other genotypes to provide more detailed understanding about the zoonotic transmission of this parasite.
Assuntos
Giardia lamblia/isolamento & purificação , Giardíase/veterinária , Animais , Genótipo , Giardia lamblia/classificação , Giardíase/epidemiologia , Emirados Árabes Unidos/epidemiologiaRESUMO
@#The aim of this study was to detect and characterize Giardia lamblia in animals in the UAE. Eighty-seven fecal samples were tested for G. lamblia using the conserved fragment of small subunit (SSU)-rRNA by nested PCR. Giardia-positive isolates were genotyped for assemblages A and B using assemblage specific primers of the triosephosphate isomerase (tpi) gene. Thirty samples (34.5%) were positive for G. lamblia. Conversely, neither genotype A nor B were detected using tpi genotyping on the studied samples. Further investigations are required using higher number of samples including both human and animals in the country taking into consideration the analysis of other genotypes to provide more detailed understanding about the zoonotic transmission of this parasite.
RESUMO
Exposure to particulate matter (PM), a major component of air pollution, contributes to increased morbidity and mortality worldwide. PM induces innate immune responses and contributes to allergic sensitization, although the mechanisms governing this process remain unclear. Lung mucosal uric acid has also been linked to allergic sensitization. The links among PM exposure, uric acid, and allergic sensitization remain unexplored. We therefore investigated the mechanisms behind PM-induced allergic sensitization in the context of lung mucosal uric acid. PM10 and house dust mite exposure selectively induced lung mucosal uric acid production and secretion in vivo, which did not occur with other challenges (lipopolysaccharide, virus, bacteria, or inflammatory/fibrotic stimuli). PM10-induced uric acid mediates allergic sensitization and augments antigen-specific T-cell proliferation, which is inhibited by uricase. We then demonstrate that human airway epithelial cells secrete uric acid basally and after stimulation through a previously unidentified mucosal secretion system. Our work discovers a previously unknown mechanism of air pollution-induced, uric acid-mediated, allergic sensitization that may be important in the pathogenesis of asthma.