RESUMO
OBJECTIVE: Investigation of the effects of interleukin (IL)-17 cytokines in Chlamydophila pneumoniae-infected mice. METHODS: Mice were infected with C. pneumoniae once or three times and the expression of IL-17 cytokines was followed by RT qPCR from day 1 to day 28 after infection and re-infection. After the treatment of mice with anti-IL-17A, ELISA was used to detect the differences in cytokine and chemokine production. The number and phenotype of the IL-17A-producing cells were determined by ELISPOT. RESULTS: Chlamydophila pneumoniae induced IL-17A and IL-17F from day 2 after infection, and their levels remained elevated on day 28. The expression of IL-17C, IL-17D and IL-17E mRNA did not change significantly in response to a single infection. The in vivo neutralization of IL-17A resulted in a higher C. pneumoniae burden in the mouse lungs, a decreased cell influx, and diminished chemokine levels. The phenotype of IL-17A-producing cells was CD4(+). The re-infection of mice led to an increased expression of IL-17E mRNA. CONCLUSION: These results facilitate an understanding of the early inflammatory response after C. pneumoniae infection and suggest that C. pneumoniae re-infection induces the production of a high amount of IL-17E, which has an important role in the pathogenesis of allergic pulmonary diseases.
Assuntos
Infecções por Chlamydophila/imunologia , Chlamydophila pneumoniae , Interleucina-17/imunologia , Animais , Linfócitos T CD4-Positivos/imunologia , Feminino , Interleucina-17/genética , Pulmão/imunologia , Camundongos , Camundongos Endogâmicos BALB C , Pneumonia/imunologia , RNA Mensageiro/metabolismo , Baço/citologia , Baço/imunologiaRESUMO
The first Hungarian report of a case of myotubular myopathy is presented here, which is a recessive congenital disorder linked to X chromosome. The patient presented at birth with severe hypotonia, weak spontaneous movements, arthrogryposis and respiratory insufficiency. The biopsy showed the appearance of myotubular myopathy. The diagnosis was further confirmed by genetic analysis revealing a novel frameshift mutation (1314-1315insT) of the myotubularin-coding MTM1 gene.
