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Histochem Cell Biol ; 130(1): 165-76, 2008 Jul.
Artículo en Inglés | MEDLINE | ID: mdl-18365236

RESUMEN

Streptococcus pneumoniae is the leading causative agent of community-acquired pneumonia. Induction of apoptosis in pulmonary epithelial cells by bacteria during pneumonia might be harmful to the host. Interleukin-15 (IL-15) has been demonstrated as an effective inhibitor of apoptosis and is expressed in lung epithelium on the mRNA and protein level. Therefore, we characterized the sub-cellular expression pattern of the short and long IL-15 isoforms in lung epithelial cells in vitro as well as its role in pneumococci-related lung epithelial cell apoptosis. We found an expression pattern for both IL-15 signal peptides in the pulmonary epithelial cell lines A549 and Beas-2B. Moreover, a strong co-localization of IL-15 and IL-15Ralpha was detected on cell surfaces. Compared to pro-inflammatory cytokine stimulation, neither IL-15 nor its trimeric receptor complex was up-regulated after pneumococcal infection. However, overexpression of IL-15 isoforms revealed IL-15LSP and IL-15Vkl as inhibitors of pneumococci induced apoptosis in pulmonary epithelial cells. Thus, IL-15 may act as an anti-apoptotic molecule in pneumococci infection, thereby suggesting IL-15 as a benefical cytokine in pulmonary host defense against infection.


Asunto(s)
Interleucina-15/metabolismo , Pulmón/inmunología , Pulmón/patología , Neumonía Neumocócica/inmunología , Neumonía Neumocócica/patología , Receptores de Interleucina-15/metabolismo , Streptococcus pneumoniae/inmunología , Apoptosis , Línea Celular Tumoral , Células Epiteliales/inmunología , Células Epiteliales/microbiología , Células Epiteliales/patología , Humanos , Pulmón/microbiología , Isoformas de Proteínas/metabolismo , Mucosa Respiratoria/inmunología , Mucosa Respiratoria/patología , Transfección
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