[Sporadic lymphangioleiomyomatosis: A rare cause of bilateral spontaneous pneumothorax in young woman]. / La lymphangioléiomyomatose sporadique : cause rare du pneumothorax spontané bilatéral chez la femme jeune.

Sporadic lymphangioleiomyomatosis is an orphan disease of the young woman. Its clinical manifestations are mainly respiratory, including spontaneous pneumothorax. The management is multidisciplinary. We report the case of a young patient with bilateral spontaneous pneumothorax revealing sporadic lymphangioleiomyomatosis.

Alpha-actinin accumulation in epithelial cells infected with attaching and effacing gastrointestinal pathogens.

Fluorescent F-actin staining utilizing phalloidin, a highly toxic mushroom poison, is used as an indirect test to detect attaching and effacing (AE) bacteria. A study was done to determine if accumulation of alpha-actinin in infected tissue culture cells is a consistent feature and whether it corresponds with the AE response. Rearrangement of alpha-actinin was detected using immunofluorescence microscopy by incubation of infected cells with a murine monoclonal anti-alpha-actinin antibody. Foci of alpha-actinin-specific fluorescence corresponding to areas of bacterial adhesion were detected by transmission electron microscopy in HEp-2 and gastric KATO-III cells infected with only those bacterial strains that formed AE lesions. Therefore, this study shows that alpha-actinin accumulation is a consistent, specific manifestation of the AE phenotype and forms the basis for the development of a safe alternative test for detecting AE bacteria.

Increased adherence of Escherichia coli RDEC-1 to human tissue culture cells results in the activation of host signaling pathways.

Attaching and effacing (AE) adhesion is associated with the pathogenesis of enteropathogenic Escherichia coli (EPEC) and rabbit diarrheogenic E. coli (RDEC-1). Although RDEC-1 provides an animal model for investigating pathophysiology of EPEC infection, RDEC-1 does not adhere to human cell lines, thereby limiting in vitro investigation. Therefore, transformed RDEC-1 strains expressing adhesins derived from human diarrheogenic E. coli were studied. These adhesins promoted AE adhesion of RDEC-1 and led to the accumulation of alpha-actinin aggregates in the cytoplasm of infected cells. Furthermore, these strains induced host signal transduction pathways, resulting in tyrosine phosphorylation of host proteins and an intracellular elevation of calcium. These results demonstrate that RDEC-1 and EPEC stimulate similar signal transduction pathways in infected epithelial cells, thus lending additional support for the use of RDEC-1 as a model for the study of human EPEC infection.