Eosinophilia and reduced STAT3 signaling affect neutrophil cell death in autosomal‐dominant Hyper‐IgE syndrome

Neutrophil cell death, activation and bacterial infection in cystic fibrosis.

BACKGROUND Cystic fibrosis (CF) is characterised by chronic endobronchial bacterial infection and neutrophil mediated inflammation. Neutrophil apoptosis is essential for the resolution of inflammation. This study assessed the relationship between levels of neutrophil apoptosis and sputum microbiology in matched clinically stable patients with CF. METHODS Sputum was induced from 34 patients (n...

STAT3 Signaling in Cancer

In recent years, signal transducers and activators of transcription (STAT) proteins have been recognized as cytoplasmic transcription factors that mediate extracellular signaling to the nucleus controlling fundamental functions, such as cell proliferation, apoptosis, differentiation, immune responses and angiogenesis. Among them, STAT3 is a major player, aberrant activation of which is involved...

PMS and eosinophilia-myalgia syndrome.

Tissue eosinophilia in oral and cutaneous squamous cell carcinoma and normal oral and cutaneous tissues

Introduction: Eosinophils produce proteases that stimulate invasion in cancers. Due to the more malignant potential of oral squamous cell carcinoma (OSCC) compared to cutaneous squamous cell carcinoma (CSCC), the aim of the present study was to compare tissue eosinophilia between OSCC and CSCC samples to understand whether tissue eosinophilia play a role in different biological...

Reduced IGF signaling prevents muscle cell death in a Caenorhabditis elegans model of muscular dystrophy.

Duchenne muscular dystrophy, a fatal degenerative muscle disease, is caused by mutations in the dystrophin gene. Loss of dystrophin in the muscle cell membrane causes muscle fiber necrosis. Previously, loss-of-function mutations in dys-1, the Caenorhabditis elegans dystrophin ortholog, were shown to cause a contractile defect and mild fiber degeneration in striated body wall muscle. Here, we sh...