Radiation-Induced Autophosphorylation of Epidermal Growth Factor Receptor in Human Malignant Mammary and Squamous Epithelial Cells

1996 ◽  
Vol 145 (1) ◽  
pp. 81 ◽  
Author(s):  
Rupert K. Schmidt-Ullrich ◽  
Kristoffer Valerie ◽  
P. Bryan Fogleman ◽  
Jay Walters
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Growth Factor Receptor ◽  
Radiation Induced ◽  
Epidermal Growth

scholarly journals Involvement of Epidermal Growth Factor Receptor-Linked Signaling Responses in Pseudomonas fluorescens-Infected Alveolar Epithelial Cells

2011 ◽  
Vol 79 (5) ◽  
pp. 1998-2005 ◽  
Author(s):  
Hye Jin Choi ◽  
Chan Hee Seo ◽  
Seong Hwan Park ◽  
Hyun Yang ◽  
Kee Hun Do ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Pseudomonas Fluorescens ◽  
Growth Factor Receptor ◽  
Airway Epithelial ◽  
Content Type ◽  
Proinflammatory Responses ◽  
Epidermal Growth

ABSTRACTPseudomonas fluorescensis an opportunistic indoor pathogen that can cause severe airway proinflammatory responses. Pulmonary epithelium, like other mucosal epithelial linings of the body, constitutes the first line of defense against airway microbial pathogens. Mucosal epithelial cells can be a sentinel of pathogenic bacteria via stimulation of specific cell surface receptors, including the epidermal growth factor receptor (EGFR) and Toll-like receptor (TLR). This study addressed the involvement of EGFR in airway epithelial pathogenesis byP. fluorescens. Human A549 pneumocytes showed prolonged production of proinflammatory interleukin-8 (IL-8) in response to infection withP. fluorescens, which was via the nuclear factor-kappa B (NF-κB) signaling pathway. Production of proinflammatory cytokine IL-8 was not mediated byP. fluorescenslipopolysaccharide, a representative TLR4 agonist, but was mediated through EGFR-linked signals activated by the opportunistic bacteria. Moreover, EGFR signals were involved in NF-κB signal-mediated production of proinflammatory cytokines. Along with persistent NF-κB activation,P. fluorescensenhanced the EGFR phosphorylation and subsequent activation of downstream mediators, including protein kinase B or extracellular-signal-regulated kinases 1/2. Blocking of EGFR-linked signals increased epithelial susceptibility to pathogen-induced epithelial cell death, suggesting protective roles of EGFR signals. Thus, airway epithelial exposure toP. fluorescenscan trigger antiapoptotic responses via EGFR and proinflammatory responses via TLR4-independent NF-κB signaling pathway in human pneumocytes.

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