TLR expression on neutrophils at the pulmonary site of infection: TLR1/TLR2-mediated up-regulation of TLR5 expression in cystic fibrosis lung disease.

Cystic fibrosis (CF) lung disease is characterized by infection with Pseudomonas aeruginosa and a sustained accumulation of neutrophils. In this study, we analyzed 1) the expression of MyD88-dependent TLRs on circulating and airway neutrophils in P. aeruginosa-infected CF patients, P. aeruginosa-infected non-CF bronchiectasis patients, and noninfected healthy control subjects and 2) studied the regulation of TLR expression and functionality on neutrophils in vitro. TLR2, TLR4, TLR5, and TLR9 expression was increased on airway neutrophils compared with circulating neutrophils in CF and bronchiectasis patients. On airway neutrophils, TLR5 was the only TLR that was significantly higher expressed in CF patients compared with bronchiectasis patients and healthy controls. Studies using confocal microscopy and flow cytometry revealed that TLR5 was stored intracellularly in neutrophils and was mobilized to the cell surface in a protein synthesis-independent manner through protein kinase C activation or after stimulation with TLR ligands and cytokines characteristic of the CF airway microenvironment. The most potent stimulator of TLR5 expression was the bacterial lipoprotein Pam(3)CSK(4). Ab-blocking experiments revealed that the effect of Pam(3)CSK(4) was mediated through cooperation of TLR1 and TLR2 signaling. TLR5 activation enhanced the phagocytic capacity and the respiratory burst activity of neutrophils, which was mediated, at least partially, via a stimulation of IL-8 production and CXCR1 signaling. This study demonstrates a novel mechanism of TLR regulation in neutrophils and suggests a critical role for TLR5 in neutrophil-P. aeruginosa interactions in CF lung disease.

Corrosion Resistance of Inconel 625 CMT-Cladded Layers after Long-Term Exposure to Biomass and Waste Ashes in High-Temperature Conversion Processes.

The present study investigated the effect of corrosion on an Inconel 625-cladded layer using the cold metal transfer (CMT) method. The corrosion was caused by various ashes and high process temperatures. The ashes were obtained from the biomasses of mixed wood and oat straw, as well as from sewage sludge, by ashing. Long-term corrosion tests were carried out at 650 °C over a period of 1000 h. The chemical composition, mineral phases, and corrosion effects were studied by X-ray fluorescence (XRF), scanning electron microscopy equipped with energy-dispersive X-rays (SEM-EDX), and X-ray diffraction (XRD) from the surface and on the cross-section of the samples. The chemical composition of the ashes was quite different, but representative of their particular fuel. Together with the effects of the operating temperature and mass transfer, significant differences in the degree of the corrosion depth were detected for the various ashes. For the investigated samples, the corrosion mechanisms were inferred based on the identified corrosion products.