The influence of nanoporous anodic aluminum oxide on the initial adhesion of Streptococcus mitis and mutans.

The use of nanoscale surface modifications offers a possibility to regulate the bacterial adherence behavior. The aim of this study was to evaluate the influence of nanoporous anodic aluminum oxide of different pore diameters on the bacterial species Streptococcus mitis and Streptococcus mutans. Nanoporous anodic aluminum oxide (AAO) surfaces with an average pore diameter of 15 and 40 nm, polished pure titanium and compact aluminum oxide (alumina) samples as reference material were investigated.

The anti-inflammatory effect of low-dose radiation therapy involves a diminished CCL20 chemokine expression and granulocyte/endothelial cell adhesion.

Background And Purpose: Low-dose radiotherapy (LD-RT) is known to exert an anti-inflammatory effect, however, the underlying molecular mechanisms are not fully understood. The manipulation of polymorphonuclear neutrophil (PMN) function and/or recruitment may be one mechanism. Chemokines contribute to this process by creating a chemotactic gradient and by activating integrins.

Expression and regulation of CCL18 in synovial fluid neutrophils of patients with rheumatoid arthritis.

Rheumatoid arthritis (RA) is characterized by the recruitment of leukocytes and the accumulation of inflammatory mediators within the synovial compartment. Release of the chemokine CCL18 has been widely attributed to antigen-presenting cells, including macrophages and dendritic cells. This study investigates the production of CCL18 in polymorphonuclear neutrophils (PMN), the predominant cell type recruited into synovial fluid (SF).

Extravasation into synovial tissue induces CCL20 mRNA expression in polymorphonuclear neutrophils of patients with rheumatoid arthritis.

Objective: Examination of expression of the chemokine macrophage inflammatory protein-3a (CCL20/Mip-3alpha) in blood polymorphonuclear neutrophils (PMN) and synovial fluid (SF) PMN of patients with rheumatoid arthritis (RA).

Methods: Paired samples of blood PMN and SF PMN were obtained from 11 patients with RA. In addition, SF was prepared from 9 patients with osteoarthritis (OA) and 10 patients with juvenile idiopathic arthritis (JIA).

A synthetic, non-peptide CXCR2 antagonist blocks MIP-2-induced neutrophil migration in mice.

Non-peptide antagonists of chemokine receptors are considered an intriguing alternative for the treatment of acute and chronic diseases. Particularly the recruitment of neutrophils to inflammatory sites often causes harmful side effects and is mediated by chemokine ligands of the CXC chemokine receptor 2 (CXCR2). Hence, this receptor has been proposed as an important target for novel drugs.