The ease with which B. anthracis can be made resistant in vitro suggests that close monitoring of patients treated for anthrax is mandatory.

We determined the prevalence and risk factors of H. pylori infection among 197 healthy 3- to 5-year-old Israeli Arab children, in a population under socioeconomic and environmental transition. Data on the socioeconomic and environmental characteristics were obtained by personal interviews. The presence of H. pylori infection was identified using an ELISA kit for detection of H. pylori antigens in stool specimens. The prevalence rate of H. pylori infection was 49.7% (95% CI 42.8-56.67). It varied significantly among the different villages. In the univariate analysis stratified by village, the risk of infection increased according to household crowding, number of siblings younger than 5 years and siblings' H. pylori positivity. In the multivariate analysis the village of residence and siblings' H. pylori positivity were the only variables that remained strongly associated with H. pylori infection. In a population such as that described in this study the socioeconomic and living conditions are major risk factors of H. pylori infection and the intra-familial transmission of H. pylori in early childhood has an important role.

Therapy with ethosomal erythromycin applied to the skin of S. aureus-infected mice was as effective as systemically administered erythromycin, suggesting a new possibility to treat deep dermal infections by local application of antibiotic in ethosomal carrier.

Many endogenous molecules, mostly proteins, purportedly activate the Toll-like receptor 4 (TLR4)–myeloid differentiation factor-2 (MD-2) complex, the innate immune receptor for lipopolysaccharide (LPS) derived from gram-negative bacteria. However, there is no structural evidence supporting direct TLR4–MD-2 activation by endogenous ligands. Sulfatides (3-O-sulfogalactosylceramides) are natural, abundant sulfated glycolipids that have variously been shown to initiate or suppress inflammatory responses. We show here that short fatty acid (FA) chain sulfatides directly activate mouse TLR4–MD-2 independent of CD14, trigger MyD88- and TRIF-dependent signaling, and stimulate tumor necrosis factor α (TNFα) and type I interferon (IFN) production in mouse macrophages. In contrast to the agonist activity toward the mouse receptor, the tested sulfatides antagonize TLR4–MD-2 activation by LPS in human macrophage-like cells. The agonistic and antagonistic activities of sulfatides require the presence of the sulfate group and are inversely related to the FA chain length. The crystal structure of mouse TLR4–MD-2 in complex with C16-sulfatide revealed that three C16-sulfatide molecules bound to the MD-2 hydrophobic pocket and induced an active dimer conformation of the receptor complex similar to that induced by LPS or lipid A. The three C16-sulfatide molecules partially mimicked the detailed interactions of lipid A to achieve receptor activation. Our results suggest that sulfatides may mediate sterile inflammation or suppress LPS-stimulated inflammation, and that additional endogenous negatively charged lipids with up to six lipid chains of limited length might also bind to TLR4–MD-2 and activate or inhibit this complex.