Asian sand dust aggregate causes atopic dermatitis-like symptoms in Nc/Nga mice.

BACKGROUND: Asian sand dust (ASD) originates from the arid and semiarid areas of China, and epidemiologic studies have shown that ASD exposure is associated with various allergic and respiratory symptoms. However, few studies have been performed to assess the relationship between skin inflammation and ASD exposure. METHODS: Twelve-week-old NC/Nga mice were divided into 6 groups (n = 8 for each group): hydrophilic petrolatum only (control); hydrophilic petrolatum plus ASD (ASD); hydrophilic petrolatum and heat inactivated-ASD (H-ASD); Dermatophagoides farinae extract (Df); Df and ASD (Df + ASD), and; Df and H-ASD (Df + H-ASD). The NC/Nga mice in each group were subjected to treatment twice a week for 4 weeks. We evaluated skin lesions by symptoms, pathologic changes, and serum IgE levels. RESULTS: ASD alone did not induce atopic dermatitis (AD)-like skin symptoms. However, Df alone, Df + H-ASD and Df + ASD all induced AD-like symptoms, and dermatitis scores in the group of Df + ASD group were significantly greater than that of the Df group (P = 0.0011 at day 21; and P = 0.017 at day 28). Mean serum IgE was markedly increased in the Df and Df + ASD groups, compared to the ASD and control groups (P < 0.0001), and serum IgE levels in the Df + ASD group were significantly higher compared to the Df group (P = 0.003). CONCLUSIONS: ASD alone did not cause AD-like symptoms in NC/Nga mice. However, AD-like symptoms induced by Df, a major allergen, were enhanced by adding ASD. Although no epidemiological studies have been conducted for the association between ASD and symptoms of dermatitis, our data suggest that it is likely that ASD may contribute to the exacerbation of not only respiratory symptoms, but also skin diseases, in susceptible individuals.

Contribution of a phytotoxic compound to the allelopathy of Ginkgo biloba.

Ginkgo (Ginkgo biloba L.) has not changed over 121 million years. There may be unknown special strategy for the survival. Gingko litter inhibited the growth of weed species ryegrass (Lolium multiflorum L.). The inhibition was greater with the litter of the close position than that of the far position from the gingko tree. A phytotoxic substance, 2-hydroxy-6-(10-hydroxypentadec-11-enyl)benzoic acid (HHPEBA) was isolated in the litter. HHPEBA concentration was greater in the litter of the close position than that of the far position from the tree. HHPEBA inhibited the ryegrass growth at concentrations greater than 3 µM. HHPEBA was estimated to be able to cause 47-62% of the observed growth inhibition of ryegrass by the gingko litter. Therefore, HHPEBA may contribute to the inhibitory effect caused by ginkgo litter and may provide a competitive advantage for gingko to survive through the growth inhibition of the neighboring plants.

A novel substance with allelopathic activity in Ginkgo biloba.

Ginkgo (Ginkgo biloba) is one of the oldest living tree species and has been widely used in traditional medicine. Leaf extracts of ginkgo, such as the standardized extract EGb761, have become one of the best-selling herbal products. However, no bioactive compound directed at plants has been reported in this species. Therefore, we investigated possible allelopathic activity and searched for allelopathically active substances in ginkgo leaves. An aqueous methanol leaf extract inhibited the growth of roots and shoots of garden cress (Lepidium sativum), lettuce (Lactuca sativa), timothy (Phleum pratense) and ryegrass (Lolium multiflorum) seedlings. The extract was purified by several chromatographic runs and an allelopathically active substance was isolated and identified by spectral analysis to be the novel compound 2-hydroxy-6-(10-hydroxypentadec-11-enyl)benzoic acid. The compound inhibited root and shoot growth of garden cress and timothy at concentrations greater than 3 µM. The activity of the compound was 10- to 52-fold that of nonanoic acid. These results suggest that 2-hydroxy-6-(10-hydroxypentadec-11-enyl)benzoic acid may contribute to the allelopathic effect caused by ginkgo leaf extract. The compound may also have potential as a template for the development of new plant control substances.

Staphylococcus aureus requires cardiolipin for survival under conditions of high salinity.

BACKGROUND: The ability of staphylococci to grow in a wide range of salt concentrations is well documented. In this study, we aimed to clarify the role of cardiolipin (CL) in the adaptation of Staphylococcus aureus to high salinity. RESULTS: Using an improved extraction method, the analysis of phospholipid composition suggested that CL levels increased slightly toward stationary phase, but that this was not induced by high salinity. Deletion of the two CL synthase genes, SA1155 (cls1) and SA1891 (cls2), abolished CL synthesis. The cls2 gene encoded the dominant CL synthase. In a cls2 deletion mutant, Cls1 functioned under stress conditions, including high salinity. Using these mutants, CL was shown to be unnecessary for growth in either basal or high-salt conditions, but it was critical for prolonged survival in high-salt conditions and for generation of the L-form. CONCLUSIONS: CL is not essential for S. aureus growth under conditions of high salinity, but is necessary for survival under prolonged high-salt stress and for the generation of L-form variants.

Transcription-coupled nucleoid architecture in bacteria.

The circular bacterial genome DNA exists in cells in the form of nucleoids. In the present study, using genetic, molecular and structural biology techniques, we show that nascent single-stranded RNAs are involved in the step-wise folding of nucleoid fibers. In Escherichia coli, RNase A degraded thicker fibers (30 and 80 nm wide) into thinner fibers (10 nm wide), while RNase III and RNase H degraded 80-nm fibers into 30-nm (but not 10-nm) fibers. Similarly in Staphylococcus aureus, RNase A treatment resulted in 10-nm fibers. Treatment with the transcription inhibitor, rifampicin, in the absence of RNase A changed most nucleoid fibers to 10-nm fibers. Proteinase-K treatment of nucleoids exposed DNA. Thus, the smallest structural unit is an RNase A-resistant 10-nm fiber composed of DNA and proteins, and the hierarchical structure of the bacterial chromosome is controlled by transcription itself. In addition, the formation of 80-nm fibers from 30-nm fibers requires double-stranded RNA and RNA-DNA hetero duplex. RNA is evident in the architecture of log-phase uncondensed and stationary-phase condensed nucleoids.

Biochemical, molecular genetic, and structural analyses of the staphylococcal nucleoid.

The nucleoid structure of an important human pathogen, Staphylococcus aureus, was dissected by atomic force microscopy (AFM). The nucleoids dispersed on a cover glass consisted of fibrous units with two different widths of 40 and 80 nm, a feature shared with those of Escherichia coli. On the other hand, cells exposed to an oxidative stress exhibited clogged nucleoids. A knock-out of mrgA (metallo regulated genes A) encoding a staphylococcal homolog of the nucleoid compaction factor (E. coli Dps) eliminated the compaction response to the oxidative stress and reduced the susceptibilities to H2O2 and UV irradiation. We also observed that the negative supercoiling of plasmids is increased by the oxidative stress. A possible interrelation between the helical density and the nucleoid compaction is discussed in relation to the oxidative stress response.

Genetic characterization of the natural SigB variants found in clinical isolates of Staphylococcus aureus.

The SigB concentrations in clinical isolates of Staphylococcus aureus were measured to examine their correlation with the antibiotic resistance. The SigB concentrations in methicillin-resistant S. aureus (MRSA) were higher than in the control strain, N315, and many of methicillin-susceptible S. aureus (MSSA). Sequencing analyses of the sigB genes revealed that the strains exhibiting the high SigB concentrations have three amino acid substitutions in SigB: I11V, D141N, and Q256K. Further analysis using isogenic mutants demonstrated that D141N (or both D141N and Q256K) is essential to maintain the high SigB concentration. These substitutions affected the UV tolerance, but had no effect on the antibiotic resistance. The SigB activity was affected by these substitutions toward the stationary phase, but not during the transient heat shock response.