Cellular Fibronectin is Induced in Ultraviolet-Exposed Human Skin and Induces IL-10 Production by Monocytes/Macrophages

CD11b+ monocytic/macrophagic cells that infiltrate human skin after in vivo ultraviolet exposure potently produce interleukin-10. We hypothesized that binding of monocyte β1 integrins to ultraviolet-induced extracellular matrix ligands, such as fibronectin, after entry of blood monocytes into the dermis, is involved in the modulation of immunoregulatory monocytic cytokines. Immunostaining of human skin and reverse transcriptase–polymerase chain reaction studies revealed that the embryonic isoform of cellular fibronectin, in which the extra domain A (EDA) segment is spliced in (EDA+ cellular fibronectin), and confers enhanced binding to β1 integrins, is newly induced and is associated with infiltrating CD11b+ cells post in vivo ultraviolet exposure. We then tested the effect of fibronectin on resting purified peripheral monocytes in vitro. We found that monocyte interleukin-10, but not interleukin-12, was significantly induced in a concentration-dependent manner by in vitro binding to cellular fibronectin (n = 6), but not plasma fibronectin. Tumor necrosis factor-α was also induced in a concentration-dependent manner, but to a lesser extent. Monoclonal antibodies to β1 integrins β-subunit (CD29) also strongly induced tumor necrosis factor-α and interleukin-10 production, but not interleukin-12. Neutralization of tumor necrosis factor-α reduced by 54% the interleukin-10 production that was induced by monocytes binding to cellular fibronectin, indicating that interleukin-10 induction is at least in part dependent upon concomitant autocrine tumor necrosis factor-α release. In conclusion, ultraviolet skin injury results in increased production and deposition of EDA+ cellular fibronectin in the papillary dermis, which may be one of the key signals capable of inducing interleukin-10 but not interleukin-12 in monocytes that infiltrate micromilieu of human skin after ultraviolet exposure

Prevalence of Childhood Atopic Dermatitis: An Urban and Rural Community-Based Study in Shanghai, China

Background: Atopic dermatitis (AD) is a common inflammatory and chronically relapsing disorder with increasing prevalence. However, little is known about its prevalence in Shanghai, the top metropolitan of China. This study will estimate and compare the prevalence of AD in urban and rural areas in representative samples of 3 to 6-year-old children in Shanghai. Methodology/Principal Findings: A descriptive cross-sectional study was performed. Pre-school children were obtained by cluster sampling from 8 communities in different districts in Shanghai. The main instrument was the core questionnaire module for AD used in the U.K. Working Party’s study. All the data were statistically analyzed by EpiData 3.1 and SPSS16.0. A total of 10436 children completed the study satisfactorily, with a response rate of 95.8%. The prevalence of AD in 3 to 6-year-old children was 8.3 % (Male: 8.5%, Female: 8.2%). The prevalence in urban areas of Shanghai was gradiently and significantly higher than that in rural areas. The highest prevalence was in the core urban area (10.2 % in Xuhui Tianping) vs. the lowest far from the urban areas (4.6 % in Chongming Baozhen). Conclusions/Significance: The prevalence of AD was 8.3 % (95%CI: 7.6%–9.1%) in children aged 3 to 6 in Shanghai. Th

Differential regulation of IL-1 and IL-1 receptor antagonist in HaCaT keratinocytes by tumor necrosis factor-Α and transforming growth factor-Β1

: Cytokines such as TNFΑ and TGFΒ1 have potent effects on keratinocyte differentiation and have been implicated in cutaneous injury, immunologic reactions, and wound healing. To determine whether such conditions might alter the balance of epidermal keratinocyte IL-1 and the IL-1 receptor antagonist (IL-1ra), TNFΑ and TGFΒ1 were added to HaCaT cells, a human adult keratinocyte cell line. mRNA levels of IL-1Α, IL-1Β, and IL-IRa were detected by polymerase chain reaction (PCR) on reverse transcribed RNA extracts, followed by Southern blot of the PCR products, 35 S-labeled probe hybridization, and quantification against standard curves. TNFΑ (100 ng/ml) at the 3-h time point significantly induced increases in mRNA expression of IliΑ (9.2±2.9 fold increase) and IL-1Β (2.5±0.7 fold increase) ( n =7) which were concordant with increases in IL-1Α protein (7.1±1.3 fold increase) and II-Β protein (4.4±1.0 fold increase) measured by ELISA 24 h after stimulation. By contrast, icIL-IRa mRNA and protein levels were not affected by TNFΑ. TGFΒl induced a mild increase in IL-lΑ mRNA (3.8±1.8 fold) and protein (3.5±1.2 fold). TGFΒl did not affect IL-1Α mRNA levels but caused variable increases in IL-1Β protein levels. TGFΒ1 did not alter icIL-1Ra mRNA or protein levels. Inhibition of RNA synthesis with actinomycin D demonstrated that the rate of degradation of IL-1Β mRNA was reduced by treatment with TNFΑ. This stabilization of IL-1Β mRNA was specific, because TGFP I did not stabilize IL-1Β mRNA, and TGFΒ1 and TNFΑ did not increase the stability of II-1Α mRNA. icIL-l Ra mRNA was fairly stable over a 20 hour period and its slow degradation was not affected by treatment with either TNFΑ or TGFΒ1, indicating a higher steady state stability of icIL-1ra mRNA relative to IL-1 mRNA's. Given the high rate of degradation of IL-1Α and IL-1Β mRNA, levels of these mRNAs may rapidly decrease while the icIL-1ra mRNA levels remain constant, thus allowing for rapid dampening of IL-1 activity soon after the stimuli provoking an inflammatory or reparative response have abated. In conclusion, TNFΑ and TGFΒl, cytokines with potent effects on inflammation and differentiation, both induce keratinocyte IL-1Α mRNA and protein levels, but differentially regulate IL-1Β mRNA. They both exert little effect on IL-1 Ra levels, which were constitutively highly stable. Such differential regulation provides mechanisms for separately controlling the relative activity of these cytokines under normal and disordered conditions.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/71526/1/j.1600-0625.1996.tb00120.x.pd

Study on the Durability of Bamboo Fiber Asphalt Mixture

To evaluate the durability of bamboo fiber asphalt mixture using four gradation schemes, the durability of the bamboo fiber asphalt mixture is studied considering three aspects: ageing durability, freeze-thaw cycle durability and fatigue durability through the Marshall test, indoor ageing test, uniaxial compression test, low-temperature bending test, immersion Marshall test, freeze-thaw splitting test and four-point bending fatigue test. Nonfiber asphalt mixture and lignin fiber asphalt mixture were used as control groups. The results show that the addition of plant fiber can effectively improve the durability of asphalt mixture. Bamboo fiber modified asphalt mastic has good ductility and adhesion due to its rough surface and good oil absorption performance. Bamboo fiber asphalt mixture has better and more stable low-temperature ageing durability and moisture ageing durability than lignin fiber asphalt mixture, but its mechanical property is weaker than the latter. The improvement effect of the two fibers on the freeze-thaw cycle durability of asphalt mixture is basically the same. Bamboo fiber can improve the flexibility of the mixture and delay the development of cracks so that the mixture has good fatigue durability. The smaller the void ratio, the thicker the asphalt film, and the denser the structure of the mixture, the better the durability. The durability of the stone mastic asphalt (SMA) gradation mixture is better than that of asphalt concrete (AC) gradation. The material composition and aggregate gradation of plant fiber asphalt mixture have a great influence on its durability. In the future, it is necessary to establish a multiparameter comprehensive evaluation index system among fiber type and properties, mixture gradation and durability so as to realize the directional regulation of the durability of different fiber asphalt mixtures. Bamboo fiber is a reliable substitute for lignin fiber, and further research on improving its surface properties and dispersion uniformity can be carried out in the future

Study on the Durability of Acid Rain Erosion-Resistant Asphalt Mixtures

Acid erosion can accelerate the process of early damage of asphalt pavement and decrease the durability of asphalt pavement. However, there are limited research results for asphalt mixtures that can resist acid rain erosion. To systematically evaluate the impact and action law of acid rain erosion on the durability of asphalt mixtures, three gradation schemes were used: periodic dry–wet cycle immersion test, contact angle test and road performance test. The acid rain erosion resistance of epoxy asphalt mixture, SBS-modified asphalt mixture and 70# matrix asphalt mixture were tested from three aspects of anti-aging performance, freeze–thaw cycle performance and fatigue performance. The results show that the erosion of acid rain can significantly decrease the adhesion between asphalt and aggregate, and affects the road performance of the asphalt mixture. Acid rain erosion can significantly decrease the mechanical properties, adhesion and durability of asphalt mixtures. Epoxy asphalt has better physical properties, adhesion and acid rain erosion resistance than 70# matrix asphalt and SBS-modified asphalt. Epoxy asphalt has excellent adhesion due to its polar group, high cohesion and thermosetting resin with low shrinkage, which can effectively resist moisture erosion, spalling and temperature stress cracking, thereby effectively resisting the erosion of acid rain. Epoxy asphalt mixture has the strongest acid rain erosion resistance, which can be further enhanced when used together with waste rubber powder and modified bamboo fiber. On the whole, asphalt mixture with high-density structure and thicker asphalt film can effectively resist acid rain erosion. The durability of asphalt concrete (AC)-type gradation mixture and stone mastic asphalt (SMA)-type gradation mixture are equivalent, and both are superior to open-graded friction courses (OGFC)-type gradation mixture. The gradation of asphalt mixtures and the type of asphalt binder have great influence on their acid rain erosion resistance and durability. In order to realize the directional control of the acid rain erosion resistance and durability of different asphalt mixtures, a multi-parameter comprehensive assessment indicator system between the type and property of asphalt, the gradation of asphalt mixture, and the acid rain resistance and durability of the mixture need to be established in the future

Phosphodiesterase Inhibition by Ro 20-1724 Reduces Hyper-IgE Synthesis by Atopic Dermatitis Cells In Vitro

Peripheral blood mononuclear leukocytes (MNL) from patients with atopic dermatitis spontaneously produce large amounts of IgE in vitro. These cells also show markedly elevated levels of cAMP phosphodiesterase (PDE) which may be responsible for the observed abnormal cAMP responsiveness. Treatment of atopic dermatitis MNL with varying concentrations of the cAMP PDE inhibitor Ro 20-1724 resulted in progressively decreasing amounts of IgE synthesis, statistically significant at the 10-4 M and 10-5 M concentrations. There was a close correlation between PDE inhibition and inhibition of IgE synthesis, r = 0.93, p <0.05. To define the cellular target of the drug, we used monoclonal antibodies directed toward MNL subsets (Lyt 3, OKT8, OKT4, monocyte-myeloid) in a modified “panning” method to perform experiments with purified subsets. With untreated subsets, removal of OKT4-positive cells significantly reduced IgE synthesis; readdition of OKT4-positive cells enhanced IgE synthesis. OKT8 cells and monocytes did not affect IgE synthesis. Pretreatment of T cell-depleted MNL with Ho 20-1724 resulted in significantly more inhibition of IgE synthesis than did pretreatment of T enriched cells prior to recombination with the reciprocal untreated subset and subsequent culture. Similarly, pretreatment of monocyte-depleted cells resulted in significantly more inhibition of IgE synthesis than pretreatment of monocyte-enriched cells prior to recombination and culture. The majority of the effect appeared to be mediated by a direct effect on the B cells. However, some inhibition of IgE synthesis was also achieved through pretreatment of T enriched cells. Since pretreatment of isolated suppressor/cytotoxic or helper/inducer T-cell subsets did not give the same degree of inhibition as with unfractionated T cells, a T-T interaction may be involved in this aspect. The imidazolidinone derivative, Ro 20-1724, significantly and consistently inhibited both the elevated cAMP phophodiesterase activity and the elevated spontaneous IgE synthesis of MNL from patients with atopic dermatitis. These findings demonstrate a previously indescribed link between cAMP PDE levels and in vitro IgE synthesis

Preparation and Properties of Wood Tar-based Rejuvenated Asphalt

In order to explore the applicability of the rejuvenated asphalt with wood tar as the main raw material, the orthogonal test was used to determine the optimal ratio of wood tar-based rejuvenator. The physical properties, rheological properties and components of matrix asphalt, aged asphalt, wood tar-based rejuvenated asphalt and commercial RA-102# rejuvenated asphalt were tested and compared. The results show that the optimal ratio of wood tar-based rejuvenator is 15wt% wood tar, 0.3wt% biomass fiber, 5wt% plasticizer, 0.3wt% compatibilizer, and 1wt% stabilizer of the mass of aged asphalt. Wood tar-based rejuvenator can restore the physical properties of the aged asphalt to meet the specification requirements. The synergistic effect of biomass fiber and plasticizer make the wood tar-based rejuvenated asphalt has good resistance to accumulated permanent deformation, but its low-temperature cracking resistance needs to be further improved. During the rejuvenation process of aged asphalt, the colloidal state changes from gel-state to sol-state, characterizing that the viscosity of asphalt decreased and the fluidity increased. Wood tar-based rejuvenator can react with aged asphalt to weaken the vibration strength of carbonyl and sulfoxide groups, so as to realize the recovery of service performance. Wood tar-based rejuvenator has better environmental protection and applicability, which is worthy of further study and promotion

iC3b Arrests Monocytic Cell Differentiation Into CD1c-Expressing Dendritic Cell Precursors: A Mechanism for Transiently Decreased Dendritic Cells in vivo After Human Skin Injury by Ultraviolet B

Our previous data indicated that C3, its bioactive product iC3b, and the iC3b ligand CD11b are critical for ultraviolet-induced immunosuppression. We thus hypothesized that iC3b is an important skin-based factor regulating CD11b+ monocytic cell function in the acute post-ultraviolet period. Although monocytic cell migration peaked at 1–3 d after ultraviolet exposure of skin, dermal CD1c dendritic cells underwent a rapid and prolonged depletion that did not recover until day 7. Because ultraviolet-induced iC3b deposits are reciprocally maximal on day 3, but fade by day 7, we next hypothesized that iC3b can be responsible for the delay in differentiation into dendritic cells of monocytic cells migrating into ultraviolet-exposed skin. Analysis of dermal cells derived from keratome biopsies suggested that iC3b exposure could inhibit the development of CD1c+ dermal cells. To model newly immigrating blood monocytes entering ultraviolet-exposed, iC3b-containing dermis, purified monocytes from human blood were induced with granulocyte-macrophage colony stimulating factor to generate a population of dendritic cell precursors expressing CD1c. Incubation with iC3b markedly inhibited the appearance of CD1c+ cells (p<0.05) and induced CD1c–CD14+ cells. This inhibition was reversed by coincubation with an anti-CD11b antibody that blocks the iC3b binding site. Other functions associated with dendritic cell maturation were also inhibited by iC3b, such as interleukin-12p70 production as well as CD80 and CD40 expression. Restimulation of monocytes for DC maturation revealed that iC3b induced a temporary inhibition of DC differentiation. Thus, a human skin response in which iC3b is transiently (3–7 d) generated in dermis, such as ultraviolet, can arrest monocytic skin-infiltrating cells from undergoing dendritic cell precursor differentiation