Isoprene-Degrading Bacteria from Soils Associated with Tropical Economic Crops and Framework Forest Trees.

Isoprene, a volatile hydrocarbon emitted largely by plants, plays an important role in regulating the climate in diverse ways, such as reacting with free radicals in the atmosphere to produce greenhouse gases and pollutants. Isoprene is both deposited and formed in soil, where it can be consumed by some soil microbes, although much remains to be understood about isoprene consumption in tropical soils. In this study, isoprene-degrading bacteria from soils associated with tropical plants were investigated by cultivation and cultivation-independent approaches. Soil samples were taken from beneath selected framework forest trees and economic crops at different seasons, and isoprene degradation in soil microcosms was measured after 96 h of incubation. Isoprene losses were 4-31% and 15-52% in soils subjected to a lower (7.2 × 105 ppbv) and a higher (7.2 × 106 ppbv) concentration of isoprene, respectively. Sequencing of 16S rRNA genes revealed that bacterial communities in soil varied significantly across plant categories (framework trees versus economic crops) and the presence of isoprene, but not with isoprene concentration or season. Eight isoprene-degrading bacterial strains were isolated from the soils and, among these, four belong to the genera Ochrobactrum, Friedmanniella, Isoptericola and Cellulosimicrobium, which have not been previously shown to degrade isoprene.

Bioremediation of Crude Oil Contaminated Desert Soil: Effect of Biostimulation, Bioaugmentation and Bioavailability in Biopile Treatment Systems.

This work was aimed at evaluating the relative merits of bioaugmentation, biostimulation and surfactant-enhanced bioavailability of a desert soil contaminated by crude oil through biopile treatment. The results show that the desert soil required bioaugmentation and biostimulation for bioremediation of crude oil. The bioaugmented biopile system led to a total petroleum hydrocarbon (TPH) reduction of 77% over 156 days while the system with polyoxyethylene (20) sorbitan monooleate (Tween 80) gave a 56% decrease in TPH. The biostimulated system with indigenous micro-organisms gave 23% reduction in TPH. The control system gave 4% TPH reduction. The addition of Tween 80 led to a respiration rate that peaked in 48 days compared to 88 days for the bioaugmented system and respiration declined rapidly due to nitrogen depletion. The residual hydrocarbon in the biopile systems studied contained polyaromatics (PAH) in quantities that may be considered as hazardous. Nitrogen was found to be a limiting nutrient in desert soil bioremediation.

Anti-IgE (omalizumab) inhibits late-phase reactions and inflammatory cells after repeat skin allergen challenge.

BACKGROUND: Anti-IgE (omalizumab) inhibited early and late asthmatic reactions and infiltration of inflammatory cells in asthmatic bronchial biopsies at baseline. The effect of chronic allergen exposure on these outcomes is unknown. Repeat allergen challenge in human skin represents a suitable model to address this question. OBJECTIVE: To study the effect of anti-IgE (omalizumab) on early-phase (EPR) and late-phase (LPR) skin reactions and cellular infiltration by using a repeat skin allergen challenge designed to imitate chronic allergen exposure. METHODS: Twenty-four atopic allergic volunteers received omalizumab or placebo for 12 weeks. Paired intradermal challenges of allergen (30 biological units) and diluent control were administered on 9 occasions at 2-week intervals. Early-phase and late-phase skin reactions and cellular infiltration in skin biopsies (using immunohistochemistry and in situ hybridization) were measured at intervals. RESULTS: Compared with placebo, omalizumab-treated patients had a progressive reduction in the LPR that was significantly greater than its effect on the EPR (median, --63% vs--24% respectively; P=.009). In addition, significant reduction of the LPR was reached within 2 weeks of commencing treatment, compared with 8 weeks for the EPR. There was a priming effect of repeated allergen challenge on infiltration of eosinophil, neutrophil, T(H)2 (CD3(+)/IL-4(+)), and total FcepsilonRI(+) cells in patients on placebo that was abrogated in those receiving omalizumab. CONCLUSION: The more marked effect of omalizumab on the LPR and prevention of the repeat-dose priming effect on several inflammatory cell types support a role for anti-IgE treatment in conditions associated with chronic allergic inflammation.

Acute allergen-induced airway remodeling in atopic asthma.

Studies in animals and in human atopic skin suggest that allergen challenge may activate acute tissue remodeling changes via transforming growth factor-beta pathways. We determined whether inhalational allergen challenge in subjects with mild asthma induces similar acute changes to the airway epithelial mesenchymal trophic unit (EMTU). Endobronchial mucosal biopsies obtained before and 24 h after challenge were examined by confocal microscopy for extracellular matrix deposition in the reticular basement membrane (RBM). Cells actively involved in extracellular matrix synthesis were identified as immunoreactive to heat shock protein 47, a chaperone of collagen synthesis. Interleukin-4/13 and transforming growth factor-beta-activated cells were identified by specific antibodies to phosphorylated (phospho-) signal transducer and activator of transcription 6 and phospho-Smad2, respectively. After allergen challenge, there was a significant increase in the number of heat shock protein 47-positive airway fibroblasts (P = 0.003) and in the thickness of tenascin in the RBM (P = 0.031). There were also increases in the number of phospho-Smad2+ epithelial cells (P = 0.04) and nuclear phospho-Smad2+ fibroblasts (P = 0.03), as well as phospho-signal transducer and activator of transcription 6+ epithelial cells (P = 0.03), after allergen challenge. Thus, allergen challenge in patients with mild asthma induces activation of epithelial cells and fibroblasts in the EMTU as well as increased tenascin deposition within the RBM. Airway remodeling in asthma may, in part, result from repeated acute activation of the EMTU by allergen exposure.