Screening of Microorganisms for Biodegradation of Simazine Pollution (Obsolete Pesticide Azotop 50 WP)

The capability of environmental microorganisms to biodegrade simazine—an active substance of 2-chloro-s-triazine herbicides (pesticide waste since 2007)—was assessed. An enormous metabolic potential of microorganisms impels to explore the possibilities of using them as an alternative way for thermal and chemical methods of utilization. First, the biotope rich in microorganisms resistant to simazine was examined. Only the higher dose of simazine (100 mg/l) had an actual influence on quantity of bacteria and environmental fungi incubated on substrate with simazine. Most simazine-resistant bacteria populated activated sludge and biohumus (vermicompost); the biggest strain of resistant fungi was found in floral soil and risosphere soil of maize. Compost and biohumus were the sources of microorganisms which biodegraded simazine, though either of them was the dominant considering the quantity of simazine-resistant microorganisms. In both cases of periodic culture (microorganisms from biohumus and compost), nearly 100% of simazine (50 mg/l) was degraded (within 8 days). After the repeated enrichment culture with simazine, the rate of its degradation highly accelerated, and just after 24 h, the significant decrease of simazine (20% in compost and 80% in biohumus) was noted. Although a dozen attempts of isolating various strains responsible for biodegradation of simazine from compost and biohumus were performed, only the strain identified as Arthrobacter urefaciens (NC) was obtained, and it biodegraded simazine with almost 100% efficiency (within 4 days)

ENHANCED beta-MANNANASE PRODUCTION FROM ALTERNATIVE SOURCES BY RECOMBINANT ASPERGILLUS SOJAE

beta-mannanases can degrade galactomannans to mannose and it has been used in various application areas. The aim of this study was to produce the beta-mannanase from carob pod extract including different nitrogen sources. The best operation values for fermentation were determined to be 8% initial sugar concentration with 0.5% yeast extract, 100 r.p.m., and 7% inoculation rate, which yielded the maximum beta-mannanase activity as 423.60 U ml(-1). Effects of nitrogen sources on beta-mannanase activity were also studied and it reached 695.6 U ml(-1) by using 0.5% of ammonium nitrate as the nitrogen source at the determined optimum conditions. Results also showed that meat bone meal and soybean meal could be used as cost effective nitrogen sources based on achieved beta-mannanase activity

Novel hybrid treatments of textile wastewater by membrane oxidation reactor: Performance investigations, optimizations and efficiency comparisons

PMID = 3114174

SAA drives proinflammatory heterotypic macrophage differentiation in the lung via CSF-1R-dependent signaling

Serum amyloid A (SAA) is expressed locally in chronic inflammatory conditions such as chronic obstructive pulmonary disease (COPD), where macrophages that do not accord with the classic M1/M2 paradigm also accumulate. In this study, the role of SAA in regulating macrophage differentiation was investigated in vitro using human blood monocytes from healthy subjects and patients with COPD and in vivo using an airway SAA challenge model in BALB/c mice. Differentiation of human monocytes with SAA stimulated the proinflammatory monokines IL-6 and IL-1β concurrently with the M2 markers CD163 and IL-10. Furthermore, SAA-differentiated macrophages stimulated with lipopolysaccharide (LPS) expressed markedly higher levels of IL-6 and IL-1β. The ALX/FPR2 antagonist WRW4 reduced IL-6 and IL-1β expression but did not significantly inhibit phagocytic and efferocytic activity. In vivo, SAA administration induced the development of a CD11chighCD11bhigh macrophage population that generated higher levels of IL-6, IL-1β, and G-CSF following ex vivo LPS challenge. Blocking CSF-1R signaling effectively reduced the number of CD11chighCD11bhigh macrophages by 71% and also markedly inhibited neutrophilic inflammation by 80%. In conclusion, our findings suggest that SAA can promote a distinct CD11chighCD11bhigh macrophage phenotype, and targeting this population may provide a novel approach to treating chronic inflammatory conditions associated with persistent SAA expression.-Anthony, D., McQualter, J. L., Bishara, M., Lim, E. X., Yatmaz, S., Seow, H. J., Hansen, M., Thompson, M., Hamilton, J. A., Irving, L. B., Levy, B. D., Vlahos, R., Anderson, G. P., Bozinovski, S. SAA drives proinflammatory heterotypic macrophage differentiation in the lung via CSF-1R-dependent signaling

IL-17A and Serum Amyloid A Are Elevated in a Cigarette Smoke Cessation Model Associated with the Persistence of Pigmented Macrophages, Neutrophils and Activated NK Cells

<div><p>While global success in cessation advocacy has seen smoking rates fall in many developed countries, persistent lung inflammation in ex-smokers is an increasingly important clinical problem whose mechanistic basis remains poorly understood. In this study, candidate effector mechanisms were assessed in mice exposed to cigarette smoke (CS) for 4 months following cessation from long term CS exposure. BALF neutrophils, CD4⁺ and CD8⁺ T cells and lung innate NK cells remained significantly elevated following smoking cessation. Analysis of neutrophil mobilization markers showed a transition from acute mediators (MIP-2α, KC and G-CSF) to sustained drivers of neutrophil and macrophage recruitment and activation (IL-17A and Serum Amyoid A (SAA)). Follicle-like lymphoid aggregates formed with CS exposure and persisted with cessation, where they were in close anatomical proximity to pigmented macrophages, whose number actually increased 3-fold following CS cessation. This was associated with the elastolytic protease, MMP-12 (macrophage metallo-elastase) which remained significantly elevated post-cessation. Both GM-CSF and CSF-1 were significantly increased in the CS cessation group relative to the control group. In conclusion, we show that smoking cessation mediates a transition to accumulation of pigmented macrophages, which may contribute to the expanded macrophage population observed in COPD. These macrophages together with IL-17A, SAA and innate NK cells are identified here as candidate persistence determinants and, we suggest, may represent specific targets for therapies directed towards the amelioration of chronic airway inflammation.</p></div

Smoke-induced weight loss was reversed 12 weeks after CS cessation.

<p>Male BALB/c mice were either exposed to 6 cigarettes/day, 6 days/week (▪) or sham handled (▴) for 16 weeks. After smoke exposure, groups of mice were then exposed to room air without cigarette smoke for either 4 weeks (∇) or 12 weeks (♦). For all groups body weight was determined weekly. Data are shown as mean ± SE for n = 14–18 per treatment group.</p