The mechanism of survival and degradation of phenol by Acinetobacter pittii in an extremely acidic environment.

The treatment efficiency of acidic phenol-containing wastewater is hindered by the absence of efficient acid-resistant phenol-degrading bacteria, and the acid-resistant mechanism of such bacteria remains poorly studied. In this study, the acid-resistant strain Hly3 was used as a research model to investigate its ability to degrade phenol and its underlying mechanism of acid resistance. Strain Hly3 exhibited robust acid resistance, capable of surviving in extremely acidic environments (pH 3) and degrading 1700 mg L-1 phenol in 72 h. Through the physiological response analysis of strain Hly3 to pH, the results indicated: firstly, the strain could reduce the relative permeability of the cell membrane and increase EPS secretion to prevent H+ from entering the cell (shielding effect); secondly, the strain could accumulate more buffering substances to neutralize the intracellular H+ (neutralization effect); thirdly, the strain could expel H+ from the cell by enhancing H+-ATPase activity (pumping effect); finally, the strain produced more active scavengers to reduce the toxicity of acid stress on cells (antioxidant effect). Subsequently, combining liquid chromatography-mass spectrometry (LC-MS) technology with exogenous addition experiments, it was verified that the acid resistance mechanism of microorganisms is achieved through the activation of acid-resistant response systems by glutamine, thereby enhancing functions such as shielding, neutralization, efflux, and antioxidation. This study elucidated the acid resistance mechanism of Acinetobacter pittii, providing a theoretical basis and guidance for the treatment of acidic phenol-containing wastewater.

Self-organized nanocrystal rings formed by microemulsion for selective recognition of proteins and immunoassays.

A simple and cheap method to fabricate a nanocrystal ring pattern was developed by utilization of a microemulsion in this study. The mixture of polystyrene and stabilizer dichloromethane solution that contained nanocrystal aqueous solution, prepared through shaking, was applied to fabricate a reverse microemulsion. After spreading and evaporating the solvent of microemulsion on a glass slide, an ordered honeycomb film was produced, accompanied by the formation of a nanocrystal ring pattern. The nanocrystal pattern could be readily applied for immunoassays and recognition of proteins. The pattern with antibody marked by a green colored nanocrystal specifically bound with antigen labeled by a red colored nanocrystal, leading to the enhancement in red fluorescent ring pattern and decrease in green fluorescent pattern. When the unlabeled antigen was added, the green fluorescent pattern was recovered. In addition, the ring pattern with immunocomplex could selectively recognize antigen and transferrin proteins. This strategy reveals that these patterns have potential applications in biochips, biosensors, imaging analysis and so forth.

Influence of subinhibitory concentrations of licochalcone A on the secretion of enterotoxins A and B by Staphylococcus aureus.

Enterotoxins produced by Staphylococcus aureus are the key pathogenicity factors that can cause a variety of illnesses in humans, including staphylococcal gastroenteritis and food poisoning. It has been proven that licochalcone A is a potentially effective antimicrobial agent against S. aureus. In this study, Western blot assays, tumour necrosis factor release assays, murine T-cell proliferation assays, and real-time reverse transcriptase-PCR were performed to evaluate the effect of subinhibitory concentrations of licochalcone A on the secretion of two major enterotoxins (SEA and SEB) by S. aureus. The results show that licochalcone A significantly decreased, in a dose-dependent manner, the secretion of SEA and SEB by both methicillin-sensitive S. aureus and methicillin-resistant S. aureus. These results may increase the desirability of using licochalcone A as a lead compound for the design of more potent antibacterial agents based on the chalcone template.

Preventive effects of valnemulin on lipopolysaccharide-induced acute lung injury in mice.

Valnemulin reportedly regulates inflammatory responses in addition to its in vitro antibacterial activity. In this study, we established a mouse model of lipopolysaccharide (LPS)-induced inflammatory lung injury and investigated the effect of valnemulin (100 mg/kg) on acute lung injury (ALI) 8 h after LPS challenge. We prepared bronchoalveolar lavage fluid (BALF) for measuring protein concentrations, cytokine levels, and superoxidase dismutase (SOD) activity, and collected lungs for assaying wet-to-dry weight (W/D) ratios, myeloperoxidase (MPO) activity, cytokine mRNA expression, and histological change. We found that the pre-administration of valnemulin significantly decreases the W/D ratio of lungs, protein concentrations, and the number of total cells, neutrophils, macrophages, and leukomonocytes, and histologic analysis indicates that valnemulin significantly attenuates tissue injury. Furthermore, valnemulin significantly increases LPS-induced SOD activity in BALF and decreases lung MPO activity as well. In addition, valnemulin also inhibits the production of tumor necrosis factor-alpha, interleukin-6, and interleukin-1beta, which is consistent with mRNA expression in lung. The results showed that valnemulin had a protective effect on LPS-induced ALI in mice.

Ceftiofur attenuates lipopolysaccharide-induced acute lung injury.

Ceftiofur is a new broad-spectrum, third-generation cephalosporin antibiotic for veterinary use. Our laboratory has previously been reported that ceftiofur can modulate early cytokine responses and increase mouse survival in endotoxemia. In the present study, we investigated the effect of ceftiofur on acute lung injury (ALI) induced by lipopolysaccharide (LPS) in vivo. Mice were pretreated with ceftiofur 1h before challenge with a dose of 0.5mg/kg LPS. Mice treated with LPS alone showed marked increased TNF-alpha, IL-6, and IL-8 levels in the bronchoalveolar lavage fluid (BALF). When pretreated with 30mg/kg of ceftiofur, the TNF-alpha, IL-6, and IL-8 levels were significantly decreased. In addition, the W/D ratio of the lung tissue and the number of total cells, neutrophils and macrophages in the BALF significantly decreased at 8h after pretreatment with ceftiofur. Furthermore, ceftiofur markedly attenuated the LPS-induced histological alteration. These studies indicate that ceftiofur significantly decreases the inflammation in a murine model of LPS-mediated ALI and may represent a novel prevention strategy for nonspecific inflammation in the lungs.

Protective effect of florfenicol on acute lung injury induced by lipopolysaccharide in mice.

Florfenicol, an antibiotic used to treat infection, has previously been shown to modulate early cytokine responses and increase mouse survival in endotoxemia. In the present study, we investigated in vivo the effect of florfenicol on acute lung injury (ALI) induced by lipopolysaccharide (LPS). In the mouse model of LPS-induced inflammatory lung injury, we found that pretreatment with a single 100mg/kg dose of florfenicol significantly decreases the W/D ratio of lungs and protein concentration in the bronchoalveolar lavage fluid (BALF) and significantly reduces the number of total cells, neutrophils and macrophages in the BALF at 24h after LPS challenge. In addition, histopathological examination indicates that florfenicol significantly attenuates tissue injury of the lungs in LPS-induced ALI. Furthermore, florfenicol also inhibits the production of several inflammatory cytokines, including tumor necrosis factor-alpha (TNF-alpha) at 6 and 12h, interleukin-6 (IL-6) at 12 and 24h, and interleukin-1ss (IL-1ss) at 12h, in the BALF after LPS challenge. These results suggest that florfenicol protects against LPS-induced ALI in mice.