High Temperature in Combination with UV Irradiation Enhances Horizontal Transfer of stx2 Gene from E. coli O157:H7 to Non-Pathogenic E. coli

Background: Shiga toxin (stx) genes have been transferred to numerous bacteria, one of which is E. coli O157:H7. It is a common belief that stx gene is transferred by bacteriophages, because stx genes are located on lambdoid prophages in the E. coli O157:H7 genome. Both E. coli O157:H7 and non-pathogenic E. coli are highly enriched in cattle feedlots. We hypothesized that strong UV radiation in combination with high temperature accelerates stx gene transfer into nonpathogenic E. coli in feedlots. Methodology/Principal Findings: E. coli O157:H7 EDL933 strain were subjected to different UV irradiation (0 or 0.5 kJ/m 2) combination with different temperature (22, 28, 30, 32, and 37uC) treatments, and the activation of lambdoid prophages was analyzed by plaque forming unit while induction of Stx2 prophages was quantified by quantitative real-time PCR. Data showed that lambdoid prophages in E. coli O157:H7, including phages carrying stx2, were activated under UV radiation, a process enhanced by elevated temperature. Consistently, western blotting analysis indicated that the production of Shiga toxin 2 was also dramatically increased by UV irradiation and high temperature. In situ colony hybridization screening indicated that these activated Stx2 prophages were capable of converting laboratory strain of E. coli K12 into new Shiga toxigenic E. coli, which were further confirmed by PCR and ELISA analysis. Conclusions/Significance: These data implicate that high environmental temperature in combination with UV irradiatio

\u3ci\u3eNurudea zhengii\u3c/i\u3e Ren, A New Species of the \u3ci\u3eRhus\u3c/i\u3e Gall Aphids (Aphididae: Eriosomatinae: Fordini) from Eastern China

A new Rhus gall aphid species Nurudea zhengii Ren, sp. nov. collected from the Mountain Qixing in Shangrao County, Jiangxi Province, China is described and illustrated from alate viviparous female. The new species differs from the other Nurudea species in the length and proportion of antennal segments, the structure of antennal secondary sensilla, and the flower-like shape of the galls that are formed on its primary host. Its primary host plant is Rhus hypoleuca, whereas other Nurudea species are on R. chinensis

Quercetin Prevents Escherichia coli O157:H7 Adhesion to Epithelial Cells via Suppressing Focal Adhesions

The attachment of Escherichia coli O157:H7 to intestinal epithelial cells is indispensable for its pathogenesis. Besides translocated-intimin receptor (Tir), E. coli O157:H7 interacts with host cell surface receptors to promote intimate adhesion. This study showed that integrin β1 was increased in Caco-2 cells upon E. coli O157:H7 infection, while Caco-2 cells subjected to integrin β1 antibody blocking or CRISPR/Cas9 knockout had reduced bacterial attachment. Infection of E. coli O157:H7 inactivated focal adhesion kinase (FAK) and paxillin, increased focal adhesion (FA) and actin polymerization, and decreased cell migration in Caco-2 cells, which were rescued by integrin β1 antibody blocking or knockout. Pre-treatment with quercetin, known for its anti-oxidant and anti-inflammatory activity, reduced bacterial infection to Caco-2 cells, which might be partially via interfering integrin β1 and FAK association augmented by E. coli O157:H7. In addition, quercetin decreased FA formation induced by bacterial infection and recovered host cell motility. Taken together, data showed that E. coli O157:H7 interacts with integrin β1 to facilitate its adhesion to host cells. Quercetin inhibits bacterial infection possibly by blocking the interaction between E. coli O157:H7 and integrin β1. Collectively, these data indicate that quercetin provides an alternative antimicrobial to mitigate and control E. coli O157:H7 intestinal infection, and suggest potential broad benefits of quercetin and related polyphenols in fighting other enteric pathogen infections

Leukotriene B4, administered via intracerebroventricular injection, attenuates the antigen-induced asthmatic response in sensitized guinea pigs

<p>Abstract</p> <p>Background</p> <p>Despite intensive studies focused on the pathophysiology of asthmatic inflammation, little is known about how cross-talk between neuroendocrine and immune systems regulates the inflammatory response during an asthmatic attack. We recently showed corresponding changes of cytokines and leukotriene B₄(LTB₄) in brain and lung tissues of antigen-challenged asthmatic rats. Here, we investigated how LTB₄interacts with the neuroendocrine-immune system in regulating antigen-induced asthmatic responses in sensitized guinea pigs.</p> <p>Methods</p> <p>Ovalbumin-sensitized guinea pigs were challenged by inhalation of antigen. Vehicle, LTB₄or U75302 (a selective LTB₄BLT1 receptor inhibitor) was given via intracerebroventricular injection (i.c.v.) 30 min before challenge. Airway contraction response was evaluated using Penh values before and after antigen challenge. The inflammatory response in lung tissue was evaluated 24 h after challenge. The LTB₄content of lung and brain homogenate preparations was detected by reversed phase high-performance liquid chromatography (RP-HPLC). Plasma levels of adrenocorticotropic hormone (ACTH) and corticosterone (CORT) were measured using ELISA kits.</p> <p>Results</p> <p>Antigen challenge impaired pulmonary function and increased inflammatory cell infiltration in lung tissue. These responses could be significantly suppressed by LTB₄, 30 ng i.c.v., in ovalbumin-sensitized guinea pigs. LTB₄content of lung and brain homogenates from antigen-challenged guinea pigs was significantly increased. In addition, administration of LTB₄via i.c.v. markedly increased CORT and ACTH level in plasma before antigen challenge, and there were further increases in CORT and ACTH levels in plasma after antigen challenge. U75302, 100 ng i.c.v., completely blocked the effects of LTB₄. In addition, U75302, 100 ng via i.c.v. injection, markedly decreased LTB₄content in lung homogenates, but not in brain homogenates.</p> <p>Conclusions</p> <p>Increased LTB₄levels in brain during asthmatic attacks down-regulates airway contraction response and inflammation through the BLT1 receptor. Stimulation of the hypothalamic-pituitary-adrenal axis by LTB₄may result in an increase in systemic glucocorticoids which, in turn, would feed back to suppress the asthmatic response.</p

4-Guanidinobenzene­sulfonic acid

In the zwitterionic title compound (systematic name: 4-{[amino(inimio)methyl]amino}benzenesulfonate), C7H9N3O3S, the dihedral angle between the plane of the guanidine grouping and the benzene ring system is 44.87 (7)°. The crystal packing is stabilized by inter­molecular N—H⋯O hydrogen bonds involving all the potential donors