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Understanding the molecular determinants underlying the interaction between the leaf and human pathogenic bacteria is key to provide the foundation to develop science-based strategies to prevent or decrease the pathogen contamination of leafy greens. In this study, we conducted a dual RNA-sequencing analysis to simultaneously define changes in the transcriptomic profiles of the plant and the bacterium when they come in contact. We used an economically relevant vegetable crop, lettuce (Lactuca sativa L. cultivar Salinas), and a model plant, Arabidopsis thaliana Col-0, as well as two pathogenic bacterial strains that cause disease outbreaks associated with fresh produce, Escherichia coli O157:H7 and Salmonella enterica serovar Typhimurium 14028s (STm 14028s). We observed commonalities and specificities in the modulation of biological processes between Arabidopsis and lettuce and between O157:H7 and STm 14028s during early stages of the interaction. We detected a larger alteration of gene expression at the whole transcriptome level in lettuce and Arabidopsis at 24 h post inoculation with STm 14028s compared to that with O157:H7. In addition, bacterial transcriptomic adjustments were substantially larger in Arabidopsis than in lettuce. Bacterial transcriptome was affected at a larger extent in the first 4 h compared to the subsequent 20 h after inoculation. Overall, we gained valuable knowledge about the responses and counter-responses of both bacterial pathogen and plant host when these bacteria are residing in the leaf intercellular space. These findings and the public genomic resources generated in this study are valuable for additional data mining.

Abnormalities in hippocampal synaptic plasticity contribute to the pathogenesis of post-traumatic stress disorder (PTSD). The Wnt/β-catenin signaling pathway is critical for the regulation of synaptic plasticity. PTSD symptoms can be alleviated by correcting impaired neural plasticity in the hippocampus (Hipp). Electroacupuncture (EA) has a therapeutic effect by relieving PTSD-like behaviors. However, little is known about whether the Wnt/β-catenin pathway is involved in EA-mediated improvements of PTSD symptoms. In this study, we found that enhanced single prolonged stress (ESPS)-induced PTSD led to abnormal neural plasticity, characterized by the decline of dendritic spines, the expression of postsynaptic density 95 (PSD95), and synaptophysin (Syn) in the stressed Hipp along with the reduction of Wnt3a and β-catenin, and increased GSK-3β. EA significantly alleviated PTSD-like behaviors, as assessed by the open field test, elevated platform maze test and conditioning fear test. This was paralleled by correcting abnormal neural plasticity by promoting the expression of PSD95 and Syn, as well as the number of dendritic spines in the Hipp. Importantly, EA exerted anti-PTSD effects by augmenting the expression levels of Wnt3a and β-catenin, and decreasing that of GSK-3β. The effects mediated by EA were abolished by XAV939, an inhibitor of the Wnt/β-catenin pathway. This suggests that EA relieved ESPS-induced PTSD-like behaviors, which can largely be ascribed to impaired neural plasticity in the Hipp. These findings provide new insights into possible mechanisms linking neural plasticity in the Hipp as potential novel targets for PTSD treatment in EA therapy.

Acute kidney injury (AKI) is one of the most challenging clinical problems in kidney disease due to serious complications and high mortality rate, which can lead to acute lung injury (ALI) through inflammatory reactions and oxidative stress. Adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR) pathway has been reported to be involved in the development of renal ischemia-reperfusion through autophagy and it remains unclear whether AMPK/mTOR pathway has an effect on the AKI-induced ALI. In this study, we aimed to investigate the effects of autophagy-related AMPK/mTOR signaling pathway on inflammatory factors and oxidative stress in an AKI-induced ALI model. The 48 male Sprague–Dawley rats were divided into four groups randomly: (i) sham, (ii) ischemia/reperfusion injury (IRI), (iii) IRI + rapamycin (RA), and (iv) IRI + 3-methyladenine (3-MA). Unilateral flank incisions were made and right kidneys were excised. The left kidney was subjected to 60 min of ischemia followed by 12, 24, 48, and 72 h of reperfusion. The levels of Scr, blood urea nitrogen (BUN), Wet/Dry ratio, indexes of inflammation, and oxidative stress were assayed. Histological examinations were performed. The protein expression of AMPK, mTOR, LC3-II/LC3-I ratio, and Beclin-1, ULK1 was evaluated by western blotting and immunohistochemistry. Compared to the rats from the sham group, IRI rats showed significantly pulmonary damage after AKI with increased Scr, BUN, Wet/Dry ratio, indexes of inflammation, and oxidative stress. The expression of AMPK, LC3-II/LC3-I ratio, Beclin-1, and ULK1 and were increased, while p62 and mTOR were decreased. In addition, RA treatment significantly attenuated lung injury by promoting autophagy through the activation of the AMPK/mTOR pathway, and 3-MA treatment exhibited adverse effects inversely. Therefore, the activation of the AMPK/mTOR pathway after renal IRI induction could significantly attenuate kidney injury and following AKI-induced ALI by inducing autophagy, which alienates inflammation, oxidative stress, and apoptosis.