Cold atmospheric plasma (CAP) is a group of various chemical active species, such as ozone and nitric oxide, generated by working gas. CAP was demonstrated to have an effect on tissue regeneration and wound healing. We conducted this study to evaluate the efficacy and safety of CAP as a novel therapy for diabetic wounds in vitro and in vivo. The plasma consists of ionised helium gas that is produced by a high‐voltage and high‐frequency power supply. Eight‐week‐old male db/db mice and C57BL mice were treated with helium gas (control group), 90s' CAP (low‐dose group), and 180s' CAP (high‐dose group). Mice were treated and observed for 2 weeks. Skin samples from around the wound and blood samples were collected. Our in vitro analysis included scratch wound‐healing assays by using human HaCaT immortalised human epidermal cells. After 14 days of treatment, CAP could obviously promote diabetic wound healing. Wound closure rates were significantly higher in the low‐dose group and high‐dose groups compared with the control group. Meanwhile, compared with the control group, the protein expression of IL‐6, tumour necrosis factor‐α, inducible nitric oxide synthase, and superoxide dismutase in two CAP groups significantly decreased, while the protein expression of vascular endothelial growth factor and transforming growth factor‐β in two CAP groups significantly increased (all P < .05); these data show good agreement with the change in mRNA level (all P < .05). In vitro, scratch wound‐healing assays showed that plasma treatment could effectively ensure healing within 3 minutes of exposure (all P < .05). In addition, no difference was found in histological observations of normal skin and the level of serum alanine transaminase, aspartate aminotransferase, blood urea nitrogen, creatinine, and white blood cells among the CAP groups and control group. CAP treatment for 3 minutes every day improves wound healing in diabetic mice by suppressing inflammation, reducing oxidative stress, and enhancing angiogenesis, involving several proteins signalling, and it is safe for the liver and kidney.

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sRNAs (small RNAs) play an important role in regulation of plant immunity against a variety of pathogens. In this study, sRNA sequencing analysis was performed to identify miRNAs (microRNAs) during the interaction of potato and Phytophthora infestans. Totally, 171 potato miRNAs were identified, 43 of which were annotated in the miRNA database and 128 were assigned as novel miRNAs in this study. Those potato miRNAs may target 878 potato genes and half of them encode resistance proteins. Fifty-three potato miRNAs may target 194 P. infestans genes. Three potato miRNAs (novel 72, 133, and 140) were predicted to have targets only in the P. infestans genome. miRNAs transient expression and P. infestans inoculation assay showed that miR396, miR166, miR6149-5P, novel133, or novel140 promoted P. infestans colonization, while miR394 inhibited colonization on Nicotiana benthamiana leaves. An artificial miRNA target (amiRNA) degradation experiment demonstrated that miR394 could target both potato gene (PGSC0003DMG400034305) and P. infestans genes. miR396 targets the multicystatin gene (PGSC0003DMG400026899) and miR6149-5p could shear the galactose oxidase F-box protein gene CPR30 (PGSC0003DMG400021641). This study provides new information on the aspect of cross-kingdom immune regulation in potato-P. infestans interaction at the sRNAs regulation level.

Oomycete pathogens secrete hundreds of cytoplasmic RxLR effectors to modulate host immunity by targeting diverse plant proteins. Revealing how effectors manipulate host proteins is pivotal to understand infection processes and to develop new strategies to control plant disease. Here we show that the Phytophthora infestans RxLR effector Pi22798 interacts in the nucleus with a potato class II knotted-like homeobox (KNOX) transcription factor, StKNOX3. Silencing the orthologue NbKNOX3 in Nicotiana benthamiana reduces host colonization by P. infestans, whereas transient and stable overexpression of StKNOX3 enhances infection. StKNOX3 forms a homodimer which is dependent on its KNOX II domain. The KNOX II domain is also essential for Pi22798 interaction and for StKNOX3 to enhance P. infestans colonization, indicating that StKNOX3 homodimerization contributes to susceptibility. However, critically, the effector Pi22798 promotes StKNOX3 homodimerization, rather than heterodimerization to another KNOX transcription factor StKNOX7. These results demonstrate that the Oomycete effector Pi22798 increases pathogenicity by promoting homodimerization specifically of StKNOX3 to enhance susceptibility.