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Acute inflammation has the potential for the recruitment of immune cells, inhibiting tumor angiogenesis, metastasis, and drug resistance thereby overcoming the tumor immunosuppressive microenvironment caused by chronic inflammation. Here, an acute inflammation inducer using bacteria outer membrane vesicles (OMVs) loaded in thermal‐sensitive hydrogel (named OMVs‐gel) for localized and controlled release of OMVs in tumor sites is proposed. OMVs trigger neutrophil recruitment and amplify acute inflammation inside tumor tissues. The hydrogel ensures drastic inflammation is confined within the tumor, addressing biosafety concerns that the direct administration of free OMVs may cause fatal effects. This strategy eradicated solid tumors safely and rapidly. The study further elucidates one of the possible immune mechanisms of OMVs‐gel therapy, which involves the assembly of antitumor neutrophils and elastase release for selective tumor killing. Additionally, tumor vascular destruction induced by OMVs‐gel results in tumor darkening, allowing for combinational photothermal therapy. The findings suggest that the use of OMVs‐gel can safely induce acute inflammation and enhance antitumor immunity, representing a promising strategy to promote acute inflammation application in tumor immunotherapy. [ABSTRACT FROM AUTHOR]

Most land plants can establish symbiosis with arbuscular mycorrhizal (AM) fungi to increase fitness to environmental challenges. The development of AM symbiosis is controlled by intricate procedures involving all phytohormones. However, the mechanisms underlying the auxin‐mediated regulation of AM symbiosis remains largely unknown. Here, we report that AM colonisation promotes auxin response and indole‐3‐acetic acid (IAA) accumulation, but downregulates IAA biosynthesis genes in tomato (Solanum lycopersicum). External IAA application modulates the AM symbiosis by promoting arbuscule formation at low concentrations but repressing it at high concentrations. An AM‐induced GH3 gene, SlGH3.4, encoding a putative IAA‐amido synthetase, negatively regulates mycorrhization via maintaining cellular auxin homoeostasis. Loss of SlGH3.4 function increased free IAA content and arbuscule incidence, while constitutively overexpressing SlGH3.4 in either tomato or rice resulted in decreased IAA content, total colonisation level and arbuscule abundance in mycorrhizal roots. Several auxin‐inducible expansin genes involved in AM formation or resistance to pathogen infection were upregulated in slgh3.4 mycorrhizal roots but downregulated in the SlGH3.4‐overexpressing plants. Taken together, our results highlight a positive correlation between the endogenous IAA content and mycorrhization level, particularly arbuscule incidence, and suggest that the SlGH3.4‐mediated auxin homoeostasis and regulation of expansin genes is involved in finely tuning the AM development. [ABSTRACT FROM AUTHOR]

Long-chain chitooligosaccharides are fungal microbe-associated molecular patterns ( MAMPs) that are recognized by LYSIN MOTIF RECEPTOR KINASE5 ( LYK5), inducing the formation of a complex with CHITIN ELICITOR RECEPTOR KINASE1 ( CERK1). Formation of this complex leads to activation of the CERK1 intracellular kinase domain and induction of plant innate immunity in Arabidopsis., We found that addition of chitooctaose induced LYK5 protein accumulation as a result of de novo gene expression and the inhibition of LYK5 protein degradation. Screening the putative E3 ligases for interaction with LYK5 identified PLANT U-BOX13 ( PUB13), which complexed with LYK5, but this complex dissociated upon addition of chitooctaose. Consistent with these results, LYK5 protein abundance was higher in pub13 mutants compared with the wild type without chitooctaose treatment, while similar abundance was detected with the addition of chitooctaose., The pub13 mutants showed hypersensitivity to chitooctaose-induced rapid responses, such as the production of reactive oxygen species ( ROS) and mitogen-activated protein ( MAP) kinase phosphorylation, but exhibited normal responses to subsequent long-term chitooctaose treatment, such as gene expression and callose deposition. In addition, PUB13 could ubiquitinate the LYK5 kinase domain in vitro., Taken together, our results suggest an important regulatory function for the turnover of LYK5 mediated by the E3 ligase PUB13. [ABSTRACT FROM AUTHOR]