Soft rot caused byBotryosphaeriadothideaandPhomopsissp. is a critical disease in kiwifruit. In order to efficiently control soft rot, a 28.6% chitosan composite film (CCF) containing chitosan, dextrin, ferulic acid, calcium, and auxiliaries was successfully developed. The results showed that CCF had a strong inhibitory effect on mycelia growth ofB. dothideaandPhomopsissp., with mycelial EC50values of 68.11 and 50.34 mg L−1, respectively. The concentration of 0.71–1.42 g L−1CCF had noticeably preventive and curative effects against soft rot. The spray of CCF before pathogen infection effectively reduced the incidence of soft rot, remarkably increased the content of resistance compounds, and activated the activity of defense enzymes. Moreover, it notably enhanced the yield and quality and prolonged the shelf life of kiwifruit. Therefore, the excellent control effects of CCF against soft rot might be associated with its film-forming property and antifungal activity, which prevent infection and induce plant defense mechanisms. The concentration of 0.71–1.42 g L−1CCF was optimal for the field application before the onset of disease symptoms in plants withB. dothideaandPhomopsissp.Keywords:chitosan composite film;kiwifruit;pathogen infection;soft rot;disease resistance;storage quality
Aeromonas caviae, an important food-borne pathogen, induces serious invasive infections and inflammation. The pro-inflammatory IL-1β functions against pathogenic infections and is elevated in various Aeromonas infection cases. However, the molecular mechanism of A. caviae-mediated IL-1β secretion remains unknown. In this study, mouse macrophages (PMs) were used to establish A. caviae infection model and multiple strategies were utilized to explore the mechanism of IL-1β secretion. IL-1β was elevated in A. caviae infected murine serum, PMs lysates or supernatants. This process triggered NLRP3 levels upregulation, ASC oligomerization, as well as dot gathering of NLRP3 and speck-like signals of ASC in the cytoplasm. MCC950 blocked A. caviae mediated IL-1β release. Meanwhile, NLRP3 inflammasome mediated the release of IL-1β in dose- and time-dependent manners, and the release of IL-1β was dependent on active caspase-1, as well as NLRP3 inflammasome was activated by potassium efflux and cathepsin B release ways. A. caviae also enhanced TLR2 levels, and deletion of TLR2 obviously decreased IL-1β secretion. What’s more, A. caviae resulted in NF-κB p65 nuclear translocation partly in a TLR2-dependent manner. Blocking NF-κB using BAY 11-7082 almost completely inhibited NLRP3 inflammasome first signal pro-IL-1β expression. Blocking TLR2, NF-κB, NLRP3 inflammasome significantly downregulated IL-1β release and TNF-α and IL-6 levels. These data illustrate that A. caviae caused IL-1β secretion in PMs is controlled by NLRP3 inflammasome, of which is mediated by NF-κB pathway and is partially dependent on TLR2, providing basis for drugs against A. caviae.
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