In this study, the mutant JX22MT1 was obtained by the EZ-Tn5 tran

In this study, the mutant JX22MT1 was obtained by the EZ-Tn5 transposon mutation and showed no antifungal activity against Fusarium oxysporum f. sp. lycopersici as compared with wild-type strain JX22.

The pqqC gene was disrupted in the mutant. Antifungal activity at the wild-type level was restored from the mutant JX22MT1 with the introduction of the functional pqqC gene, which encodes pyrroloquinoline–quinone synthesis protein C. The results suggest that pqqC is essential for antifungal activity of P. kilonensis JX22 against F. oxysporum f. sp. lycopersici. “
“Consumption see more of Vibrio parahaemolyticus via contaminated shellfish results in inflammatory gastroenteritis characterised by severe diarrhoea, nausea and stomach cramps. This study investigated

the translocation of V. parahaemolyticus across a Peyer’s patch M cell-like Caco-2/Raji B co-culture model system, as M cells represent a primary site of infection for many pathogenic bacteria. Vibrio parahaemolyticus translocated across co-culture monolayers in higher numbers as compared to Caco-2 monolayers. Moreover, the bacteria induced a greater disruption of the transepithelial resistance in M cell-like co-cultures than in Caco-2 monocultures. Virulence factors associated with this pathogen include two type three secretion systems (TTSS-1 and Olaparib cost TTSS-2). TTSS-1 had no effect on translocation efficiency, with TTSS-2 exhibiting a modest enhancing effect. ERK activity was required for optimal translocation 1 h postinfection, however,

neither ERK nor the JNK and p38 MAPK were required at 2 h pi. Additionally, TER disruption in response to bacterial infection occurred independently of the TTSS and MAPK activation. It was concluded that V. parahaemolyticus causes TER disruption of M cell-like co-cultures and translocates in high numbers across the M cell-like co-culture monolayer. These data implicate M cells as important sites for V. parahaemolyticus invasion across the intestinal epithelium during infection. The human gastrointestinal pathogen ID-8 Vibrio parahaemolyticus is a Gram-negative bacterium whose natural habitat is marine and estuarine sediment (Daniels et al., 2000; Makino et al., 2003). Infection is characterised by severe gastroenteritis following consumption of contaminated, uncooked shellfish. Infection of the host epithelium by V. parahaemolyticus is associated with the presence of two haemolysins and two type three secretion systems, namely TTSS-1 and TTSS-2. While TTSS-1 is involved in the cytotoxic effects of the bacterium, TTSS-2 is responsible for bacterial enterotoxicity (Park et al., 2004a, b). The intestinal monolayer is an important defensive barrier following the consumption of contaminated seafood (Catalioto et al., 2011).

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