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Taibi, A.

Publications and source records attributed to Taibi, A..

2 recordsLinked to original sources

Exploring the phytobeneficial and biocontrol capacities of endophytic bacteria isolated from hybrid vanilla pods

Few studies have been conducted on endophytic bacteria of vanilla. In this study, 58 bacterial strains were isolated from two hybrid vanilla plants from Madagascar, Manitra ampotony and Tsy taitra. They were genetically characterised and divided into four distinct phylotypes. A selection of twelve strains corresponding to the identified genetic diversity were tested in vitro for four phytobeneficial capacities: phosphate solubilisation, free nitrogen fixation, phytohormone and siderophore production. They were also evaluated in vitro for their ability to biocontrol the growth of the vanilla pathogenic fungi, Fusarium oxysporum f. sp. radicis vanillae and Cholletotrichum orchidophilum. Bacteria belonging to three different phyla were found to be highly competent in each of the phytobeneficial capacities tested. Bacteria belonging to the phylum related to Bacillus siamensis showed the best capacity to inhibit fungal growth making them good candidates for controlling fungal diseases of vanilla. This competence was highlighted with spectral imaging showing the production of lipopeptides by the bacterial strains confronted with the pathogenic fungi of vanilla.

microbiology↗

The neonatal microenvironment programs conventional and intestinal Tbet+ γδT17 cells through the transcription factor STAT5

Interleukin(IL)-17-producing ROR{gamma}t+ {gamma}{delta} T ({gamma}{delta}T17) cells develop in the embryonic thymus and participate in type 3 immune responses. Herein we show that {gamma}{delta}T17 cells rapidly proliferate within neonatal lymph nodes and gut, where upon entry they uniquely upregulate Tbet and co-express IL-17, IL-22 and interferon(IFN) {gamma} in a STAT3 and retinoic acid dependent manner. Neonatal expansion was halted in mice conditionally deficient in STAT5 and its loss resulted in {gamma}{delta}T17 cell depletion from all adult organs. Hyperactive STAT5 mutant mice showed that the STAT5A homologue had a dominant role over STAT5B in promoting {gamma}{delta}T17 cell expansion and downregulating gut-associated Tbet. In contrast, STAT5B preferentially expanded IFN{gamma}-producing {gamma}{delta} populations. Importantly, mice lacking {gamma}{delta}T17 cells due to STAT5 deficiency displayed a profound resistance to experimental autoimmune encephalomyelitis. Our data identify for the first time STAT5 as a key molecular checkpoint allowing {gamma}{delta}T17 cells to pass through a critical neonatal developmental window to acquire tissue-specific characteristics essential for infection and autoimmunity.

immunology↗