Abiotic stresses such as salt stress are the major limiting factors for agricultural productivity, and cause global food insecurity. It is well known that plant associated beneficial microorganisms can stimulate plant growth and enhance resistance to abiotic stresses. In this context, bacterial endophytes are a group of bacteria that colonize the host plant and play a fundamental role in plant growth enhancement under stress condition. Recently, our group reported that the beneficial bacteria Enterobacter sp.SA187 induces plant growth in Arabidopsis under salt stress conditions by manipulation of the plant ethylene signaling pathway. We therefore compared inoculation of plants by SA187 with virulent and non-virulent strains Pst DC3000. Although both strains inhibit plant growth at ambient conditions, Pst DC3000 hrcC-, but not Pst DC3000, induced salt stress tolerance, suggesting that Pst DC3000 hrcC- also contains plant growth promoting activity under stress conditions. Our results indicate that Pst DC3000 hrcC- shares features with beneficial bacteria by inducing salt tolerance through reduction of the shoot and root Na+/K+ ratio. To further elucidate the underlying mechanisms of this interaction with Arabidopsis, RNAseq, hormone and biochemical analyses were performed. Genetic studies also show that Pst DC3000 hrcC- induced salt stress tolerance involving several phytohormone pathways, including auxin, ethylene and salicylic acid. Transcriptome and genetic analyses indicate that glucosinolates play an important role in this beneficial interaction. We found that indolic and alkyl glucosinolates act as negative factors on Pst DC3000 hrcC-, alkyl glucosinolates are positive and indolic glucosinolates negative regulators in SA187 interaction with Arabidopsis. These results reveal that besides a repertoire of effectors, Pst DC3000 hrcC- also produces factors that can be beneficial for plant growth under certain stress conditions, as observed with Enterobacter sp. SA187.

Early innate response of intestinal epithelial cells is the first line defense against enteric pathogens. Toxoplasma gondii infections acquired naturally via the peroral route, encounter intestinal epithelial cells early post-infection. Although the population structure of T. gondii is known to be highly clonal, clinical strains of T. gondii have been classified into three genotypes based on their virulence. In this study we investigated whether human intestinal epithelial cell immune response to T. gondii is virulence dependent. We demonstrated distinct virulence of the three T. gondii genotype strains evaluated in human intestinal epithelial cells by their capacity to replicate and induce host cell cytotoxicity. The early host innate mechanisms such as activation of signaling pathways and induction of innate effectors were likewise differentially elicited by the three T. gondii strains. Low levels of TLR dependent NF-kB activation and a failure to rapidly up-regulate innate cytokine and chemokine genes was observed after virulent Type I strain infection. In contrast, early innate response to the less virulent Type II strain was rapid, efficient and led to high levels of IL-8 and IL-6 secretion, whereas response to Type III parasites was intermediate. Early expression of b-defensin 2 gene was suppressed specifically by virulent Type I strain and its activation prior to infection in intestinal epithelial cells led to decreased parasite viability. These findings provide evidence for T. gondii strain virulence dependent down-modulation of early human intestinal epithelial cell innate responses and highlight the importance of these cells in host defense against this infection.

Early innate response of intestinal epithelial cells is the first line defense against enteric pathogens. Toxoplasma gondii infections acquired naturally via the peroral route, encounter intestinal epithelial cells early post-infection. Although the population structure of T. gondii is known to be highly clonal, clinical strains of T. gondii have been classified into three genotypes based on their virulence. In this study we investigated whether human intestinal epithelial cell immune response to T. gondii is virulence dependent. We demonstrated distinct virulence of the three T. gondii genotype strains evaluated in human intestinal epithelial cells by their capacity to replicate and induce host cell cytotoxicity. The early host innate mechanisms such as activation of signaling pathways and induction of innate effectors were likewise differentially elicited by the three T. gondii strains. Low levels of TLR dependent NF-kB activation and a failure to rapidly up-regulate innate cytokine and chemokine genes was observed after virulent Type I strain infection. In contrast, early innate response to the less virulent Type II strain was rapid, efficient and led to high levels of IL-8 and IL-6 secretion, whereas response to Type III parasites was intermediate. Early expression of b-defensin 2 gene was suppressed specifically by virulent Type I strain and its activation prior to infection in intestinal epithelial cells led to decreased parasite viability. These findings provide evidence for T. gondii strain virulence dependent down-modulation of early human intestinal epithelial cell innate responses and highlight the importance of these cells in host defense against this infection. / Doctorat en Sciences biomédicales et pharmaceutiques / info:eu-repo/semantics/nonPublished