Project description:Disease outbreaks due to the consumption of legume seedlings contaminated with human enteric bacterial pathogens like Escherichia coli O157:H7 and Salmonella enterica are reported every year. We found surface and internal colonization of Medicago truncatula by Salmonella enterica and Escherichia coli O157:H7 even with inoculum levels as low as two bacteria per plant. Expression analyses using microarray revealed that some Medicago truncatula genes were regulated in a similar manner in response to both of these enteric pathogens. Medicago truncatula roots were inoculated with low inoculum levels of two enteric bacteria per plant (E. coli O157:H7 and Salmonella). 10 days post inoculated plants were used for RNA extraction and hybridization on Affymetrix microarrays.
Project description:Disease outbreaks due to the consumption of legume seedlings contaminated with human enteric bacterial pathogens like Escherichia coli O157:H7 and Salmonella enterica are reported every year. We found surface and internal colonization of Medicago truncatula by Salmonella enterica and Escherichia coli O157:H7 even with inoculum levels as low as two bacteria per plant. Expression analyses using microarray revealed that some Medicago truncatula genes were regulated in a similar manner in response to both of these enteric pathogens.
Project description:The enteric nervous system (ENS) controls several intestinal functions including motility and nutrient handling, which can be disrupted by infection-induced neuropathies or neuronal cell death. We investigated possible tolerance mechanisms preventing neuronal loss and disruption in gut motility after pathogen exposure. We found that following enteric infections, muscularis macrophages (MMs) acquire a tissue-protective phenotype that prevents neuronal loss and dysmotility during subsequent challenge with unrelated pathogens. Bacteria-induced neuroprotection relied on activation of gut-projecting sympathetic neurons and signaling via b2-adrenergic receptors (b2AR) on MMs. In contrast, helminth-mediated neuroprotection was dependent on T cells and systemic production of interleukin (IL)-4 and -13 by eosinophils, which induced arginase-expressing MMs that prevented neuronal loss from an unrelated infection located in a different intestinal region. Collectively, these data suggest that distinct enteric pathogens trigger a state of disease- or tissue tolerance that preserves ENS number and functionality.
Project description:Xyloglucans are highly substituted polysaccharides found in the primary cell walls of all vascular plants, acting as a first barrier against pathogens. Herein, we revealed that the diverse and economically relevant Xanthomonas phytopathogens are endowed with an enzymatic system targeting xyloglucans. Furthermore, we demonstrate that the products generated by this system elicit the expression of multiple virulence factors including the type III secretion system, a membrane-embedded machinery to deliver effector proteins into the host cells. Together, these findings illuminate the intricate enzymatic apparatus employed by Xanthomonas to break down xyloglucans and connect this system to the pathogenesis through activating the expression of key virulence factors.