This bias can be minimised by specific library preparation (i.e. Nevertheless, such an approach is seriously impaired by the unbalanced representation of the sequences from each compartment, most often favouring the host compartment. During tenacibaculosis outbreaks in Platax, Tenacibaculum maritimum burden is also commonly associated with other pathogen co-occurrences, namely Vibrio spp. when a host interacts simultaneously with multiple pathogens during co-infection. Despite their commonness, remarkably few studies have explored such models, i.e. Species interactions can be neutral, antagonistic or facilitative and most often shape strain virulence plasticity, resulting in increased disease virulence. In nature, co-occurrence of multiple pathogen species (co-infection) is frequent. Yet, none of these studies have simultaneously explored dysbiosis and associated changes in microbiota. Studies applying this approach to fish bacterial infection systems have flourished recently and show promise for deciphering the complexity of host–pathogen interplay. ĭual RNAseq sequencing fulfils the need to simultaneously assess the expression of both host and pathogen genes. A more in-depth understanding of host–pathogen interactions could potentially improve our mechanistic understanding of pathogenicity and virulence, thereby defining novel preventive, therapeutic and vaccine targets. Although changes in gene expression as a result of host–pathogen interactions appear to be common, the mechanisms involved often remain poorly understood. Reciprocally, the host adapts to counteract and limit pathogen virulence. Through constant selective pressure, pathogens evolve mechanisms to overcome the host’s immune system. Host–pathogen interactions rely on a complex balance between host defences and pathogen virulence. Pathogens remain a significant threat to biodiversity, livestock farming and human health. In resistant individuals, we detected up-regulation of specific immune-related genes differentiating resistant individuals from controls at 96 hpi, which suggests a possible genomic basis of resistance, although no genetic variation in coding regions was found. maritimum in resistant fish skin and the total absence of any skin lesions suggest that these fish did not escape contact with the pathogen, but rather that some mechanisms prevented pathogens entry. These surviving fish showed no evidence of stress (cortisol levels) or significant difference in microbiome diversity compared with controls at the same sampling time. Fish were, however, largely sensitive to infection, and less than 25% survived after 96 hpi. In addition, our results suggest that fish activate an adaptive immune response visible through the stimulation of T-helper cells, Th17, with congruent reduction of Th2 and T-regulatory cells. The fish host concurrently displays a large panel of immune effectors, notably involving innate response and triggering acute inflammatory response. We showed that the infection of the host is characterised by an enhancement of functions associated with antibiotic and glucans catabolism functions but a reduction of sulfate assimilation process in T.
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