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Reduction of post-weaning diarrhoea caused by ETEC is a principal objective in pig farming in terms of welfare benefits. This study determined the effects of genetic susceptibility and dietary strategies targeting inflammation and fimbriae adherence on F4-ETEC shedding and diarrhoea in weaned piglets in an experimental challenge model. A DNA marker test targeting single nucleotide polymorphism 2 (SNP2) identified piglets as heterozygous (SNP2+, susceptible) or homozygous (SNP2-, resistant) to developing F4ac-ETEC diarrhoea. A total of 50 piglets, 25 SNP2+ and 25 SNP2-, were weaned at 30 days of age and equally distributed to different treatments (n = 10): Positive control (PC): piglets fed with a negative control diet and provided with colistin via drinking water; Negative control (NC): piglets fed with a negative control diet; Tall oil fatty acids (TOFA): piglets fed with a negative control diet + 1.0 g TOFA/kg feed; Yeast hydrolysate (YH): piglets fed with a negative control diet + 1.5 g YH/kg feed derived from Saccharomyces cerevisiae; and Combination (COM): piglets fed with a negative control diet + 1.0 g TOFA and 1.5 g YH/kg feed. On day 10 post-weaning, all piglets were infected with F4-ETEC by oral administration. Piglets fed with PC, TOFA, YH or COM had a lower faecal shedding of F4-ETEC than NC piglets (P < 0.001), which was also shorter in duration for PC and TOFA piglets than for NC piglets (P < 0.001). Piglets in PC, TOFA, YH and COM had a shorter diarrhoea duration versus NC when classified as SNP2+ (P = 0.02). Furthermore, PC, TOFA and YH piglets grew more than NC and COM piglets in the initial post-inoculation period (P < 0.001). In addition, the level of faecal F4-ETEC shedding and the percentage of pigs that developed F4-ETEC diarrhoea (72 vs. 32%, P < 0.01) following infection were higher, and the duration of F4-ETEC diarrhoea longer (2.6 vs. 0.6 days, P < 0.001), in SNP2+ piglets than in SNP2- piglets, and led to reduced growth performance (P = 0.03). In conclusion, piglets fed with TOFA, YH or their combination, irrespective of their SNP2 status, are more resilient to F4-ETEC infection. Moreover, SNP2+ piglets show a higher level of F4-ETEC shedding and diarrhoea prevalence than SNP2- piglets, confirming an association between SNP2 and F4ac-ETEC susceptibility., (© 2024. The Author(s).)

The root microbiome consists of commensal, pathogenic, and plant-beneficial microbes [1]. Most members of the root microbiome possess microbe-associated molecular patterns (MAMPs) similar to those of plant pathogens [2]. Their recognition can lead to the activation of host immunity and suppression of plant growth due to growth-defense tradeoffs [3, 4]. We found that 42% of the tested root microbiota, including the plant growth-promoting rhizobacteria Pseudomonas capeferrum WCS358 [5, 6] and Pseudomonas simiae WCS417 [6, 7], are able to quench local Arabidopsis thaliana root immune responses that are triggered by flg22 [8], an immunogenic epitope of the MAMP flagellin [9], suggesting that this is an important function of the root microbiome. In a screen for WCS358 mutants that lost their capacity to suppress flg22-induced CYP71A12 pro :GUS MAMP-reporter gene expression, we identified the bacterial genes pqqF and cyoB in WCS358, which are required for the production of gluconic acid and its derivative 2-keto gluconic acid. Both WCS358 mutants are impaired in the production of these organic acids and consequently lowered their extracellular pH to a lesser extent than wild-type WCS358. Acidification of the plant growth medium similarly suppressed flg22-induced CYP71A12 pro :GUS and MYB51 pro :GUS expression, and the flg22-mediated oxidative burst, suggesting a role for rhizobacterial gluconic acid-mediated modulation of the extracellular pH in the suppression of root immunity. Rhizosphere population densities of the mutants were significantly reduced compared to wild-type. Collectively, these findings show that suppression of immune responses is an important function of the root microbiome, as it facilitates colonization by beneficial root microbiota., (Copyright © 2019 Elsevier Ltd. All rights reserved.)