Dataset Information

Hen raising helps chicks establish gut microbiota in their early life and improve microbiota stability after H9N2 challenge.

ABSTRACT:

Background

Early gut microbial colonization is important for postnatal growth and immune development of the chicken. However, at present, commercial chickens are hatched and raised without adult hens, thus are cut off from the microbiota transfer between hens and chicks. In this study, we compared the gut microbiota composition between hen-reared and separately reared chicks, and its impact on the resistance to H9N2 avian influenza virus, with the motive of investigating the impact of this cutoff in microbiota transfer.

Results

We used the 16SrRNA sequencing method to assess the composition of the gut microbiota in chicks represented by three hen-reared groups and one separately reared group. We found that the diversity of gut microbes in the chicks from the three hen-reared groups was more abundant than in the separately reared group, both at the phylum and genus levels. Our findings highlight the importance of early parental care in influencing the establishment of gut microbiota in the early life of chicks. SourceTracker analysis showed that the feather and cloaca microbiota of hens are the main sources of gut microbiota of chicks. After H9N2 exposure, the viral infection lasted longer in the separately reared chicks, with the viral titers in their oropharyngeal swabs being higher compared to the hen-reared chicks at day 5 post-infection. Interestingly, our results revealed that the gut microbiota of the hen-reared chicks was more stable after H9N2 infection in comparison to that of the separately reared chicks.

Conclusions

Microbiota transfer between the hens and their chicks promotes the establishment of a balanced and diverse microbiota in the early life of the chicks and improves microbiota stability after H9N2 challenge. These findings advance our understanding of the protective role of gut microbiota in the early life of chicks and should be instrumental in improving chick rearing in the commercial poultry industry. Video Abstract.

SUBMITTER: Li X

PROVIDER: S-EPMC8785444 | biostudies-literature |

REPOSITORIES: biostudies-literature

ACCESS DATA

Similar Datasets

Project description:BackgroundAntibiotics are widely used for prophylactic therapy and for improving the growth performance of chicken. The problem of bacterial drug resistance caused by antibiotic abuse has previously attracted extensive attention; however, the influence of early-day use of prophylactic antibiotics on the gut microflora and on the disease resistance ability in chicks has not been explored. Here, we comprehensively evaluate the growth performance, gut microbial dynamics, level of antibiotic resistance genes (ARGs) in the gut microbial community, and resistance to H9N2 avian influenza virus (AIV) in chickens following long-term and short-term early-day prophylactic antibiotic treatment.ResultsUnexpectedly, long-term prophylactic enrofloxacin treatment slowed the growth rate of chickens, whereas short-term antibiotics treatments were found to increase the growth rate, but these changes were not statistically significant. Strikingly, expansions of Escherichia-Shigella populations were observed in early-life prophylactic antibiotics-treated groups of chickens, which is in contrast to the general perception that antibiotics should control their pathogenicity in chicks. The gut microbiota composition of chickens treated long term with antibiotics or received early-day antibiotics treatment tend to be more dramatically disturbed compared to the gut microbiome of chickens treated with antibiotics for a short term at a later date, especially after H9N2 AIV infection.ConclusionsOur data provide evidence that early-day and long-term antibiotic treatments have a more adverse effect on the intestinal microbiome of chickens, compared to short-term late age antibiotic treatment. Furthermore, our metagenomic data reveal that both long-term and short-term antibiotic treatment increase the relative abundance of ARGs. Our findings highlight the adverse effects of prophylactic antibiotic treatment and provide a theoretical basis for the cautious administration of antibiotics in food-producing animal management. Video Abstract.

Project description:Background and aimsLactulose is a common food ingredient and widely used as a treatment for constipation or hepatic encephalopathy and a substrate for hydrogen breath tests. Lactulose is fermented by the colon microbiota resulting in the production of hydrogen (H2). H2 is a substrate for enteropathogens including Salmonella Typhimurium (S. Typhimurium) and increased H2 production upon lactulose ingestion might favor the growth of H2-consuming enteropathogens. We aimed to analyze effects of single-dose lactulose ingestion on the growth of intrinsic Escherichia coli (E. coli), which can be efficiently quantified by plating and which share most metabolic requirements with S. Typhimurium.Methods32 healthy volunteers (18 females, 14 males) were recruited. Participants were randomized for single-dose ingestion of 50 g lactulose or 50 g sucrose (controls). After ingestion, H2 in expiratory air and symptoms were recorded. Stool samples were acquired at days -1, 1 and 14. We analyzed 16S microbiota composition and abundance and characteristics of E. coli isolates.ResultsLactulose ingestion resulted in diarrhea in 14/17 individuals. In 14/17 individuals, H2-levels in expiratory air increased by ≥20 ppm within 3 hours after lactulose challenge. H2-levels correlated with the number of defecations within 6 hours. E. coli was detectable in feces of all subjects (2 x 10(2)-10(9) CFU/g). However, the number of E. coli colony forming units (CFU) on selective media did not differ between any time point before or after challenge with sucrose or lactulose. The microbiota composition also remained stable upon lactulose exposure.ConclusionIngestion of a single dose of 50 g lactulose does not significantly alter E. coli density in stool samples of healthy volunteers. 50 g lactulose therefore seems unlikely to sufficiently alter growth conditions in the intestine for a significant predisposition to infection with H2-consuming enteropathogens such as S. Typhimurium (www.clinicaltrials.gov NCT02397512).