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Effects of T‐2 Toxin on the Intestinal Cecum Microbiome of Broiler Chickens

Many of the World's studies are aimed at identifying specific microbial markers of chicken intestines, including those markers that are associated with diseases. While mycotoxins can lead to bacterial disorder, gut microbiota could play a useful role in the prevention of mycotoxicosis. For this reason, it is important to characterize the bacterial populations that are involved in the dysbacteriosis caused by mycotoxins. This study was aimed the influence of diet contaminated with T‐2 toxin on caecum microbiome of Smena‐8 broilers. The experiment was carried out on 33‐day‐old broiler chickens for 14 days according to the Basic Principles of the Declaration of Helsinki. 4 experimental groups (5 chickens in each) were formed based on the concentration of the added T‐2 toxin: control 1, that received a diet without the contamination of T‐2 toxin, trial 2 ‐ received a diet with the addition of T‐2 toxin at a concentration of 100 μg/kg, trial 3 ‐ 200 μg/kg, trial 3 ‐ 400 μg/kg. Broiler chicken caecal content's genomic DNA was extracted and amplified of 16S rRNA NGS sequencing by the Miseq sequencer (Illumina, USA). The results showed that some microorganisms, in comparison with the control group, completely disappeared, and some, on the contrary, appeared when the feed was contaminated with T‐2 toxin. Members of the Mycoplasmataceae family and the phylum Candidatus Saccharibacteria have appeared in the intestines of chickens in trials 2,3 and 4. The average number of representatives of the Mycoplasmataceaefamily, among which pathogens are often found, increased (P≤0.05) under the influence of the toxin. The number of the Mycoplasmataceae family in groups in trial 2,3,4 was 0.0063 ± 0.0003, 0.0093 ± 0.0005 and 0.0130 ± 0.0007% respectively. On the contrary, representatives of other families (including Anaerolineaceae, Rickettsiaceae, Neisseriaceae), which are found in the control, completely disappeared from the intestines of chickens when contaminated with T‐2 toxin (trials 2,3 and 4). Thus, it can be concluded that T‐2 toxin provokes dysbiosis in the intestines of chickens. The number of the Lactobacillaceaefamily increased depending on the increase in the dose of mycotoxin – in trials 2,3 and 4 it was higher than in controls by 31.6, 45.6 and 46.3%, respectively. In all likelihood, lactobacilli are more resistant to mycotoxins than other members of the microbiota. This may be due to the fact that Lactobacillaceaemay play a role in the mycotoxin detoxification process. We believe that Lactobacillaceae, Mycoplasmataceae, Candidatus Saccharibacteria, Anaerolineaceae, Rickettsiaceae, Neisseriaceae are indicator groups of microorganisms that could be relevant biomarkers of toxicity of T‐2 toxin in chickens.