Mycotoxins, which are widely found in feed ingredients and human food, can exert harmful effects on animals and pose a serious threat to human health. As the first barrier against external pollutants, the intestinal mucosa is protected by a mechanical barrier, chemical barrier, immune barrier, and biological barrier. Firstly, mycotoxins can disrupt the mechanical barrier function of the intestinal mucosa, by destroying the morphology and tissue integrity of the intestinal epithelium. Secondly, mycotoxins can cause changes in the composition of mucin monosaccharides and the expression of intestinal mucin, which in turn affects mucin function. Thirdly, mycotoxins can cause damage to the intestinal mucosal immune barrier function. Finally, the microbiotas of animals closely interact with ingested mycotoxins. Based on existing research, this article reviews the effects of mycotoxins on the intestinal mucosal barrier and its mechanisms.

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The metabolic responses of cows undergo substantial changes during the transition from late pregnancy to early lactation. However, the molecular mechanisms associated with these changes in physiological metabolism have not been clearly elucidated. The objective of this study was to investigate metabolic changes in transition cows from the perspective of plasma metabolites. Plasma samples collected from 24 multiparous dairy cows on approximately d 21 prepartum and immediately postpartum were analyzed using ultrahigh-performance liquid chromatography/time-of-flight mass spectrometry in positive and negative ion modes. In conjunction with multidimensional statistical methods (principal component analysis and orthogonal partial least squares discriminant analysis), differences in plasma metabolites were identified using the t-test and fold change analysis. Sixty-seven differential metabolites were identified consisting of AA, lipids, saccharides, and nucleotides. The levels of 32 plasma metabolites were significantly higher and those of 35 metabolites significantly lower after parturition than on d 21 prepartum. Pathway analysis indicated that the metabolites that increased from late pregnancy to early lactation were primarily involved in lipid metabolism and energy metabolism, whereas decreased metabolites were related to AA metabolism.

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ObjectiveObesity has been associated with impaired immunity and increased susceptibility to bacterial infection. It also exerts protective effects against mortality secondary to acute lung injury. The effects of obesity on immune responses to acute lung injury induced by Escherichia coli were investigated to determine if the above‐mentioned differences in its effects were related to infection severity.MethodsDiet‐induced obesity (DIO) and lean control mice received intranasal instillations of 109 or 1010 CFUs of E. coli. The immune responses were examined at 0 h (uninfected), 24 h, and 96 h postinfection.ResultsFollowing infection, the DIO mice exhibited higher leukocyte, interleukin (IL)−10, IL‐6, and tumor necrosis factor‐α levels and more severe lung injury than the lean mice. Following inoculation with 1010 CFUs of E. coli, the DIO mice exhibited higher mortality and more severe inflammation‐induced injury than the lean mice, but no differences in E. coli counts were noted between the two groups. However, inoculated with 109 CFUs of E. coli, the DIO mice exhibited smaller E. coli burdens at 24 h and 96 h after infection, as well as lower concentrations of IL‐10 and tumor necrosis factor‐α and less severe lung injury at 96 h after infection.ConclusionsThe results support the emerging view that obesity may be beneficial in the setting of milder infection but detrimental in the setting of more severe infection.