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Influence of Eimeria falciformis Infection on Gut Microbiota and Metabolic Pathways in Mice.

ABSTRACT: Coccidiosis, caused by different species of Eimeria parasites, is an economically important disease of poultry and livestock worldwide. Here we report previously unknown alterations in the gut microbes and metabolism of BALB/c mice infected with Eimeria falciformis Specifically, we observed a significant shift in the abundance of cecal bacteria and disrupted metabolism in parasitized animals. The relative abundances of Lachnospiraceae bacterium NK4A136, Ruminiclostridium, Alistipes, and Lactobacillus declined in response to E. falciformis infection, whereas Escherichia, Shigella, Helicobacter, Klebsiella, and Bacteroides were increased. Carbohydrate and amino acid metabolites in the serum samples of infected mice were significantly altered compared to naïve controls. Levels of amino acids, including asparagine, histidine, l-cysteine, tryptophan, lysine, glycine, serine, alanine, proline, ornithine, methionine, and valine, decreased on day 7 postinfection before returning to baseline on day 14. In addition, increased levels of indolelactate and mannitol and a reduced amount of oxalic acid indicated impaired carbon metabolism upon parasitic infection. These data demonstrate that intestinal coccidial infection perturbs the microbiota and disrupts carbon and nitrogen metabolism.

SUBMITTER: Huang G

PROVIDER: S-EPMC5913850 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature

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Influence of Eimeria falciformis Infection on Gut Microbiota and Metabolic Pathways in Mice.

Huang Guangping G Zhang Sixin S Zhou Chunxue C Tang Xiaoli X Li Chao C Wang Chaoyue C Tang Xinming X Suo Jingxia J Jia Yonggen Y El-Ashram Saeed S Yu Zhengquan Z Cai Jianping J Gupta Nishith N Suo Xun X Liu Xianyong X

Infection and immunity 20180423 5

Coccidiosis, caused by different species of Eimeria parasites, is an economically important disease of poultry and livestock worldwide. Here we report previously unknown alterations in the gut microbes and metabolism of BALB/c mice infected with Eimeria falciformis Specifically, we observed a significant shift in the abundance of cecal bacteria and disrupted metabolism in parasitized animals. The relative abundances of Lachnospiraceae bacterium NK4A136, Ruminiclostridium< ...[more]

PMID: 29440368

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Project description:The hygiene hypothesis proposes that decreased exposure to infectious agents in developed countries may contribute to the development of allergic and autoimmune diseases. Trichinella spiralis, a parasitic roundworm, causes trichinellosis, also known as trichinosis, in humans. T. spiralis had many hosts, and almost any mammal could become infected. Adult worms lived in the small intestine, while the larvae lived in muscle cells of the same mammal. T. spiralis was a significant public health threat because it could cause severe illness and even death in humans who eat undercooked or raw meat containing the parasite. The complex interactions between gastrointestinal helminths, gut microbiota, and the host immune system present a challenge for researchers. Two groups of mice were infected with T. spiralis vs uninfected control, and the experiment was conducted over 60 days. The 16S rRNA gene sequences and untargeted LC/MS-based metabolomics of fecal and serum samples, respectively, from different stages of development of the Trichinella spiralis-mouse model, were examined in this study. Gut microbiota alterations and metabolic activity accompanied by parasite-induced immunomodulation were detected. The inflammation parameters of the duodenum (villus/crypt ratio, goblet cell number and size, and histological score) were involved in active inflammation and oxidative metabolite profiles. These profiles included increased biosynthesis of phenylalanine, tyrosine, and tryptophan while decreasing cholesterol metabolism and primary and secondary bile acid biosynthesis. These disrupted metabolisms adapted to infection stress during the enteral and parenteral phases and then return to homeostasis during the encapsulated phase. There was a shift from an abundance of Bacteroides in the parenteral phase to an abundance of probiotic Lactobacillus and Treg-associated-Clostridia in the encapsulated phase. Th2 immune response (IL-4/IL-5/IL-13), lamina propria Treg, and immune hyporesponsiveness metabolic pathways (decreased tropane, piperidine and pyridine alkaloid biosynthesis and biosynthesis of alkaloids derived from ornithine, lysine, and nicotinic acid) were all altered. These findings enhanced our understanding of gut microbiota and metabolic profiles of Trichinella -infected mice, which could be a driving force in parasite-shaping immune system maintenance.

Project description:Intracellular parasites reprogram the host functions for their survival and reproduction. Conversely, the infected host attempts to defend the microbial insult. The extent and relevance of parasite-mediated host response in vivo remains poorly studied. We utilized Eimeria falciformis, an obligate intracellular parasite completing its entire life cycle in the mouse intestinal epithelium, to identify and validate the host determinants of the parasite infection. The most prominent mouse genes induced during the onset of asexual (24 hrs) and sexual (144 hrs) parasite cycle include IFNg-regulated factors, e.g., immunity-related GTPases IRGA6/B6/D/M2/M3, guanylate-binding proteins GBP2/3/5/8, chemokines CxCL9-11 and several enzymes of the kynurenine pathway including indoleamine 2,3-dioxygenase 1 (IDO1). These results indicated a multifarious innate defense (tryptophan catabolism, IRG, GBP, chemokines signaling) mounted by epithelial cells, and a consequential adaptive immune response (chemokines-cytokines signaling, lymphocyte recruitment). A notable increase in the inflammation- and immunity-associated transcripts correlated with the severity of infection and influx of B-cells, T-cells and macrophages to the parasitized tissue. Indeed, parasite growth was enhanced in the animals inhibited for CxCr3, a major chemokine receptor on immune cells. Interestingly, despite a prominent induction, the mouse IRGB6 failed to recognize and disrupt the parasitophorous vacuole in the parasite cultures, implying an immune evasion by E. falciformis. Likewise, the oocyst output was impaired in IFNg-R-/- and IDO1-/- mice, which signifies a subversion of IFNg-signaling by the parasite to promote its growth. In brief, the Eimeria-rodent model shows contrasting roles of IFNg-signaling for parasite development, identifies a retinue of potential host determinants, and epitomizes its efficacy for in vivo parasite-host interaction studies. Microarray experiments were performed as dual-color hybridizations on Agilent mouse whole genome catalog 44K arrays. To compensate for dye-specific effects, a dye-reversal color-swap was applied.

Dataset Information

Influence of Eimeria falciformis Infection on Gut Microbiota and Metabolic Pathways in Mice.

Publications

Influence of Eimeria falciformis Infection on Gut Microbiota and Metabolic Pathways in Mice.

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