Dataset Information

Intestinal parasitic infection alters bacterial gut microbiota in children.

ABSTRACT: The study of the burden that parasites can exert upon the bacterial gut microbiota was restricted by the available technologies and their costs. Currently, next-generation sequencing coupled with traditional methodologies allows the study of eukaryotic parasites (protozoa and helminths) and its effects on the human bacterial gut microbiota diversity. This diversity can be altered by a variety of factors such as age, diet, genetics and parasitic infections among others. The disturbances of the gut microbiota have been associated with a variety of illnesses. Children population in developing countries, are especially susceptible to parasitic infections because of the lack of proper sanitation and undernutrition, allowing both, the thriving of intestinal parasites and profound alteration of the gut microbiota. In this work, we have sampled the stool of 23 children from four different children's care-centers in Medellin, Colombia, and we have identified the eukaryotic parasites by traditional and molecular methodologies coupled with microbial profiling using 16S rDNA sequencing. This mixed methodology approach has allowed us to establish an interesting relationship between Giardia intestinalis and helminth infection, having both effects upon the bacterial gut microbiota enterotypes, causing a switch from a type I to a type II enterotype upon infection.

SUBMITTER: Toro-Londono MA

PROVIDER: S-EPMC6327884 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature

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Intestinal parasitic infection alters bacterial gut microbiota in children.

Toro-Londono Miguel A MA Bedoya-Urrego Katherine K Garcia-Montoya Gisela M GM Galvan-Diaz Ana L AL Alzate Juan F JF

PeerJ 20190107

The study of the burden that parasites can exert upon the bacterial gut microbiota was restricted by the available technologies and their costs. Currently, next-generation sequencing coupled with traditional methodologies allows the study of eukaryotic parasites (protozoa and helminths) and its effects on the human bacterial gut microbiota diversity. This diversity can be altered by a variety of factors such as age, diet, genetics and parasitic infections among others. The disturbances of the gu ...[more]

PMID: 30643702

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Project description:Respiratory viral infections are extremely common, but their impacts on the composition and function of the gut microbiota are poorly understood. We previously observed a significant change in the gut microbiota after viral lung infection. Here, we show that weight loss during respiratory syncytial virus (RSV) or influenza virus infection was due to decreased food consumption, and that the fasting of mice altered gut microbiota composition independently of infection. While the acute phase tumor necrosis factor alpha (TNF-α) response drove early weight loss and inappetence during RSV infection, this was not sufficient to induce changes in the gut microbiota. However, the depletion of CD8+ cells increased food intake and prevented weight loss, resulting in a reversal of the gut microbiota changes normally observed during RSV infection. Viral infection also led to changes in the fecal gut metabolome, with a significant shift in lipid metabolism. Sphingolipids, polyunsaturated fatty acids (PUFAs), and the short-chain fatty acid (SCFA) valerate were all increased in abundance in the fecal metabolome following RSV infection. Whether this and the impact of infection-induced anorexia on the gut microbiota are part of a protective anti-inflammatory response during respiratory viral infections remains to be determined.IMPORTANCE The gut microbiota has an important role in health and disease: gut bacteria can generate metabolites that alter the function of immune cells systemically. Understanding the factors that can lead to changes in the gut microbiome may help to inform therapeutic interventions. This is the first study to systematically dissect the pathway of events from viral lung infection to changes in gut microbiota. We show that the cellular immune response to viral lung infection induces inappetence, which in turn alters the gut microbiome and metabolome. Strikingly, there was an increase in lipids that have been associated with the resolution of disease. This opens up new paths of investigation: first, what is the (presumably secreted) factor made by the T cells that can induce inappetence? Second, is inappetence an adaptation that accelerates recovery from infection, and if so, does the microbiome play a role in this?

Project description:Giardia lamblia is a common intestinal parasitic infection that although often acutely asymptomatic, is associated with debilitating chronic intestinal and extra-intestinal sequelae. In previously healthy adults, a primary sporadic Giardia infection can lead to gut dysfunction and fatigue. These symptoms correlate with markers of inflammation that persist well after the infection is cleared. In contrast, in endemic settings, first exposure occurs in children who are frequently malnourished and also co-infected with other enteropathogens. In these children, Giardia rarely causes symptoms and associates with several decreased markers of inflammation. Mechanisms underlying these disparate and potentially enduring outcomes following Giardia infection are not presently well understood. A body of work suggests that the outcome of experimental Giardia infection is influenced by the nutritional status of the host. Here, we explore the consequences of experimental Giardia infection under conditions of protein sufficiency or deficiency on cytokine responses of ex vivo bone marrow derived dendritic cells (BMDCs) to endotoxin stimulation. We show that BMDCs from Giardia- challenged mice on a protein sufficient diet produce more IL-23 when compared to uninfected controls whereas BMDCs from Giardia challenged mice fed a protein deficient diet do not. Further, in vivo co-infection with Giardia attenuates robust IL-23 responses in endotoxin-stimulated BMDCs from protein deficient mice harboring enteroaggregative Escherichia coli. These results suggest that intestinal Giardia infection may have extra-intestinal effects on BMDC inflammatory cytokine production in a diet dependent manner, and that Giardia may influence the severity of the innate immune response to other enteropathogens. This work supports recent findings that intestinal microbial exposure may have lasting influences on systemic inflammatory responses, and may provide better understanding of potential mechanisms of post-infectious sequelae and clinical variation during Giardia and enteropathogen co-infection.

Dataset Information

Intestinal parasitic infection alters bacterial gut microbiota in children.

Publications

Intestinal parasitic infection alters bacterial gut microbiota in children.

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