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Fetal exposure to maternal inflammation interrupts murine intestinal development and increases susceptibility to neonatal intestinal injury.
Elgin TG, Fricke EM, Gong H, Reese J, Mills DA, Kalantera KM, Underwood MA, McElroy SJ
(2019) Dis Model Mech 12:
MeSH Terms: Animals, Animals, Newborn, Biomarkers, Cecum, Cytokines, Disease Susceptibility, Female, Fetus, Goblet Cells, Inflammation, Intestine, Small, Lipopolysaccharides, Mice, Inbred C57BL, Microbiota, Paneth Cells, Pregnancy
Show Abstract · Added July 28, 2020
Fetal exposure to chorioamnionitis can impact the outcomes of the developing fetus both at the time of birth and in the subsequent neonatal period. Infants exposed to chorioamnionitis have a higher incidence of gastrointestinal (GI) pathology, including necrotizing enterocolitis (NEC); however, the mechanism remains undefined. To simulate the fetal exposure to maternal inflammation (FEMI) induced by chorioamnionitis, pregnant mice (C57BL/6J, , or ) were injected intraperitoneally on embryonic day (E)15.5 with lipopolysaccharide (LPS; 100 µg/kg body weight). Pups were delivered at term, and reared to postnatal day (P)0, P7, P14, P28 or P56. Serum and intestinal tissue samples were collected to quantify growth, inflammatory markers, histological intestinal injury, and goblet and Paneth cells. To determine whether FEMI increased subsequent susceptibility to intestinal injury, a secondary dose of LPS (100 µg/kg body weight) was given on P5, prior to tissue harvesting on P7. FEMI had no effect on growth of the offspring or their small intestine. FEMI significantly decreased both goblet and Paneth cell numbers while simultaneously increasing serum levels of IL-1β, IL-10, KC/GRO (CXCL1 and CXCL2), TNF and IL-6. These alterations were IL-6 dependent and, importantly, increased susceptibility to LPS-induced intestinal injury later in life. Our data show that FEMI impairs normal intestinal development by decreasing components of innate immunity and simultaneously increasing markers of inflammation. These changes increase susceptibility to intestinal injury later in life and provide novel mechanistic data to potentially explain why preterm infants exposed to chorioamnionitis prior to birth have a higher incidence of NEC and other GI disorders.
© 2019. Published by The Company of Biologists Ltd.
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Probiotics Modulate a Novel Amphibian Skin Defense Peptide That Is Antifungal and Facilitates Growth of Antifungal Bacteria.
Woodhams DC, Rollins-Smith LA, Reinert LK, Lam BA, Harris RN, Briggs CJ, Vredenburg VT, Patel BT, Caprioli RM, Chaurand P, Hunziker P, Bigler L
(2020) Microb Ecol 79: 192-202
MeSH Terms: Amino Acid Sequence, Animals, Antifungal Agents, Chytridiomycota, Microbiota, Peptides, Probiotics, Ranidae, Skin
Show Abstract · Added March 3, 2020
Probiotics can ameliorate diseases of humans and wildlife, but the mechanisms remain unclear. Host responses to interventions that change their microbiota are largely uncharacterized. We applied a consortium of four natural antifungal bacteria to the skin of endangered Sierra Nevada yellow-legged frogs, Rana sierrae, before experimental exposure to the pathogenic fungus Batrachochytrium dendrobatidis (Bd). The probiotic microbes did not persist, nor did they protect hosts, and skin peptide sampling indicated immune modulation. We characterized a novel skin defense peptide brevinin-1Ma (FLPILAGLAANLVPKLICSITKKC) that was downregulated by the probiotic treatment. Brevinin-1Ma was tested against a range of amphibian skin cultures and found to inhibit growth of fungal pathogens Bd and B. salamandrivorans, but enhanced the growth of probiotic bacteria including Janthinobacterium lividum, Chryseobacterium ureilyticum, Serratia grimesii, and Pseudomonas sp. While commonly thought of as antimicrobial peptides, here brevinin-1Ma showed promicrobial function, facilitating microbial growth. Thus, skin exposure to probiotic bacterial cultures induced a shift in skin defense peptide profiles that appeared to act as an immune response functioning to regulate the microbiome. In addition to direct microbial antagonism, probiotic-host interactions may be a critical mechanism affecting disease resistance.
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9 MeSH Terms
Endogenous Enterobacteriaceae underlie variation in susceptibility to Salmonella infection.
Velazquez EM, Nguyen H, Heasley KT, Saechao CH, Gil LM, Rogers AWL, Miller BM, Rolston MR, Lopez CA, Litvak Y, Liou MJ, Faber F, Bronner DN, Tiffany CR, Byndloss MX, Byndloss AJ, Bäumler AJ
(2019) Nat Microbiol 4: 1057-1064
MeSH Terms: Animal Experimentation, Animals, Biomarkers, Biosynthetic Pathways, Disease Models, Animal, Enterobacteriaceae, Escherichia coli, Fecal Microbiota Transplantation, Gastrointestinal Microbiome, Germ-Free Life, Mice, Mice, Inbred C57BL, Microbial Interactions, Phenotype, Probiotics, Reproducibility of Results, Salmonella, Salmonella Infections, Animal
Show Abstract · Added March 30, 2020
Lack of reproducibility is a prominent problem in biomedical research. An important source of variation in animal experiments is the microbiome, but little is known about specific changes in the microbiota composition that cause phenotypic differences. Here, we show that genetically similar laboratory mice obtained from four different commercial vendors exhibited marked phenotypic variation in their susceptibility to Salmonella infection. Faecal microbiota transplant into germ-free mice replicated donor susceptibility, revealing that variability was due to changes in the gut microbiota composition. Co-housing of mice only partially transferred protection against Salmonella infection, suggesting that minority species within the gut microbiota might confer this trait. Consistent with this idea, we identified endogenous Enterobacteriaceae, a low-abundance taxon, as a keystone species responsible for variation in the susceptibility to Salmonella infection. Protection conferred by endogenous Enterobacteriaceae could be modelled by inoculating mice with probiotic Escherichia coli, which conferred resistance by using its aerobic metabolism to compete with Salmonella for resources. We conclude that a mechanistic understanding of phenotypic variation can accelerate development of strategies for enhancing the reproducibility of animal experiments.
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Cuts Both Ways: Proteases Modulate Virulence of Enterohemorrhagic .
Palmer LD, Skaar EP
(2019) mBio 10:
MeSH Terms: Enterohemorrhagic Escherichia coli, Escherichia coli Proteins, Humans, Microbiota, Peptide Hydrolases, Virulence
Show Abstract · Added April 2, 2019
Enterohemorrhagic (EHEC) is a major cause of foodborne gastrointestinal illness. EHEC uses a specialized type III secretion system (T3SS) to form attaching and effacing lesions in the colonic epithelium and outcompete commensal gut microbiota to cause disease. A recent report in (E. A. Cameron, M. M. Curtis, A. Kumar, G. M. Dunny, et al., mBio 9:e02204-18, 2018, https://doi.org/10.1128/mBio.02204-18) describes a new role for gut commensals in potentiating disease caused by EHEC. Proteases produced by EHEC and the prevalent human commensal cleave proteins in the EHEC T3SS translocon that modulate T3SS function. protease activity promotes translocation of bacterial effectors required for lesion formation. These results describe a new role for the microbiota in gastrointestinal disease that could uncover future treatments to prevent the spread of gastroenteritis.
Copyright © 2019 Palmer and Skaar.
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Microbiota-nourishing Immunity and Its Relevance for Ulcerative Colitis.
Byndloss MX, Litvak Y, Bäumler AJ
(2019) Inflamm Bowel Dis 25: 811-815
MeSH Terms: Colitis, Ulcerative, Dysbiosis, Humans, Microbiota, Probiotics
Added March 30, 2020
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Distinct mucosal microbial communities in infants with surgical necrotizing enterocolitis correlate with age and antibiotic exposure.
Romano-Keeler J, Shilts MH, Tovchigrechko A, Wang C, Brucker RM, Moore DJ, Fonnesbeck C, Meng S, Correa H, Lovvorn HN, Tang YW, Hooper L, Bordenstein SR, Das SR, Weitkamp JH
(2018) PLoS One 13: e0206366
MeSH Terms: Age Factors, Anti-Bacterial Agents, Biodiversity, Enterocolitis, Necrotizing, Female, Humans, Infant, Infant, Newborn, Intestinal Mucosa, Male, Microbiota, Pregnancy
Show Abstract · Added October 27, 2018
OBJECTIVE - Necrotizing enterocolitis (NEC) is the most common surgical emergency in preterm infants, and pathogenesis associates with changes in the fecal microbiome. As fecal samples incompletely represent microbial communities in intestinal mucosa, we sought to determine the NEC tissue-specific microbiome and assess its contribution to pathogenesis.
DESIGN - We amplified and sequenced the V1-V3 hypervariable region of the bacterial 16S rRNA gene extracted from intestinal tissue and corresponding fecal samples from 12 surgical patients with NEC and 14 surgical patients without NEC. Low quality and non-bacterial sequences were removed, and taxonomic assignment was made with the Ribosomal Database Project. Operational taxonomic units were clustered at 97%. We tested for differences between NEC and non-NEC samples in microbiome alpha- and beta-diversity and differential abundance of specific taxa between NEC and non-NEC samples. Additional analyses were performed to assess the contribution of other demographic and environmental confounding factors on the infant tissue and fecal microbiome.
RESULTS - The fecal and tissue microbial communities were different. NEC was associated with a distinct microbiome, which was characterized by low diversity, higher abundances of Staphylococcus and Clostridium_sensu_stricto, and lower abundances of Actinomyces and Corynebacterium. Infant age and vancomycin exposure correlated with shifts in the tissue microbiome.
CONCLUSION - The observed low diversity in NEC tissues suggests that NEC is associated with a bacterial bloom and a distinct mucosal bacterial community. The exact bacterial species that constitute the bloom varied by infant and were strongly influenced by age and exposure to vancomycin.
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12 MeSH Terms
Microbial-Host Interactions in Inflammatory Bowel Disease, Functional Bowel Disease, Obesity and Obesity-Related Metabolic Disease.
Shah SC, Faith J, Colombel JF
(2018) Gastroenterology 155: 1283-1286
MeSH Terms: Host-Pathogen Interactions, Humans, Inflammatory Bowel Diseases, Irritable Bowel Syndrome, Metabolic Diseases, Microbiota, Obesity
Added March 3, 2020
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Healthy hosts rule within: ecological forces shaping the gut microbiota.
Byndloss MX, Pernitzsch SR, Bäumler AJ
(2018) Mucosal Immunol 11: 1299-1305
MeSH Terms: Animals, Ecology, Epithelial Cells, Gastrointestinal Microbiome, Homeostasis, Host Microbial Interactions, Humans, Intestinal Mucosa, Intestines, Microbiota
Show Abstract · Added March 30, 2020
A balanced gut microbiota is important for human health, but the mechanisms that maintain homeostasis are incompletely understood. Recent insights suggest the host plays a key role in shaping its gut microbiota to be beneficial. While host control in the small intestine curbs bacterial numbers to avoid competition for simple sugars and amino acids, the host limits oxygen availability in the large intestine to obtain microbial fermentation products from fiber. Epithelial cells are major players in imposing ecological control mechanisms, which involves the release of antimicrobial peptides by small-intestinal Paneth cells and maintenance of luminal anaerobiosis by epithelial hypoxia in the colon. Harnessing these epithelial control mechanisms for therapeutic means could provide a novel lynchpin for strategies to remediate dysbiosis.
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Interpreting heterogeneity in intestinal tuft cell structure and function.
Banerjee A, McKinley ET, von Moltke J, Coffey RJ, Lau KS
(2018) J Clin Invest 128: 1711-1719
MeSH Terms: Animals, Goblet Cells, Humans, Immunity, Intestinal Mucosa, Microbiota, Microvilli
Show Abstract · Added October 16, 2018
Intestinal tuft cells are a morphologically unique cell type, best characterized by striking microvilli that form an apical tuft. These cells represent approximately 0.5% of gut epithelial cells depending on location. While they are known to express chemosensory receptors, their function has remained unclear. Recently, numerous groups have revealed startling insights into intestinal tuft cell biology. Here, we review the latest developments in understanding this peculiar cell type's structure and function. Recent advances in volumetric microscopy have begun to elucidate tuft cell ultrastructure with respect to its cellular neighbors. Moreover, single-cell approaches have revealed greater diversity in the tuft cell population than previously appreciated and uncovered novel markers to characterize this heterogeneity. Finally, advanced model systems have revealed tuft cells' roles in mucosal healing and orchestrating type 2 immunity against eukaryotic infection. While much remains unknown about intestinal tuft cells, these critical advances have illuminated the physiological importance of these previously understudied cells and provided experimentally tractable tools to interrogate this rare cell population. Tuft cells act as luminal sensors, linking the luminal microbiome to the host immune system, which may make them a potent clinical target for modulating host response to a variety of acute or chronic immune-driven conditions.
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7 MeSH Terms
Nasopharyngeal Lactobacillus is associated with a reduced risk of childhood wheezing illnesses following acute respiratory syncytial virus infection in infancy.
Rosas-Salazar C, Shilts MH, Tovchigrechko A, Schobel S, Chappell JD, Larkin EK, Gebretsadik T, Halpin RA, Nelson KE, Moore ML, Anderson LJ, Peebles RS, Das SR, Hartert TV
(2018) J Allergy Clin Immunol 142: 1447-1456.e9
MeSH Terms: Acute Disease, Child, Preschool, Cohort Studies, Female, Humans, Infant, Lactobacillus, Male, Microbiota, Nasopharynx, RNA, Ribosomal, 16S, Respiratory Sounds, Respiratory Syncytial Virus Infections, Risk
Show Abstract · Added March 14, 2018
BACKGROUND - Early life acute respiratory infection (ARI) with respiratory syncytial virus (RSV) has been strongly associated with the development of childhood wheezing illnesses, but the pathways underlying this association are poorly understood.
OBJECTIVE - To examine the role of the nasopharyngeal microbiome in the development of childhood wheezing illnesses following RSV ARI in infancy.
METHODS - We conducted a nested cohort study of 118 previously healthy, term infants with confirmed RSV ARI by RT-PCR. We used next-generation sequencing of the V4 region of the 16S ribosomal RNA gene to characterize the nasopharyngeal microbiome during RSV ARI. Our main outcome of interest was 2-year subsequent wheeze.
RESULTS - Of the 118 infants, 113 (95.8%) had 2-year outcome data. Of these, 46 (40.7%) had parental report of subsequent wheeze. There was no association between the overall taxonomic composition, diversity, and richness of the nasopharyngeal microbiome during RSV ARI with the development of subsequent wheeze. However, the nasopharyngeal detection and abundance of Lactobacillus was consistently higher in infants who did not develop this outcome. Lactobacillus also ranked first among the different genera in a model distinguishing infants with and without subsequent wheeze.
CONCLUSIONS - The nasopharyngeal detection and increased abundance of Lactobacillus during RSV ARI in infancy are associated with a reduced risk of childhood wheezing illnesses at age 2 years.
Copyright © 2018 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
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14 MeSH Terms