scholarly journals Infection with a small intestinal helminth Heligmosomoides polygyrus bakeri consistently alters microbial communities throughout the small and large intestine

2019 ◽  
Author(s):  
Alexis Rapin ◽  
Audrey Chuat ◽  
Luc Lebon ◽  
Mario M. Zaiss ◽  
Benjamin Marsland ◽  
...  
Keyword(s):  
Microbial Communities ◽  
Large Intestine ◽  
Helminth Infection ◽  
Entire Length ◽  
Intestinal Helminth ◽  
Mammalian Host ◽  
Heligmosomoides Polygyrus ◽  
Small Intestinal ◽  
The Impact ◽  
Small And Large Intestine

AbstractIncreasing evidence suggests that intestinal helminth infection can alter intestinal microbial communities with important impacts on the mammalian host. However, all of the studies to date utilize different techniques to study the microbiome and access different sites of the intestine with little consistency noted between studies. In the present study, we set out to perform a comprehensive analysis of the impact of intestinal helminth infection on the mammalian intestinal bacterial microbiome. For this purpose, we investigated the impact of experimental infection using the natural murine small intestinal helminth,Heligmosomoides polygyrus bakeri(Hpb) and examined possible alterations in both the mucous and luminal bacterial communities along the entire small and large intestine. We also explored the impact of common experimental variables, including the parasite batch and pre-infection microbiome, on the outcome of helminth-bacterial interactions. This work provides evidence that helminth infection reproducibly alters intestinal microbial communities – with an impact of infection noted along the entire length of the intestine. Although the exact nature of helminth-induced alterations to the intestinal microbiome differed depending on the parasite batch and microbiome community structure present prior to infection, changes extended well beyond the introduction of new bacterial species by the infecting larvae. Moreover, striking similarities between different experiments were noted, including the consistent outgrowth of a bacterium belonging to the Peptostreptococcaceae family throughout the intestine.Author SummaryIncreasing evidence indicates a role for interactions between intestinal helminths and the microbiome in regulating mammalian health, and a greater understanding of helminth-microbiota interactions may open the path for the development of novel immunomodulatory therapies. However, such studies are hampered by the inconsistent nature of the data reported so far. Such inconsistancies likely result from variations in the experimental and technological methodologies employed to investigate helminth-microbiota interactions and well has natural variation in the starting microbiome composition and/or worm genetics. We conducted a thorough study in which the reproducibility of helminth-induced alterations of microbial communities was determined and impact of common experimental variables – such as the starting microbiome and parasite batch - was determined. Our work reveals the robust ability of small intestinal helminth infection to alter microbial communities along the entire length of the intestine and additionally identifies a single bacterium that is strongly associated with infection across multiple experiments.

scholarly journals Impaired host resistance to Salmonella during helminth co-infection is restored by anthelmintic treatment prior to bacterial challenge

2021 ◽  
Vol 15 (1) ◽  
pp. e0009052
Author(s):  
Tara P. Brosschot ◽  
Katherine M. Lawrence ◽  
Brandon E. Moeller ◽  
Mia H. E. Kennedy ◽  
Rachael D. FitzPatrick ◽  
...  
Keyword(s):  
Small Intestine ◽  
Host Resistance ◽  
Helminth Infection ◽  
Bacterial Colonization ◽  
Drug Clearance ◽  
Anthelmintic Treatment ◽  
Intestinal Lumen ◽  
Intestinal Helminth ◽  
Heligmosomoides Polygyrus ◽  
Small Intestinal

Intestinal helminth infection can impair host resistance to co-infection with enteric bacterial pathogens. However, it is not known whether helminth drug-clearance can restore host resistance to bacterial infection. Using a mouse helminth-Salmonella co-infection system, we show that anthelmintic treatment prior to Salmonella challenge is sufficient to restore host resistance to Salmonella. The presence of the small intestine-dwelling helminth Heligmosomoides polygyrus at the point of Salmonella infection supports the initial establishment of Salmonella in the small intestinal lumen. Interestingly, if helminth drug-clearance is delayed until Salmonella has already established in the small intestinal lumen, anthelmintic treatment does not result in complete clearance of Salmonella. This suggests that while the presence of helminths supports initial Salmonella colonization, helminths are dispensable for Salmonella persistence in the host small intestine. These data contribute to the mechanistic understanding of how an ongoing or prior helminth infection can affect pathogenic bacterial colonization and persistence in the mammalian intestine.

Region-specific ontogeny of α-2,6-sialyltransferase during normal and cortisone-induced maturation in mouse intestine

2002 ◽  
Vol 282 (3) ◽  
pp. G480-G490 ◽  
Author(s):  
Dingwei Dai ◽  
N. Nanda Nanthakumar ◽  
Tor C. Savidge ◽  
David S. Newburg ◽  
W. Allan Walker
Keyword(s):  
Large Intestine ◽  
Regional Differences ◽  
Trophic Factors ◽  
Mrna Levels ◽  
Age Dependent ◽  
Regional Specificity ◽  
Microvillus Membrane ◽  
Mouse Intestine ◽  
Small Intestinal ◽  
Small And Large Intestine

Regional differences in the ontogeny of mouse intestinal α-2,6-sialyltransferase activities (α-2,6-ST) and the influence of cortisone acetate (CA) on this expression were determined. High ST activity and α-2,6-ST mRNA levels were detected in immature small and large intestine, with activity increasing distally from the duodenum. As the mice matured, ST activity (predominantly α-2,6-ST) in the small intestine decreased rapidly to adult levels by the fourth postnatal week. CA precociously accelerated this region-specific ontogenic decline. A similar decline of ST mRNA levels reflected ST activity in the small, but not the large, intestine. Small intestinal sialyl α-2,6-linked glycoconjugates displayed similar developmental and CA induced-precocious declines when probed using Sambucus nigraagglutinin (SNA) lectin. SNA labeling demonstrated age-dependent diminished sialyl α2,6 glycoconjugate expression in goblet cells in the small (but not large) intestine, but no such regional specificity was apparent in microvillus membrane. This suggests differential regulation of sialyl α-2,6 glycoconjugates in absorptive vs. globlet cells. These age-dependent and region-specific differences in sialyl α-2,6 glycoconjugates may be mediated in part by altered α-2,6-ST gene expression regulated by trophic factors such as glucocorticoids.

Identification and localization of extracellular Ca2+-sensing receptor in rat intestine

1998 ◽  
Vol 274 (1) ◽  
pp. G122-G130 ◽  
Author(s):  
Naibedya Chattopadhyay ◽  
Ivan Cheng ◽  
Kimberly Rogers ◽  
Daniela Riccardi ◽  
Amy Hall ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Large Intestine ◽  
Rat Kidney ◽  
Cell Types ◽  
Northern Analysis ◽  
Reaction Products ◽  
Polymerase Chain ◽  
Small Intestinal ◽  
Small And Large Intestine

The extracellular calcium ([Formula: see text])-sensing receptor (CaR) plays vital roles in [Formula: see text] homeostasis, but no data are available on its expression in small and large intestine. Polymerase chain reaction products amplified from reverse-transcribed duodenal RNA using CaR-specific primers showed >99% homology with the rat kidney CaR. Northern analysis with a CaR-specific cRNA probe demonstrated 4.1- and 7.5-kb transcripts in all intestinal segments. Immunohistochemistry with CaR-specific antisera showed clear basal staining of epithelial cells of small intestinal villi and crypts and modest apical staining of the former, whereas there was both basal and apical staining of colonic crypt epithelial cells. In situ hybridization and immunohistochemistry also demonstrated CaR expression in Auerbach’s myenteric plexus of small and large intestines and in the submucosa in the region of Meissner’s plexus. Our results reveal CaR expression in several cell types of small and large intestine, in which it may modulate absorptive and/or secretomotor functions.

scholarly journals Duodenal Helminth Infection Alters Barrier Function of the Colonic Epithelium via Adaptive Immune Activation

2011 ◽  
Vol 79 (6) ◽  
pp. 2285-2294 ◽  
Author(s):  
Chien-wen Su ◽  
Yue Cao ◽  
Jess Kaplan ◽  
Mei Zhang ◽  
Wanglin Li ◽  
...  
Keyword(s):  
Immune Response ◽  
Barrier Function ◽  
Helminth Infection ◽  
Scid Mice ◽  
Ultrastructural Changes ◽  
Intestinal Helminth ◽  
Epithelial Barrier ◽  
Epithelial Permeability ◽  
Content Type ◽  
The Impact

ABSTRACTChronic infection with intestinal helminth parasites is a major public health problem, particularly in the developing world, and can have significant effects on host physiology and the immune response to other enteric infections and antigens. The mechanisms underlying these effects are not well understood. In the current study, we investigated the impact of infection with the murine nematode parasiteHeligmosomoides polygyrus, which resides in the duodenum, on epithelial barrier function in the colon. We found thatH. polygyrusinfection produced a significant increase in colonic epithelial permeability, as evidenced by detection of elevated serum levels of the tracer horseradish peroxidase following rectal administration. This loss of normal barrier function was associated with clear ultrastructural changes in the tight junctions of colonic epithelial cells and an alteration in the expression and distribution of the junctional protein E-cadherin. These parasite-induced abnormalities were not observed in SCID mice but did occur in SCID mice that were adoptively transferred with wild-type T cells, indicating a requirement for adaptive immunity. Furthermore, the helminth-induced increase in gut permeability was not seen in STAT6 knockout (KO) mice. Taken together, the results demonstrate that one of the mechanisms by which helminths exert their effects involves the lymphocyte- and STAT6-dependent breakdown of the intestinal epithelial barrier. This increase in epithelial permeability may facilitate the movement of lumenal contents across the mucosa, thus helping to explain how helminth infection can alter the immune response to enteric antigens.

scholarly journals PGD2 and CRTH2 counteract Type 2 cytokine–elicited intestinal epithelial responses during helminth infection

2021 ◽  
Vol 218 (9) ◽  
Author(s):  
Oyebola O. Oyesola ◽  
Michael T. Shanahan ◽  
Matt Kanke ◽  
Bridget M. Mooney ◽  
Lauren M. Webb ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Goblet Cell ◽  
Helminth Infection ◽  
Intestinal Helminth ◽  
Prostaglandin D2 ◽  
Intestinal Epithelial ◽  
Cell Hyperplasia ◽  
Goblet Cell Hyperplasia ◽  
Small Intestinal

Type 2 inflammation is associated with epithelial cell responses, including goblet cell hyperplasia, that promote worm expulsion during intestinal helminth infection. How these epithelial responses are regulated remains incompletely understood. Here, we show that mice deficient in the prostaglandin D2 (PGD2) receptor CRTH2 and mice with CRTH2 deficiency only in nonhematopoietic cells exhibited enhanced worm clearance and intestinal goblet cell hyperplasia following infection with the helminth Nippostrongylus brasiliensis. Small intestinal stem, goblet, and tuft cells expressed CRTH2. CRTH2-deficient small intestinal organoids showed enhanced budding and terminal differentiation to the goblet cell lineage. During helminth infection or in organoids, PGD2 and CRTH2 down-regulated intestinal epithelial Il13ra1 expression and reversed Type 2 cytokine–mediated suppression of epithelial cell proliferation and promotion of goblet cell accumulation. These data show that the PGD2–CRTH2 pathway negatively regulates the Type 2 cytokine–driven epithelial program, revealing a mechanism that can temper the highly inflammatory effects of the anti-helminth response.

scholarly journals Neural motor complexes propagate continuously along the full length of mouse small intestine and colon

2020 ◽  
Vol 318 (1) ◽  
pp. G99-G108 ◽  
Author(s):  
Marcello Costa ◽  
Timothy James Hibberd ◽  
Lauren J. Keightley ◽  
Lukasz Wiklendt ◽  
John W. Arkwright ◽  
...  
Keyword(s):  
Small Intestine ◽  
Large Intestine ◽  
Motor Behavior ◽  
Neural Mechanism ◽  
Distal Colon ◽  
Full Length ◽  
Propagating Waves ◽  
Mouse Small Intestine ◽  
Small Intestinal ◽  
Small And Large Intestine

Cyclical propagating waves of muscle contraction have been recorded in isolated small intestine or colon, referred to here as motor complexes (MCs). Small intestinal and colonic MCs are neurogenic, occur at similar frequencies, and propagate orally or aborally. Whether they can be coordinated between the different gut regions is unclear. Motor behavior of whole length mouse intestines, from duodenum to terminal rectum, was recorded by intraluminal multisensor catheter. Small intestinal MCs were recorded in 27/30 preparations, and colonic MCs were recorded in all preparations ( n = 30) with similar frequencies (0.54 ± 0.03 and 0.58 ± 0.02 counts/min, respectively). MCs propagated across the ileo-colonic junction in 10/30 preparations, forming “full intestine” MCs. The cholinesterase inhibitor physostigmine increased the probability of a full intestine MC but had no significant effect on frequency, speed, or direction. Nitric oxide synthesis blockade by Nω-nitro-l-arginine, after physostigmine, increased MC frequency in small intestine only. Hyoscine-resistant MCs were recorded in the colon but not small intestine ( n = 5). All MCs were abolished by hexamethonium ( n = 18) or tetrodotoxin ( n = 2). The enteric neural mechanism required for motor complexes is present along the full length of both the small and large intestine. In some cases, colonic MCs can be initiated in the distal colon and propagate through the ileo-colonic junction, all the way to duodenum. In conclusion, the ileo-colonic junction provides functional neural continuity for propagating motor activity that originates in the small or large intestine. NEW & NOTEWORTHY Intraluminal manometric recordings revealed motor complexes can propagate antegradely or retrogradely across the ileo-colonic junction, spanning the entire small and large intestines. The fundamental enteric neural mechanism(s) underlying cyclic motor complexes exists throughout the length of the small and large intestine.

scholarly journals Inhibition of miR-99a-5p prevents allergen-driven airway exacerbations without compromising type-2 memory responses in the intestine following helminth infection

2021 ◽  
Author(s):  
Lewis Entwistle ◽  
Helena Aegerter ◽  
Stephanie Czieso ◽  
Eleni Amaniti ◽  
Riccardo Guidi ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Helminth Infection ◽  
Smooth Muscle Contraction ◽  
Therapeutic Interventions ◽  
Transcriptional Analysis ◽  
Intestinal Helminth ◽  
Heligmosomoides Polygyrus ◽  
Minimal Impact ◽  
Acute Exacerbations

AbstractAcute exacerbations (AE) of asthma, remain one of the biggest concerns for patients living with asthma. As such, identifying the causes, the molecular mechanisms involved and new therapeutic interventions to prevent AE is a high priority. Immunity to intestinal helminths involves the reactivation of type-2 immune responses leading to smooth muscle contraction and mucus hypersecretion–physiological processes very similar to acute exacerbations in the airways following allergen exposure. In this study, we employed a murine model of intestinal helminth infection, using Heligmosomoides polygyrus, to identify miRNAs during active expulsion, as a system for the identification of miRNAs that may contribute to AE in the airways. Concomitant with type-2 immunity and expulsion of H. polygyrus, we identified miR-99a-5p, miR-148a-3p and miR-155-5p that were differentially regulated. Systemic inhibition of these miRNAs, alone or in combination, had minimal impact on expulsion of H. polygyrus, but inhibition of miR-99a-5p or miR-155-5p significantly reduced house dust mite (HDM)-driven acute inflammation, modelling human acute exacerbations. Immunological, pathological and transcriptional analysis identified that miR-155-5p or miR-99a-5p contribute significantly to HDM-driven AE and that transient inhibition of these miRNAs may provide relief from allergen-driven AE, without compromising anti-helminth immunity in the gut.

Small intestinal levels of the branched short-chain fatty acid isovalerate are elevated during infection with Heligmosomoides polygyrus and can promote helminth fecundity

2021 ◽  
Author(s):  
Mia H. E. Kennedy ◽  
Tara P. Brosschot ◽  
Katherine M. Lawrence ◽  
Rachael D. FitzPatrick ◽  
Jenna M. Lane ◽  
...  
Keyword(s):  
Small Intestine ◽  
Short Chain Fatty Acid ◽  
Helminth Infection ◽  
Chain Fatty Acid ◽  
Isovaleric Acid ◽  
Heligmosomoides Polygyrus ◽  
Bacterial Microbiota ◽  
Proximal Small Intestine ◽  
Small Intestinal ◽  
Helminth Fecundity

Heligmosomoides polygyrus is a helminth which naturally infects mice and is widely used as a laboratory model of chronic small intestinal helminth infection. While it is known that infection with H. polygyrus alters the composition of the host’s bacterial microbiota, the functional implications of this alteration are unclear. We investigated the impact of H. polygyrus infection on short-chain fatty acid (SCFA) levels in the mouse intestine and sera. We found that helminth infection resulted in significantly upregulated levels of the branched SCFA isovaleric acid, exclusively in the proximal small intestine, which is the site of H. polygyrus colonization. We next set out to test the hypothesis that elevating local levels of isovaleric acid was a strategy used by H. polygyrus to promote its own fitness within the mammalian host. To test this, we supplemented the drinking water of mice with isovalerate during H. polygyrus infection and examined whether this affected helminth fecundity or chronicity. We did not find that isovaleric acid supplementation affected helminth chronicity, however, we found that it did promote helminth fecundity, as measured by helminth egg output in the feces of mice. Through antibiotic-treatment of helminth-infected mice, we found that the bacterial microbiota was required in order to support elevated levels of isovaleric acid in the proximal small intestine during helminth infection. Overall, our data reveal that during H. polygyrus infection there is a microbiota-dependent localized increase in the production of isovaleric acid in the proximal small intestine and this supports helminth fecundity in the murine host.

scholarly journals In vitro study for investigating the impact of decreasing the molecular weight of oat bran dietary fibre components on the behaviour in small and large intestine

2020 ◽  
Vol 11 (7) ◽  
pp. 6680-6691 ◽  
Author(s):  
Natalia Rosa-Sibakov ◽  
Noora Mäkelä ◽  
Anna-Marja Aura ◽  
Tuula Sontag-Strohm ◽  
Emilia Nordlund
Keyword(s):  
Molecular Weight ◽  
Large Intestine ◽  
Dietary Fibre ◽  
In Vitro Study ◽  
Vitro Study ◽  
Oat Bran ◽  
The Impact ◽  
Small And Large Intestine

The objective of this work was to evaluate the role of β-glucan molecular weight (Mw) and the presence of other carbohydrates on the physiological functionality of oat bran via an in vitro digestion study.

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