Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Renewal of Intestinal Stem Cells01:23

Renewal of Intestinal Stem Cells

The intestinal epithelial lining rapidly renews every 4 to 5 days. The renewal is facilitated by intestinal stem cells (ISCs) located at the base of the crypt– a gland located at the bottom of each villus. ISCs divide asymmetrically to form new stem cells and progenitor daughter cells. The daughter cells are called transit-amplifying (TA) cells which move upwards along the crypt and either differentiate into absorptive cells– the enterocytes or secretory cells– including the goblet,...
Anthelminthic Agents01:15

Anthelminthic Agents

Anthelmintic drugs differ significantly from antiparasitic therapies targeting protozoa, primarily due to differences in parasite biology. Whereas most protozoal treatments act on proliferating cells, anthelmintics are typically directed against mature, nonproliferative helminths. The therapeutic approach considers the helminth's reliance on neuromuscular coordination, glucose metabolism, and microtubular integrity for survival, reproduction, and localization within the host. Most anthelmintics...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Identification of a persistent Ascaris-derived Kalirin epitope associated with chronic T cell activation in the lung.

PLoS neglected tropical diseases·2026
Same author

Borrelia turicatae in Ticks from Animals in a Public Park, Aguascalientes, Mexico.

Emerging infectious diseases·2026
Same author

A Scoping Review of the Associations Between Ascariasis, Helicobacter pylori Infection and Gastric Pathologies.

Parasite immunology·2026
Same author

Malaria in Children at 9 US Hospitals: 2016-2023.

Pediatrics·2026
Same author

Ixodid and flea infestations and associated bacteria on two sympatric felid species in South Texas.

Ticks and tick-borne diseases·2026
Same author

Geographically Distinct Circulation of Genotype II and III St. Louis Encephalitis Virus, Texas, USA, 2009-2024.

Emerging infectious diseases·2026

Related Experiment Video

Updated: May 11, 2026

Trichuris muris Infection: A Model of Type 2 Immunity and Inflammation in the Gut
10:05

Trichuris muris Infection: A Model of Type 2 Immunity and Inflammation in the Gut

Published on: May 24, 2011

16.3K

Repeat Ascaris challenge reduces worm intensity through gastric cellular reprograming.

Yifan Wu1, Charlie Suarez-Reyes1, Nina L Tang1

  • 1Department of Pediatrics, Division of Tropical Medicine, Baylor College of Medicine, Houston, Texas, United States of America.

Plos Neglected Tropical Diseases
|May 30, 2025
PubMed
Summary
This summary is machine-generated.

Repeated exposure to roundworm (Ascaris) infection causes gastric cellular changes that reduce worm burden. These changes may explain why infection intensity decreases with age in humans.

More Related Videos

The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions
11:58

The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions

Published on: October 18, 2017

9.3K
Experimental Infection of Mice with the Parasitic Nematode Strongyloides ratti ratti Infection
10:12

Experimental Infection of Mice with the Parasitic Nematode Strongyloides ratti ratti Infection

Published on: January 17, 2025

430

Related Experiment Videos

Last Updated: May 11, 2026

Trichuris muris Infection: A Model of Type 2 Immunity and Inflammation in the Gut
10:05

Trichuris muris Infection: A Model of Type 2 Immunity and Inflammation in the Gut

Published on: May 24, 2011

16.3K
The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions
11:58

The Nematode Caenorhabditis Elegans - A Versatile In Vivo Model to Study Host-microbe Interactions

Published on: October 18, 2017

9.3K
Experimental Infection of Mice with the Parasitic Nematode Strongyloides ratti ratti Infection
10:12

Experimental Infection of Mice with the Parasitic Nematode Strongyloides ratti ratti Infection

Published on: January 17, 2025

430

Area of Science:

  • Parasitology
  • Immunology
  • Gastroenterology

Background:

  • Ascariasis is a widespread parasitic nematode infection, with intensity peaking in children and declining in adults.
  • The gastric mucosa is crucial for Ascaris larval hatching, utilizing acidic mammalian chitinase (AMCase) and gastric acid.
  • Previous studies showed Tamoxifen-induced mucosal injury impairs larval hatching and translocation.

Purpose of the Study:

  • To investigate the impact of repeated Ascaris exposures on the gastric mucosa and infection intensity.
  • To understand the mechanisms behind age-dependent changes in Ascariasis infection intensity.

Main Methods:

  • Establishment of a repeated Ascaris suum challenge mouse model.
  • Assessment of cellular changes in the gastric mucosa.
  • Quantification of worm intensity in the liver.

Main Results:

  • Repeated Ascaris challenge induced cellular alterations in the gastric mucosa.
  • These gastric changes led to a reduction in liver worm intensity.
  • The reduction in infection intensity was independent of the adaptive immune response.

Conclusions:

  • Gastric cellular changes resulting from repeated Ascaris exposure can decrease infection intensity.
  • These findings suggest a potential mechanism for the observed age-dependent decline in Ascariasis intensity.