BLACKSBURG, Va., October 7, 2013 -- A new computational model developed by researchers at the Center for Modeling Immunity to Enteric Pathogens (MIEP) offers new ways to study host immune responses to Helicobacter pylori. Using the model, MIEP researchers identified an abnormal immune response linked to development of lesions during H. pylori infection of the stomach. Their findings may help clinicians pinpoint how best to treat such infections.

Computational simulations in combination with mouse mechanistic studies revealed that whereas Helicobacter pylori plays a crucial role in the disruption of the epithelial cell layer at the initial stages of the infection, the inflammatory lesions found at chronic stages are mainly driven by components of the effector immune response to the bacterium.











“This large-scale computational model of host responses to H. pylori infection combines cutting-edge approaches in computational modeling and experimental research to help elucidate immune responses to H. pylori,” said Dr. Raquel Hontecillas, co-director of the Nutritional Immunology and Molecular Medicine Laboratory (NIMML) and MIEP.

H. pylori is a bacterium that lives in the human gut and sometimes causes ulcers and cancers. Currently, doctors treat H. pylori infections with antibiotics that destroy the bacteria. However, H. pylori also can protect against diseases such as asthma, obesity and diabetes. Understanding how a harmless bacterial population becomes virulent and leads to disease has been difficult, but the computational model developed by MIEP researchers has led to new insights.

Based on results from experimental work with mouse models, NIMML researchers built a computational simulation that can predict how and when infection begins and progresses. The model shows the position of cells during infection and accounts for the non-uniformity and randomness of immune responses. Using the computational model, NIMML researchers found that, although H. pylori may be responsible for starting an infection, abnormal immune responses can contribute to chronic ulcers or cancers.

“The knowledge gained from such models will accelerate the development of novel drugs and vaccines for H. pylori-associated diseases,” said Dr. Hontecillas, “The ultimate aim may not be to destroy H. pylori but to learn how to manipulate the interaction of the bacterium and host immune system to produce beneficial effects.”

The PLoS paper is available here.

MIEP is funded by the National Institute of Allergy and Infectious Diseases, part of the National Institutes of Health, under Contract No. HHSN272201000056C. PI: Josep Bassaganya-Riera.

About the Nutritional Immunology and Molecular Medicine Laboratory:
The Nutritional Immunology and Molecular Medicine Laboratory (NIMML) conducts translational research aimed at developing novel therapeutic and prophylactic approaches for modulating immune and inflammatory responses. The Laboratory has over 20 researchers and combines computational modeling, bioinformatics approaches, pre-clinical experimentation and human clinical studies to better understand the mechanisms of immune regulation at mucosal surfaces and ultimately accelerate the development of novel treatments for infectious and immune-mediated diseases. In addition, the NIMML team leads the NIAID-funded Center for Modeling Immunity to Enteric Pathogens (MIEP).

About Virginia Bioinformatics Institute

Established in 2000, Virginia Bioinformatics Institute is one of seven acclaimed research institutes designed to support Virginia Tech’s research mission. Our emphasis on informatics of complex interacting systems scales from the microbiome to the entire globe, helping to solve challenges posed to human health, security, and sustainability. Headquartered on the Blacksburg, Virginia campus, the institute occupies 154,600 square feet in research facilities, including state-of-the-art core laboratory and high performance computing facilities, as well as research offices in the Virginia Tech Research Center in Arlington, Virginia.


Tiffany Trent

October 07, 2013