Processed diets may promote diseases characterized by low-grade infection and inflammation

Processed diets, which are low in fiber, may initially reduce the incidence of foodborne infectious diseases such as E. coli infections, but might also increase the incidence of diseases characterized by low-grade chronic infection and inflammation such as diabetes, according to researchers in the Institute for Biomedical Sciences at Georgia State University.

This study used mice to investigate how changing from a grain-based diet to a highly processed, high-fat Western style diet impacts infection with the pathogen Citrobacter rodentium, which resembles Escherichia coli (E. coli) infections in humans. The findings are published in the journal PLOS Pathogens.

Gut microbiota, the microorganisms living in the intestine, provide a number of benefits, such as protecting a host from infection by bacterial pathogens. These microorganisms are influenced by a variety of environmental factors, especially diet, and rely heavily on complex carbohydrates such as fiber.

The Western-style diet, which contains high amounts of processed foods, red meat, high-fat dairy products, high-sugar foods and pre-packaged foods, lacks fiber, which is needed to support gut microbiota. Changes in dietary habits, especially a lack of fiber, are believed to have contributed to increased prevalence of chronic inflammatory diseases such as inflammatory bowel disease, metabolic syndrome and cancer.

In this study, the researchers found switching mice from a standard grain-based rodent chow to a high-fat, low-fiber Western-style diet resulted in a rapid reduction in the number of gut bacteria. Mice fed the Western-style diet were frequently unable to clear the pathogen Citrobacter rodentium from the colon. They were also prone to developing chronic infection when re-challenged by this pathogen.

The researchers conclude the Western-style diet reduces the numbers of gut bacteria and promotes encroachment of microbiota into the intestine, potentially influencing immune system readiness and the body's defense against pathogenic bacteria.

We observed that feeding mice a Western-style diet, rather than standard rodent grain-based chow, altered the dynamics of Citrobacter infection, reducing initial colonization and inflammation, which was surprising. However, mice consuming the Western-style diet frequently developed persistent infection that was associated with low-grade inflammation and insulin resistance. These studies demonstrate potential of altering microbiota and their metabolites by diet to impact the course and consequence of infection following exposure to a gut pathogen."

Dr. Andrew Gewirtz, senior co-author of the study and professor, Institute for Biomedical Sciences

"We speculate that reshaping gut microbiota by nutrients that promote beneficial bacteria that out-compete pathogens may be a means of broadly promoting health," said Dr. Jun Zou, senior co-author of the study and assistant professor in the Institute for Biomedical Sciences at Georgia State.

Source:
Journal reference:

An, J., et al. (2021) Western-style diet impedes colonization and clearance of Citrobacter rodentium. PLOS Pathogens. doi.org/10.1371/journal.ppat.1009497.

Comments

The opinions expressed here are the views of the writer and do not necessarily reflect the views and opinions of News Medical.
Post a new comment
Post

While we only use edited and approved content for Azthena answers, it may on occasions provide incorrect responses. Please confirm any data provided with the related suppliers or authors. We do not provide medical advice, if you search for medical information you must always consult a medical professional before acting on any information provided.

Your questions, but not your email details will be shared with OpenAI and retained for 30 days in accordance with their privacy principles.

Please do not ask questions that use sensitive or confidential information.

Read the full Terms & Conditions.

You might also like...
Rare variant analysis reveals genetic spectrum of monogenic diabetes genes