University Of Texas Southwestern researchers report that animal models fed a plant-rich diet
are less susceptible to gastrointestinal (GI) infection
from a pathogen such as the one currently under investigation for a widespread E. coli
outbreak tied to romaine lettuce. A strain of E. coli
known as EHEC, which causes debilitating and potentially deadly inflammation in the colon with symptoms such as bloody diarrhea and vomiting, is implicated in several foodborne
outbreaks worldwide each year.
Dr Vanessa Sperandio, Ph.D., Professor of Microbiology and Biochemistry at UT Southwestern told Thailand Medical
News, "There has been a lot of hearsay about whether a plant
is better for intestinal health than a typical Western diet
, which is higher in oils and protein but relatively low in fruits and vegetables. So we decided to test it."
She added, "Plant-rich diets
are high in pectin,
a gel-like substance found in many fruits and vegetables. Pectin
is digested by the gut microbiota into galacturonic acid
, which we find can inhibit the virulence of EHEC. This is relevant to public health because EHEC outbreaks lead to hemorrhagic colitis, which is debilitating and sometimes causes death, particularly in the very young and the elderly.”
Typically intestinal pathogens
like EHEC sense the complex chemistry inside the GI tract to compete with the gut's resident microbiota
to establish a foothold, Dr Sperandio says. Over centuries, the pathogens
have developed different strategies to compete against the so-called good, or commensal,
microbes that normally line the gut.
Those beneficial commensals include harmless strains of E. coli
living in the colons of humans and other mammals, where they help the host's normal digestion process, she adds. The word commensal
means "eating at the same table" and that is what the symbiotic bacteria that make up the gut's microbiota do.
The normal commensals
that line the gut present a significant barrier to intestinal pathogens
, Dr Sperandio explains. EHEC and similar gram-negative bugs overcome that barrier by deploying a secretion system called T3SS.
The T3SSs act like molecular syringes to inject a mix of virulence proteins into the cells lining the host's colon, setting off inflammation and symptoms of infection
. Because mice are unaffected by EHEC, researchers use a similar pathogen
, Citrobacter rodentium, in mouse studies, Dr Sperandio explains.
She further commented, adding that the two
types of E. coli
may have evolved to avoid competing for the same energy sources, "Our study finds first that the good E. coli
and the pathogenic ones like EHEC use different sugars as nutrients. Second, we find that dietary pectin protects against the pathway the pathogenic EHEC uses to become more virulent."
A certain type of commensal
gut bacteria breaks down dietary pectin
from fruit and vegetables, creating galacturonic acid
, a sugar acid that the EHEC and C. rodentium use in two ways. Initially, the pathogen
uses that sugar acid as an energy source to expand in the gut, Dr Sperandio says.
She added, "Once the sugar acid becomes depleted, the pathogen changes its survival strategy, almost like flipping a switch."
Instead of using the galacturonic acid
for nourishment, the infectious bacteria employs it in a signaling pathway that increases the EHEC's and similar bacteria's virulence using the syringe-like T3SS.
The research showed that mice fed pectin
for about a week withstood infection. Comparing the colons of six mice fed a chow diet with 5 percent extra pectin from citrus peel with four mice on a typical diet, the researchers found a much lower rate of infection
in the pectin
-eating mice, Dr Sperandio says.
The detailed amount of bacteria in the mouse gut was measured by daily stool checks and by analysis of the amount of bacteria in a pouch at the juncture of the small and large intestines, called the cecum, at the experiment's end.
The medical researchers found that mice on the pectin
-enriched chow had about 10,000 bacteria in the cecum compared to 1 million bacteria in mice on the typical diet. The pectin group also had fewer symptoms, she says, adding that a pectin
level of 5 percent appears to prevent the pathogen
from activating its virulence repertoire.
Dr Sperandio stressed that the research is one step in a journey to define the molecular mechanisms that govern how the commensal
species in the gut impact the virulence of intestinal pathogens
She added, "This is not translatable to humans yet. We hope a better understanding of how intestinal disease develops will lead to strategies to reduce the incidence or, at least, the symptoms caused by these gram-negative pathogens
, possibly through new vaccines or drugs."
Reference : Diet-derived galacturonic acid regulates virulence and intestinal colonization in enterohaemorrhagic Escherichia coli and Citrobacter rodentium, Nature Microbiology (2019). DOI: 10.1038/s41564-019-0641-0 ,