The most cost-effective method of stopping invasive species is to put a halt to their introduction. In order for this to happen, managers need to know exactly what plants are invasive. Existing lists of global invasive plants include species that have been reported by scientists, but species that haven’t yet been reported as invasive still pose a risk. the team at UMass Amherst, led by Brittany Laginhas, who completed the research as part of her graduate work at UMass, mined a database of 5,893 studies, stretching back to 1959, to paint the most complete picture of the world’s invasive species yet.

“Trade and climate change have facilitated the widespread movement of species around the globe,” says Brittany Laginhas, who completed this research as part of her graduate studies at UMass Amherst and is the paper’s lead author. “In some cases, these species will establish and spread in their new environment, causing devastating ecological and economic damages. Basic information on invasive species, including which species are invasive, where they have invaded, and their timing of invasion, is critical for developing strategies to prevent their spread and subsequent damages.”

And yet, one of the most basic pieces of information — how many invasive plant species are there in the world? — is not precisely known.

“We’re capturing about two-thirds of the invasives that have been reported in the literature,” says Bethany Bradley, professor of environmental conservation at UMass Amherst, and the paper’s senior author.

Perhaps the most shocking result is that the numbers of invasive species seem to be increasing exponentially, with no sign of starting to level off. Though the team uncovered 3,008 total invasive species reported in the 5,893 papers, their statistical modelling suggests that there should be 4,721 species — though the identity of those missing 1,713 species remains a mystery.

Though there could be many explanations for why so many invasive species are missing from the literature, it’s also clear that there has been a systemic and geographically uneven undercount. While North America has been relatively well studied, Central and South America and Oceania haven’t been given equal attention. “There are vast differences in the studies conducted across different continents,” says Matthew Fertakos, one of the paper’s co-authors and a graduate student in organismic and evolutionary biology at UMass Amherst. “We have statistical methods that can help tell us how many species there should be, but real data is always better than an estimation.”

And that leads to the paper’s final conclusion: a comprehensive map of the world’s invasive species can’t be generated in the lab alone. “We need floristic surveys,” says Bradley, “where researchers actually go out into the field, especially in the places that have been understudied, like Africa, Southeast Asia, and South America, and identify the exact species causing problems.”

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The finding resolves a controversy about the possible redundancy of ILC2s with other cells in the body. The study also suggests that a unique set of regulatory networks controlled by neurons in the gut may be viable targets for future drug therapies to combat chronic inflammatory diseases including asthma, allergy and inflammatory bowel disease (IBD).

The study, published Nov. 2 in Nature, shows that although ILC2s have many functional similarities to immune cells called T helper type 2 cells (Th2 cells), the latter cell type cannot adequately compensate for loss of the protective response of ILC2s against parasitic worm infection in the gut as well as gut inflammation. Underscoring the clinical relevance of the study, the researchers found evidence that ILC2s in humans respond in a manner similar to mouse ILC2s.

“This advances our understanding of the complexity of the immune system, and gives us a potential new set of targets for future therapies,” said study senior author Dr. David Artis, director of the Jill Roberts Institute for Research in Inflammatory Bowel Disease, director of the Friedman Center for Nutrition and Inflammation and the Michael Kors Professor of Immunology at Weill Cornell Medicine.

ILC2s are part of a family of cells, innate lymphoid cells, that were discovered by multiple groups only about 12 years ago. With their strong presence in barrier tissues, innate lymphoid cells are generally considered to serve as sentinels and first responders against various types of infection. But scientists also recognize that ILCs may hold the keys to understanding common inflammatory and autoimmune conditions such as asthma and IBD.

It is thought that both ILC2s and Th2 cells evolved at least in part to defend the body from parasitic worm infections, biting insects and other environmental triggers. When triggered by such challenges, both help marshal what is called a type 2 immune response. These similarities have led researchers to suggest that they are functionally almost the same but ILC2s specialize in earlier, more localized responses, whereas T cells are more blood-borne and mobile, concentrating in multiple tissues where needed. However, in the new study, the researchers found that ILC2s have an essential immune role rather than being redundant as type 2 immune responders.

When ILC2s and Th2 cells are activated by a worm infection, they both produce an anti-worm, tissue-protecting protein called amphiregulin (AREG). To determine if Th2 cells can compensate for loss of this protein from ILC2s, the researchers engineered mice in which AREG production is selectively deleted in ILC2s, but not in Th2 cells. They found that these mice were more susceptible to parasitic worm infection in the gut due to reduced capacity to mount an anti-parasitic immune response, compared with mice with normal ILC2s. The mice lacking ILC2 AREG were also much more susceptible to gut damage from inflammation.

“This finding clarifies that ILC2s are playing the major role in this tissue protective response — without them the response is inadequate,” said study co-first author Dr. Hiroshi Yano, a postdoctoral research associate in the Artis laboratory.

Clarifying the functional importance of a major immune cell type is a significant achievement in basic immunology and the results of the study also suggest clinical applications. The researchers showed that the ILC2 immune response, either to worm infection or inflammatory gut damage, is selectively controlled by a signaling molecule produced by neurons in the gut. Giving the molecule to mice with experimental gut inflammation boosted AREG production in ILC2s and protected the animals from gut damage. Preliminary experiments with gut ILC2s taken from patients with inflammatory bowel disease showed that the molecule could boost the protective response in the human cells as well. These findings suggest that neurons in the gut communicate with ILC2s to generate a protective response that cannot be replaced by other immune cells, thus offering new therapeutic opportunities, Dr. Artis said.

This work was supported in part by the National Institutes of Health (DK126871, AI151599, AI095466, AI095608, AI142213, AR070116, AI172027, DK132244), a WCM Department of Pediatrics Junior Faculty Pilot Award, the Jill Roberts Center Pilot Award for Research in IBD, a Thomas C. King Pulmonary Fellowship, the LEO foundation, Cure for IBD, Jill Roberts Institute, the Sanders Family, and the Rosanne H. Silbermann Foundation.

The study, published Nov. 2 in Nature, found that dietary inulin fiber alters the metabolism of certain gut bacteria, which in turn triggers what scientists call type 2 inflammation in the gut and lungs. This type of inflammation is thought to have evolved in mammals chiefly to defend against parasitic worm (“helminth”) infections, and is also part of normal wound-healing, although its inappropriate activation underlies allergies, asthma and other inflammatory diseases.

“There’s a lot to think about here, but, in general, these findings broaden our understanding of the relationship between diet, immunity, and the normally beneficial microorganisms that constitute our microbiota and colonize our bodies,” said study co-senior author Dr. David Artis, director of the Friedman Center for Nutrition and Inflammation and the Michael Kors Professor of Immunology at Weill Cornell Medicine.

The study’s scientific participants reflect the Friedman Center’s highly cross-collaborative research mission, drawing on expertise in bacterial genetics, biochemistry and immunology at Weill Cornell Medicine in New York City and Cornell’s Ithaca campus. Dr. Chun-Jun Guo, assistant professor of immunology in medicine at Weill Cornell Medicine, and Dr. Frank Schroeder, professor at the Boyce Thompson Institute and in the Department of Chemistry and Chemical Biology in the College of Arts and Sciences on Cornell’s Ithaca campus teamed up with the Artis laboratory to gain a detailed understanding of how an important dietary component affects the microbiome and the immune response. The study’s first author is Dr. Mohammad Arifuzzaman, a postdoctoral researcher in the Artis laboratory.Dr. Artis is also director of the Jill Roberts Institute for Inflammatory Bowel Disease at Weill Cornell Medicine.

Small amounts of inulin are present in a wide variety of fruits and vegetables, including bananas, asparagus, and garlic. It is also frequently concentrated in commonly available high-fiber dietary supplements. Previous studies have found that inulin boosts populations of beneficial gut bacterial species which in turn boost levels of anti-inflammatory immune cells called regulatory T (Treg) cells.

In this new study, the researchers examined inulin’s effects more comprehensively. They gave mice an inulin-based, high-fiber diet for two weeks, and then analyzed the many differences between these mice and mice that had been fed a diet lacking inulin. A major difference was that the inulin diet, while increasing Treg cells, also induced markedly higher levels of white blood cells called eosinophils in the gut and lungs. A high level of eosinophils is a classic sign of type 2 inflammation and is typically seen in the setting of seasonal allergies and asthma.

Ultimately the researchers found that the eosinophil response was mediated by immune cells called group 2 innate lymphoid cells (ILC2s), which were activated by elevated levels of small molecules called bile acids in the blood. The bile acid levels were elevated due to the inulin-induced growth of certain bacterial species — a group called Bacteroidetes, found in both mice and humans — which have a bile acid-metabolizing enzyme.

“We were amazed to find such a strong association between inulin supplementation and increased bile acid levels,” Dr. Schroeder said. “We then found that deletion of the bile acid receptor abrogates the inulin-induced inflammation, suggesting that microbiota-driven changes in bile acid metabolism underlie the effects of inulin.”

“When we colonized germ-free mice (mice without microbiota) with one of these bacterial species, and then knocked out the gene for one bacterial enzyme that promotes bile acid production, the whole pathway leading from inulin to eosinophilia and allergic inflammation was blocked,” Dr. Guo said.

The finding that inulin promotes type 2 inflammation does not mean that this type of fiber is always “bad,” the researchers said. They found that inulin did worsen allergen-induced type 2 airway inflammation in mice. But the experiments also confirmed inulin’s previously reported effect at boosting anti-inflammatory Treg cells, which may in many cases, outweigh some pro-inflammatory impact. Moreover, a type 2 immune response, which in the gut and lungs involves an increased production of tissue-protecting mucus, is not necessarily harmful in healthy people — indeed, the researchers found in their mouse experiments that the inulin-induced type 2 inflammation enhances the defense against helminth infection.

“It could be that this inulin to type-2-inflammation pathway represents an adaptive, beneficial response to endemic helminth parasite infection, though its effects in a more industrialized, helminth-free environment are more complex and harder to predict,” said Dr. Arifuzzaman.

The researchers now plan to use their multi-disciplinary, multi-platform approach to study systematically the immune effects of the different types of dietary fiber as well as a range of other dietary supplements in different states of health and disease.

This work was supported in part by the National Institutes of Health (5T32HL134629, DP2 HD101401-01, AI140724, KL2 TR002385, R35 GM131877, DK126871, AI151599, AI095466, AI095608, AR070116, AI172027 and DK132244) the AGA Research Foundation, the WCM-RAPP Initiative, the W. M. Keck Foundation, the Howard Hughes Medical Institute, the LEO Foundation, CURE for IBD, the Jill Roberts Institute for Research in IBD, the Sanders Family Foundation and the Rosanne H. Silbermann Foundation.