Fight infection with glycan-rich foods – onions, asparagus, apples, kiwi, carrots

Analysis of Asn-linked glycans from vegetable foodstuffs: widespread occurrence of Lewis a, core alpha1,3-linked fucose and xylose substitutions.

Wilson IB, et al. Glycobiology. 2001.

From: https://www.ncbi.nlm.nih.gov/m/pubmed/11358875/

The N-glycans from 27 “plant” foodstuffs, including one from a gymnospermic plant and one from a fungus, were prepared by a new procedure and examined by means of matrix-assisted laser desorption/ionization time-of-flight mass spectrometry (MALDI-TOF-MS). For several samples, glycan structures were additionally investigated by size-fractionation and reverse-phase high-performance liquid chromatography in conjunction with exoglycosidase digests and finally also (1)H-nuclear magnetic resonance spectroscopy. The glycans found ranged from the typical vacuolar “horseradish peroxidase” type and oligomannose to complex Le(a)-carrying structures. Though the common mushroom exclusively contained N-glycans of the oligomannosidic type, all plant foods contained mixtures of the above-mentioned types.

Apple, asparagus, avocado, banana, carrot, celery, hazelnut, kiwi, onion, orange, pear, pignoli, strawberry, and walnut were particularly rich in Le(a)-carrying N-glycans.

Although traces of Le(a)-containing structures were also present in almond, pistachio, potato, and tomato, no such glycans could be found in cauliflower. Coconut exhibited almost exclusively N-glycans containing only xylose but no fucose. Oligomannosidic N-glycans dominated in buckwheat and especially in the legume seeds mung bean, pea, peanut, and soybean. Papaya presented a unique set of hybrid type structures partially containing the Le(a) determinant.

These results are not only compatible with the hypothesis that the carbohydrate structures are another potential source of immunological cross-reaction between different plant allergens, but they also demonstrate that the Le(a)-type structure is very widespread among plants.

 

FRom: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005082/

The dense microbial community (microbiota) that is established in the human intestine shortly after birth has a profound effect on health and physiology, providing benefits such as modulation of immune development, digestion of recalcitrant dietary nutrients, and inhibition of pathogen colonization. However, abnormalities in microbiota composition (dysbiosis) have been implicated in several disease states, including inflammatory bowel disease (IBD), colon cancer, antibiotic-associated colitisand obesity. Dysbiosis is postulated to result when a typically healthy microbial community becomes unbalanced, due to either increased abundance of potentially harmful microorganismsor increased flux through harmful metabolic pathways. The normal composition of the gut microbiota, both at single time points and over longer periods of human life, has only been deeply probed within the last several years. Current investigations seek to define the dominant forces shaping the microbiota in order to better understand the causes of dysbiosis and develop strategies to restore a healthy community.

One major factor shaping the composition and physiology of the microbiota is the influx of glycans into the intestine, mostly from diet and host mucosal secretions. Humans consume dozens of different plant and animal-derived dietary glycans, most of which cannot be degraded by enzymes encoded in the human genome. Microbial fermentation transforms these indigestible glycans into short chain fatty acids (SCFA), which serve as nutrients for colonocytes and other gut epithelial cells. Gut microorganisms therefore play a pivotal symbiotic role in helping humans access calories from otherwise indigestible nutrients. Individual microorganisms prefer different glycans. Thus, selective consumption of these nutrients can influence which microbial groups proliferate and persist in the gastrointestinal tract, pointing to dietary glycans as a non-invasive strategy with which humans can directly influence the balance of species in the gut.

In addition to dietary glycans, which fluctuate in composition and abundance, some members of the microbiota are able to degrade glycans found in host mucus secretions or shed epithelial cells. These endogenous glycans provide consistent sources of nutrients to the microbiota, despite potentially drastic changes in diet. Endogenous host glycans are presented to bacteria in the intestinal lumen as O-linked glycans attached to secreted or cell-associated mucin glycoproteins (the major component of mucus), or as N-linked glycans present in shed epithelial cells. Some proportion of endogenous glycans are likely to be concentrated directly adjacent to host tissue in the protective mucus layer. The ability of certain microorganisms to penetrate and degrade mucus as a nutrient source positions them in close proximity to host cells. As a consequence, species that are adept at utilizing these endogenous glycans may exert a disproportionate effect on colonic health, especially during states of dysbiosis.

This review explores the role of glycans in shaping the microbiota by first considering its assembly from birth to adulthood and how this process is catalyzed by changes in glycan availability. We then consider the glycan acquisition mechanisms that have been evolved by some of the most abundant (and therefore successful) members of the human gut microbiota. Finally, we consider how the spatial abundance and diversity of glycans in different gut regions (i.e., lumen versus mucosa, proximal versus distal) may select for regional sub-populations, some of which may be of particular interest in pathologies resulting from dysbiosis.

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