Acceptive Immunity: The Role of Fucosylated Glycans in Human Host–Microbiome Interactions

Abstract

The growth in the number of chronic non-communicable diseases in the second half of the past century and in the first two decades of the new century is largely due to the disruption of the relationship between the human body and its symbiotic microbiota, and not pathogens. The interaction of the human immune system with symbionts is not accompanied by inflammation, but is a physiological norm. This is achieved via microbiota control by the immune system through a complex balance of pro-inflammatory and suppressive responses, and only a disturbance of this balance can trigger pathophysiological mechanisms. This review discusses the establishment of homeostatic relationships during immune system development and intestinal bacterial colonization through the interaction of milk glycans, mucins, and secretory immunoglobulins. In particular, the role of fucose and fucosylated glycans in the mechanism of interactions between host epithelial and immune cells is discussed.

<i>Helicobacter pylori</i>. The survival strategy of a commensal symbiont in the <i>Homo sapiens</i> population

“…Это косвенно подтверждается тем фактом, что α1,2-фукозилированные гликаны эпителия ЖКТ, которые являются важной частью врожденной и адаптивной иммунной системы (они создают симбиотическую среду для хозяина и микробиоты и защищают от патогенов), опосредуют адгезию H. py lo ri к поверхности желудочного эпителия, способствуя успешной колонизации [35]. Наблюдаемая у детей ранняя колонизация H. py lo ri может иметь положительный эффект на хозяина, оказывая влияние, например, на регуляцию гормонов лептина и грелина и, кроме того, предохраняя от развития некоторых аллергических (астма) и аутоиммунных заболеваний, а также воспалительных заболеваний кишечника (ВЗК) [36,37].…”

Gastrointestinal microbiome and Helicobacter pylori: Eradicate, leave it as it is, or take a personalized benefit–risk approach?

“…Unlike other pathogenic/opportunistic bacteria, H. pylori colonization of newborns/infants is facilitated by T helper type 2 immunity and leads to the development of immune tolerance[ 34 ]. Most likely, the co-evolution of H. pylori and the human host over millennia has led to the fact that this bacterium is considered a commensal symbiont, not a pathogen, by the host’s immune system.…”

“…This is indirectly confirmed by the fact that α1,2-fucosylated glycans of the GI epithelium, which are an important part of the innate and adaptive immune system (they create a symbiotic environment for the host and microbiota and protect against pathogens), mediate the adhesion of H. pylori to the surface of the gastric epithelium, contributing to successful colonization[ 35 ]. As a result, early colonization of H. pylori can have a positive effect on the host, for example on the regulation of the hormones leptin and ghrelin as well as on protection against some allergic ( e.g., asthma) and autoimmune diseases and against inflammatory bowel disease (IBD)[ 36 , 34 ]. The inverse association between H. pylori and some potentially proinflammatory and/or procarcinogenic bacteria found in various studies[ 20 , 22 - 24 ] may suggest a regulatory function of H. pylori toward the GI microbiota.…”

Infant Gut Microbial Metagenome Mining of α- l -Fucosidases with Activity on Fucosylated Human Milk Oligosaccharides and Glycoconjugates

“…In addition, α1,6-linked l -fucose can be also added to the innermost GlcNAc residue in N -glycans constituting the so-called core fucosylation ( 5 ). Fucosylated glycoconjugates play fundamental roles in a wide range of physiological processes, including immune responses, receptor signaling, fertilization, tumor metastasis, and host-microbiome interactions ( 2 , 5 – 8 ). The l -fucose residue is essential in the molecular interactions occurring in many of these processes.…”