Currently, the concept of “human microflora” has lost its relevance: we carry in our body not just a set of bacteria, but a real biome — microbiome. But if the biome is a large ecosystem from the point of view of ecologists, then our body is a habitat for a large population of microorganisms, a kind of microbial ecosystem characterized by its genetic regulation and complex interactions and responding to the influence of environmental and internal factors. It is so unique that there are no two people in the world with an identical microbiome. Differences in microbial composition depend on environmental factors such as nutrient intake, pH, humidity, and temperature. Their various values contribute to the reproduction of bacteria and mediate the benefits they can bring to the human host [1], [2]. The microbiome is unevenly distributed in our body; according to its topography and species composition, it is customary to distinguish the microbiome of the skin, oral cavity, respiratory tract, urogenital tract and intestines. The largest microbiome of our body is undoubtedly the intestinal one. It can consist of hundreds of different types of microorganisms, but two types of bacteria predominate in an adult: Firmicutes and Bacteroidetes [3]. The intestinal microbiome has been studied better than other human bacterial communities, and long-term studies, which will be described below, have shown that it is it that has a greater impact on the health of its host. Let’s take a trip back in time and look at how our gut microbiome is formed.

Until recently, it was believed that the fetus in the womb is completely protected from contact with the world of microorganisms, that is, a person is born completely sterile, and its colonization by bacteria occurs later. But there is evidence that the first colonizers master the human body even before it is born. A number of studies have revealed that birth bacteria are present in the placenta, amniotic fluid, umbilical cord blood, and primary feces. Enterococcus, Escherichia, Leuconostoc, Lactococcus, and Streptococcus, and premature infants have traces of Enterobacter, Enterococcus (to a lesser extent than full—term infants), Lactobacillus, Photorhabdus, and Tannerella [4-14]. Also, in one of the studies, evidence of intrauterine bacterial translocation was obtained — the penetration of bacteria from the intestine of the mother to the fetus [13]. Researchers suggest that this happens through blood flow: a mechanism similar to the “enteromammary axis,” which we’ll talk about later. This hypothesis is supported by data from another experiment in which pregnant mice were orally treated with labeled Enterococcus faecium, after which these bacteria “declared themselves” in the placenta and even the meconium of unborn mice [13]. But still, really serious contact with the world of microorganisms occurs after birth, and in many ways, the future health of a person depends on how this meeting takes place. Colonization of the intestine in healthy children fits into four consecutive time phases. The first one lasts from the moment of birth to two weeks. The microbial population during this period is mainly represented by streptococci and E. coli. Depending on the type of breastfeeding — breast or artificial — after a while, bifidobacteria or lactobacilli join, respectively. Representatives of the genera Clostridium and Bacteroides are also found in small quantities. After two weeks, the second phase begins, which continues until complementary foods are introduced into the diet. At this time, the number of representatives of the genus increases Bacteroides. From the moment of introduction of complementary foods, the third phase begins, lasting until the end of breastfeeding. During this phase, the baby’s microbiome is finally formed: gradually, as the proportion of solid food in the diet increases and the proportion of breast milk decreases, the number of bacteroids and anaerobic gram-positive cocci (peptococci and peptostreptococci) increases. The end of breastfeeding marks the transition to the fourth phase. It is characterized by the relative stability of the microbial composition, which persists throughout an individual’s life [15]. Now let’s take a closer look at how the processes of colonization and the formation of an immune response occur during and after birth.

As it turned out, even the nature of delivery (a child can be born naturally, or maybe surgically, by caesarean section) affects the composition of the baby’s microbiome. The first thing a child encounters is the microbial world of his mother’s birth canal. Six types of lactobacilli have been identified in non-pregnant women, based on the ratio of which at least five qualitatively different types of the vaginal microbiome are distinguished [16]. In four of them, which are typical, as a rule, for representatives of European and Asian peoples, the following representatives of the genus predominate Lactobacillus:

• L. crispatus (type I microbiome);
• L. gasseri (type II microbiome);
• L. iners (type III microbiome);
• L. jensenii (type V microbiome).

Type IV microbiome is often found in black and Latin American women and is characterized by low levels of Lactobacillus spp. and a large number of anaerobic bacteria. During pregnancy, due to changes in the pH of the vagina, bacterial diversity decreases, but the stability of the microbiota composition increases. As a rule, during this period, the microbiome is dominated by Lactobacillus crispatus and Lactobacillus iners. The quantitative superiority of these species highlights their importance for maintaining a healthy birth canal environment. In European and Asian women, shifts between types of microbiomes may occur during pregnancy, but, as a rule, they rarely transition to type IV [18]. Thus, depending on the characteristics of the microbiota of the mother’s vagina, the child begins his life by “getting to know” a certain specific set of microorganisms, which emphasizes the importance of microbiome research in various population groups. But what does this acquaintance mean? Why is microbial colonization so important for a child? The fact is that bacteria actually activate the host’s immune system due to their symbiotic relationship with the epithelial and immune structures of the intestine (Pic. 1) [21]. Leaving the birth canal naturally, a full-term newborn ingests small amounts of representatives of the mother’s vaginal and intestinal microbiota. These are mainly bacteria of childbirth Prevotella, Sneathia, and Lactobacillus [15]. If delivery occurs by caesarean section, representatives of the skin microbiomes of the mother and medical staff, mainly the bacteria of childbirth, are among the first to colonize the newborn’s body Propionibacterium, Corynebacterium, and Streptococcus [19], [20]. In such infants, a slowdown in intestinal colonization is noted. Bacteroidetes and low bacterial diversity during the first two years of life [22]. However, from the age of four months, differences in bacterial diversity with naturally born children begin to fade, and by the age of 12 months they practically disappear [19]. Picture 1. Scheme of immune protection of the intestinal mucosa of the fetus depending on gestational age. a — In a baby born on time, all the components of the immune defense of the mucous membrane are mature. b — However, in order for the immune system to become functional, it must be stimulated by primary colonizers. The immune defense of the intestine includes: specialized epithelium, or M-cells (1), Peyer’s plaques (2), interstitial (3) and intraepithelial (4) lymphocytes mediating the development of immune reactions. Among the lymphoid formations of the intestine, single lymph nodes (located mainly in the distal intestine) and Peyer’s plaques (located mainly in the ileum) are distinguished. The latter are formed by grouped lymphatic follicles protruding the epithelium into the intestinal lumen in the form of a dome, and interstitial clusters of lymphoid tissue. The epithelium of the mucous membrane in the plaque area contains up to 10% of specific micro-folded (M—) cells that provide transepithelial transport, the mechanism of which is transcytosis: due to a thin glycocalyx, they actively absorb macromolecules (including antigens) from the intestinal lumen with the apical surface, transfer them through their cytoplasm as part of the endosome and transfer them to immunocompetent Peyer’s cells through exocytosis. plaques. To speed up the process, M cells form “pockets” from below, filled with an “immune vinaigrette” of B cells, plasmocytes, T cells, macrophages, and antigen-presenting dendritic cells. Nevertheless, it is obvious that the nature of delivery affects the microbiome of the newborn (Pic. 2). However, it is still unclear whether these differences affect the health of an adult individual.: Although some epidemiological studies demonstrate a link between cesarean section and various diseases (Table. 1), the reason for their development has not been definitively clarified. Picture 2. Changes in the microbiome in newborns. The text color and arrows indicate changes in specific varieties (green), general changes (pink), and community diversity (orange). but — Changes in infants born naturally, relative to surgically extracted ones. b — Changes in breastfed infants relative to “artificial babies”. α-diversity is the species diversity within the studied community, β-diversity is the species diversity between communities of a given area (according to R. Whittaker).

An equally important factor in the formation of the newborn’s microbiome is the nature of nutrition. Breast milk is an optimally balanced food for an infant, ensuring its normal development [23]. As is known, in the first days of life, it protects the child from infectious diseases and helps reduce mortality from them [24] due to the content of many immune factors: T and B lymphocytes, plasma cells, immunoglobulins (primarily IdA) and antimicrobial enzymes (lysozyme and lactoferrin). It has been established that breastfeeding to some extent prevents the development of chronic diseases such as diabetes mellitus [25] and obesity [26]. And, undoubtedly, breast milk contributes to the formation of a “healthy” microbiome. The first data on the detection of bacteria in human milk were obtained in 1950, but researchers of those years were interested only in pathogenic microorganisms [27]. Although the first symbiont bacteria were found in breast milk as early as the 1970s, scientists were unable to identify them [27]. It was only in 2003, when related lactobacilli were found in the milk, breast skin, and nipple areoles of eight nursing mothers, and in the mouth and feces of their children, that scientists assumed that these bacteria were not introduced accidentally from the outside, but were of endogenous origin [28]. Regardless of whether maternal or donor breast milk is used for breastfeeding, each baby has its own special microbiome. The credit for this belongs to the oligosaccharides of human milk [29], [30]. In the composition of human milk, about 8% is devoted to digested PM prebiotics that support the growth of Bifidobacterium longumsubsp. infantis [31]. At the same time, each woman’s HPV profile is unique, which in turn ensures the individuality of the infant microbiome (Pic. 3) [32]. Pic 3. Interaction of human milk glycans and microbiota. The interaction of the newborn with maternal and environmental microorganisms is mediated by the consumption of colostrum and the glycans contained in it (human milk oligosaccharides, OHMS). PMPS have prebiotic, anti—adhesive, and anti—inflammatory activities, facilitate the expansion of symbionts, especially Bacteroides and Bifidobacterium, and inhibit the growth and adhesion of opportunistic and obligate pathogens. Another factor mediating the formation of the microbiome is the so—called enteromammary axis, a system that ensures the transport of bacteria from the intestine (future) the mother’s mammary glands. Its primary link is intestinal dendritic cells, which capture bacteria and transport them to local lymphoid follicles [1]. A specific immunoglobulin is produced there. These dendritic cells and immunoglobulin-secreting lymphocytes circulate in the blood, but can selectively return to the intestine due to the interaction between β7-integrins and adhesion molecules secreted by endotheliocytes (addressins, MAdCAM-1). Mammary endothelial cells synthesize MAdCAM-1 molecules during pregnancy, ensuring the selective entry of “programmed” dendritic cells containing intestinal bacteria into the gland [33]. In addition to bacteria, colostrum and mother’s milk contain T cells producing β7-integrins and plasma cells producing specific IdA [34]. There are also cytokines in milk, the composition of which depends on the immunological experience of the mother acquired during life. There is a theory suggesting the transfer of microorganisms from the baby’s mouth to the mother’s mammary gland, followed by the production of specific antibodies in her body and their entry into the child’s gastrointestinal tract [34]. The assumption is confirmed by the fact that identical bacteria are found in the mouth of the newborn and in breast milk. Gemella, Veillonella, Staphylococcus and Streptococcus [35], [36]. Although there is evidence that they are present in colostrum even before breastfeeding (even after careful hygienic treatment of the gland, samples of expressed milk contain bacteria from the skin and intestinal microbiome of the mother [37]), this still does not negate the possibility of implementing a reverse skid mechanism. In 2011, scientists from the United States found nine taxonomic units of bacteria in milk samples from 16 women. Having thus established that the microbial composition of milk is extremely diverse, they proposed the concept of the “core of the microbiome of human milk” (pic. 4) [35]. Later, it became clear that the microbiome changes throughout the lactation period. For example, colostrum is dominated by bacteria. Weissella, Leuconostoc, Staphylococcus, Streptococcus, and Lactococcus, and in the milk produced in the first six months after birth, apparently due to frequent contact with the inhabitants of the baby’s mouth, there is a “bias” towards Veillonella, Leptotrichia and Prevotella — which again confirms the theory of reverse drift [37]. Picture 4. Nine bacterial taxonomic units found in milk samples from 16 women in 2011. The observed communities turned out to be quite complex, and with the relative constancy of the composition of one group of subjects, the other showed changes over time. Maternal health also plays an important role in shaping the microbial composition of milk. In the first month of lactation, the milk of obese women is dominated by Lactobacillus, however, after six months they are replaced by representatives of the genus Staphylococcus [37], which, as studies show, begin to prevail in the intestines of obese infants, and therefore scientists have suggested the existence of a link between the features of the human milk microbiome and paratrophy in children. The gradual weaning of the baby and the transition to solid foods also play an important role in the formation of bacterial diversity. After breast—feeding is completed, bacteria typical of an adult appear in the microbiome of the baby’s intestine. Bacteroidetes, Firmicutes, and the Clostridia class: Clostridium, Ruminococcus, Faecalibacterium, Roseburia, and Anaerostipes [19], [38].

Recent studies have confirmed the important role of intestinal microflora in the development of immune protection. A review was published in Nature Reviews Immunology that highlighted the important contribution of commensal bacteria to the functioning of the intestinal epithelial barrier (Pic. 5). Picture 5. Intestinal epithelial barrier. The simple cylindrical epithelium has mechanisms of physical and biochemical adaptation to microbial colonization that maintain the integrity of the barrier. These include: actin-rich microvilli; dense contacts of epithelial cells (a); mucins that form a “sieve— for sieving glycocalyx molecules; production of various antimicrobial peptides. M cells covering Peyer’s plaques and single lymphoid follicles provide translocation of molecules from the intestinal lumen under the epithelium to antigen-presenting cells. Dendrites of specialized dendritic cells (DCS) can penetrate into the intestinal lumen through tight contacts (b). Scientists have suggested that intestinal bacteria not only stimulate its lymphoid elements, but also affect the intestinal mucosal barrier, stimulating the formation of microvilli [39], [40] and dense contacts [41]. Picture 6. The interaction between the intestinal immune system and the baby’s microbiome. The development of secondary lymphoid structures, including Peyer’s plaques and single lymph nodes, occurs in utero, long before bacterial colonization begins. With its onset, the mechanisms of interaction between the host’s immune system and symbiont bacteria are adjusted. M cells transfer bacterial antigens to dendritic cells by transcytosis, which present them, mediating the T-dependent maturation of B lymphocytes and promoting the secretion of IgA by plasma cells, which plays an important role in protecting against pathogens. Bacteria can also translocate through dendritic cells and be presented to lymph node T cells, inducing their differentiation. The lower left panel is an AMPM — associated molecular pattern with microorganisms. Under conditions of homeostasis, AMPS associated with symbiont bacteria stimulate the production of regulatory cytokines (IL-25, IL-33, thymus stromal lymphopoietin and transforming growth factor, TGF-β). Signal transduction to dendritic cells stimulates the development of regulatory T cells and promotes the secretion of IL-10.Lower right panel — In a state of dysbiosis, a decrease in the number of symbiont bacteria leads to the proliferation of pathogens. Pathogenic AMPS induce the secretion of pro-inflammatory cytokines (IL-1, IL-6, and IL-18), promoting the proliferation of effector T cells. These T cells differentiate into CD4+Th1 and Th17 and secrete IL-17, tumor necrosis factor (TNF-α) and interferon-γ (IFN-γ), which attract neutrophils to the inflammatory site, protecting the host body from pathogens. Investigating the effect of bacteria on the protective mechanisms of the intestine (Fig. 6), scientists artificially colonized bacteria Bacteroides thetaiotaomicron intestines of antimicrobial mice. The intestinal epithelial RNA was then analyzed for changes in gene expression [42]. Extensive activation of epitheliocyte genes was noted, which regulated the function of the epithelial barrier and promoted increased production of the IdA receptor. This study perfectly reflects the effect of bacterial colonization on the intestines of a newborn, because in this context it is the same, practically bacterial-free organism. All new works emphasize the important role of bacterial colonization in the formation and maintenance of mammalian health. In a recent experiment devoted to studying the functions of Toll-like receptors, a gene for an important component of innate immunity, the TLR5 receptor, located on the basolateral surface of mouse enterocytes, was knocked out. This led to the following: the mice began to overeat regularly and eventually developed a metabolic syndrome accompanied by a change in the composition of the intestinal microbiota. It has been suggested that the microbiome may serve as an indicator of the development of many diseases. But the scientists went further and transplanted the “pathological” microbiota from TLR5-deficient individuals into antimicrobial mice with a normal receptor, and those also showed signs of metabolic syndrome. That is, the microbiome may serve not only as an indicator of systemic problems, but also directly participate in their occurrence. Interestingly, dietary restriction in TLR5-deficient mice prevented the development of obesity, but not insulin resistance [43]. In general, the connection of colonization by symbiont bacteria with the development of both acquired and innate immunity has been demonstrated repeatedly. It was found that the interaction of enterocyte receptors and intestinal immune cells with microbial antigens causes a natural, self-limiting inflammatory response. In this way, the mechanisms of the innate immune response make it possible to prevent pathogens from penetrating the intestinal epithelial barrier, while distinguishing them from harmless symbionts (Pic. 6) [44], [45]. When a baby leaves the womb, it comes into contact with a large number of bacteria. And in order to avoid a continuous inflammatory reaction in response to intestinal colonization, the expression of these receptors, in particular TLR2 and TLR4, decreases [46]. Unfortunately, in children born prematurely, the described mechanisms are still immature, which often leads to the development of necrotizing enterocolitis [47]. Recent studies have shown that intestinal bacteria can also contribute to the development of immune tolerance, that is, protection against excessive immune reactions. These observations are extremely relevant for the development of possible therapeutic interventions, because many bacterial species have a quantitative advantage only in the early stages of colonization, during breastfeeding (see the chapter “Microbiome and breastfeeding”). How were the symbionts linked to immunotolerance? For example, polysaccharide And the capsules Bacteroides fragilis can interact with TLR2 receptors of intestinal dendritic cells, activating the production of anti-inflammatory cytokines that create a specific microenvironment for bacteria [48]. Some species of clostridia similarly increase the number of regulatory T-cells — controllers that suppress the immune response if the T-effectors are unreasonably rampant, thereby preventing IgE-mediated diseases [49]. Thus, specific microorganisms present in breast milk can determine the degree of an individual’s “allergy” even in infancy: these mechanisms make it possible to develop tolerance to “beneficial” antigens and bacteria, preventing the further development of allergies and autoimmune diseases.

In addition to genetic factors, the nature of delivery and feeding, the formation of the microbiome and immunity in a newborn is influenced to one degree or another by dietary habits, experience with antibiotics, and environmental factors (Pic. 7). Picture 7. Factors that ensure the formation of the baby’s microbiome. Infections of a woman’s genital tract can lead to bacterial contamination of the uterus. The intestinal and oral microflora can be transported with blood to the fetus. The nature of delivery forms the primary microflora. Genetics and postnatal factors such as diet, antibiotic use, and environmental exposure have additional effects on the microbiome. Antibiotics are one of the most commonly prescribed medications for children. Prescribing them to the mother in the postpartum period or to a newborn can disrupt the fragile processes that underlie the formation of the microbiome and cause a number of diseases (Table 1). Recent studies regularly emphasize the importance of understanding the processes leading to neonatal dysbiosis and the further development of pathologies such as type II diabetes and inflammatory bowel diseases or an allergic reaction to milk components [51-56]. Changes in the microbiome caused by antibiotics depend on the method of administration, target, type and dosage of the drug. All this is still poorly understood in infants, which makes it difficult to understand the effect of antibiotic therapy on the formation of normal microflora.

Table 1. The main factors that serve as a link between the imbalance of the microbiome at an early age and the propensity for the subsequent development of diseases. The table is from [71].

The factor causing the imbalance	Characteristics of the cohort	Outcomes
Caesarean section	1.9 million Danish children aged 0-15 years	Asthma, systemic connective tissue diseases, juvenile rheumatoid arthritis, inflammatory bowel diseases, immunodeficiency and leukemia
	1,255 three-year-olds from the USA	Obesity, high BMI
	2,803 Norwegian children 0-3 years old	Allergic reaction to chicken eggs, fish or nuts
Антибиотикотерапия	1401 children 0-6 months old from the USA	Asthma and allergies
	5,780 British children 0-2 years old	Asthma and eczema
	12,062 Finnish children 0-2 years old	Overweight and obesity
	162820 children aged 2-18 from the USA	Overweight
	9 million British children	Inflammatory bowel diseases
Probiotics	215 Spanish children 0-6 months old	Reducing the frequency of gastrointestinal and upper respiratory tract infections
	European Society of Specialists in Pediatric Gastroenterology, Hepatology and Nutrition, Nutrition Commission	Reducing the incidence of nonspecific gastrointestinal infections
Food additives	139 African children aged 6-14	Inflammatory bowel diseases are more common, and colic is less common.
Hygiene	184 children 0-3 years old (study of the purity of pacifiers)	The cleanliness of the pacifiers reduced the risk of asthma, allergies, and sensitization.
Pets	3143 Finnish children 0-1 years old	Reducing the risk of type I diabetes

It is worth mentioning separately about probiotics and prebiotics, which are widely enriched in artificial feeding mixtures, despite the lack of evidence of their effectiveness [57]. Probiotics are living microorganisms that are supposed to participate in the formation of the microbiome, while prebiotics are substances that promote the growth of beneficial microorganisms. The use of probiotics in pediatric practice is still a controversial issue, although their effect on various childhood diseases has been studied quite widely. Thus, some meta-analyses have found their effectiveness in the treatment of atopic dermatitis, while others have not revealed a significant effect on children younger than 12 months [58-61]. The impact of the most popular probiotic supplements in baby food (Lactobacillus and Bifidobacterium spp., L. reuteri) on colic in infants was evaluated. After three weeks of their use, the number of lactobacilli in the intestines of newborns increased and the content of E. coli decreased [62]. However, to date, most studies show that pre- or probiotics do not significantly affect the qualitative and quantitative composition of the intestinal microbiome. The environment is not sterile, and the household items that a newborn encounters also serve as sources of microorganisms involved in the formation of the microbiome. For example, the probability of bacterial exchange through household items and indoor air increases in proportion to the number of people living in the house. A study of 60 families from the USA revealed that members of the same family (households) have more similar microbiomes than members of different families [63]. The maximum similarity of the skin microbiota between the spouses is especially significant, as well as the exchange of surface bacterial communities between the owners and their dogs. Frequent contact with house dust components and a large family in the first two months of life can lead to changes in the microbiome associated with allergies. They consist in an increase in the number of bifidobacteria in infants (with the exception of B. adolescentis) and a decrease in the number of Lactobacillus spp., Bifidobacterium adolescentis and Clostridium difficile [64]. It is likely that frequent contact with animals, and consequently with their microbiota, has a protective effect in the first year of life, increasing immune tolerance. For example, interaction with pets from an early age reduces the risk of developing allergic conditions and asthma, but the mechanisms of this phenomenon have not yet been fully identified [65]. And after all that has been said, of course, the conclusion of scientists that bacterial diversity is much higher in rural children than in urban children will not come as a surprise [66]. In conclusion, it is worth noting that a number of bacterial strains are found simultaneously in mothers and their adult daughters, which means that some bacteria temporarily “rent” living space, while others receive a lifetime “residence permit” in the macroorganism.

Recent studies have explored therapeutic interventions that could alter the microbe and prevent microbial imbalance in early childhood. Approaches to microbiome modification, as a rule, are divided into three main groups: purification from microorganisms, their modulation and replacement, restoration of microbiota. For example, antibiotics, due to their ability to effectively cleanse the intestines of bacteria, are often used to treat conditions caused by a non-specific pathogenic microbiota (Pic. 8). Picture 8. “Microbial therapy” depending on the stage of the disease. In the preclinical stages, the disease is not yet fully manifested: its symptoms (if any) are minimal and non-specific, but subtle biological changes are already taking place. The use of cultures of certain bacterial communities in the early stages of the disease can prevent dysbiosis and the development of pathology with maximum effectiveness. As the disease progresses, the microbiome is enriched with pathogens (shown in red) that produce pro-inflammatory metabolites and thereby activate inflammatory pathways (Fig. 6). The mucous layer protected by the epithelium becomes thinner as pathogens accumulate, exacerbating the course of the disease. At this stage, diet therapy and antibiotics can be used as a radical measure that changes the quantitative and qualitative composition of bacteria. In the later stages, the continued thinning of the mucous layer allows bacteria to break through the epithelial barrier. Then aggressive antibiotic therapy combined with microbiota transplantation can help restore microbial balance. AMP is a microbial—associated molecular pattern. However, in young children, prolonged use of antibiotics is fraught with a significant risk of complications. The composition of the microbiota can also be changed through diet therapy by eating foods that promote the growth of “beneficial” microorganisms. One example of such a diet is a special enteral nutrition used for the symptomatic treatment of Crohn’s disease in children. It is a specific mixture of all the necessary micro- and macronutrients and therefore can serve as the only source of nutrients for a long time. It is supplied exclusively in liquid form — orally or through a probe — and contributes to achieving clinical remission by creating a kind of “resting mode”: reducing the functional load on the inflamed intestine and reducing its injury [67]. Research in the field of nutrition deficiency has demonstrated that today it is impossible, using diet therapy alone, to significantly influence the composition of the intestinal microbiome, although the study of the influence of nutrition on it continues. Given the significant impact on health of the microbiota in early childhood, methods aimed at timely, preventive, restoration of microbial balance look very relevant. Recently, it has been shown that the microbiome of newborns born by caesarean section can be restored to a state similar to babies born naturally. Wiping such children with tampons, which were inserted into the mother’s vagina an hour before cesarean section, led to a significant enrichment of their microbiome with representatives of Lactobacillus and Bacteroides. However, the possible health consequences of such a procedure have not yet been clarified [68]. The gut microbiome can be considered as a whole separate organ of our body. We acquire it at birth, and what it will be like depends on many factors. But one thing is for sure: it will be unlike any other microbiome. This is almost as unique a feature as the papillary lines and vascular pattern of the retina. And just as fingerprints can tell investigators the criminal history of a criminal, the gut microbiome can show scientists the milestones of its host’s ontogenesis. And the process of bacterial colonization and its significance for the body is reflected in the famous proverb: “What you sow, you reap.” Take care of your microbiome and be healthy! Source: Biomolecule