Microbiota in Healthy Individuals: Comparison
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Please note this is a comparison between Version 2 by Conner Chen and Version 1 by Vasile Valeriu Lupu.

Although the microbiome is dynamic, changing in relation with human age and health status, there is an equilibrium between different types of species maintaining eubiosis and sustaining an absence of pathology. “All diseases begin in the gut” is an ancient quote that still maintains its truth: alteration of the composition and function of the healthy microbial structure leads to dysbiosis, resulting in various gastrointestinal (GI) disorders, systemic metabolic diseases, and neurological impairments.

  • microbiome
  • human
  • digestive pathology

1. Introduction

It is known that humans are living ecosystems including human cells as well as microorganisms. The population of microorganisms found in our body or on its surface consists of bacteria, viruses, fungi and protozoa, and it is called microbiota, while the term “microbiome” is used to describe their genomes [1,2][1][2].
The human microbiome can be found on the skin, in the oral cavity, in the gastrointestinal (GI) tract, the respiratory tract, and the genitourinary tract, including epithelial barriers and body fluids; however due to the bioavailability of nutrients; the largest concentration and diversity of microbiota can be found in the GI tract. Studies estimate that the human GI microbiota accounts for about 1012 microbes per gram of content, representing around 5000 distinct species [2,3][2][3]. Interactions between the human and its associated microbiota involve numerous complexities with implications in various immunological, neuronal, metabolic and endocrine responses attained through multiple biological systems such as the intestinal neuro-immune axis [2,3,4,5][2][3][4][5].
The medical literature illustrates the idea that all individuals share a core microbiome; however, each individual has a unique composition and diversity of microbes [6]. Although the microbiome is dynamic, changing in relation with human age and health status, there is an equilibrium between different types of species maintaining eubiosis and sustaining an absence of pathology [1,3][1][3]. “All diseases begin in the gut” is an ancient quote that still maintains its truth: alteration of the composition and function of the healthy microbial structure leads to dysbiosis, resulting in various GI disorders, systemic metabolic diseases, and neurological impairments. Many of these affections depend on their metabolic programing early in life and can be alleviated or prevented through early intervention via flora disruption [7,8][7][8].
Besides bacteria, the human body is host to an impressive amount of viruses, their number exceeding even 10 times the number of commensal bacteria [9]. The human virome has a specific site composition over different anatomical segments of the human body. The largest number of viruses is found in the GI tract. The GI virome has a highly individualized composition, depending on age, diet, lifestyle and geographical location. Its composition consists of both DNA and RNA viruses, in addition to prokaryotic and eukaryotic viruses. Similar to human microbiota, the human GI virome composition and diversity changes over time, evolving gradually to its stable adult form. Infants within their first days of life are characterized by high phageome and a low bacteriome diversity, shifting to a low phageome and a high bacteriome diversity across the age of two years [9,10,11][9][10][11].
In the past, fungi were studied as individual species as they were considered human pathogens. CurrSoment studies showed that fungi are a component of the human body’s ecosystem, described as the human “mycobiome”. Similar to the bacterial and viral microbiome, the mycobiome has a variable composition shaped by several factors [12]. The presence of the mycobiome has been detected in the gut of at least 70% of healthy adults [13]. Ascomycota is the most prevalent phylum, covering 48% to 99% of all present species. In contrast, Basidiomycota is the less abundant phylum, ranging between 0.5% to 14% of identified microscopic fungi, followed by the phylum Mucoromycota [14,15][14][15]. Two mycotypes can be distinguished in the gut. Mycotype 1 is defined by a high abundance of the genus Saccharomyces and also other unclassified genera, while mycotype 2 consists of the genera Penicillium, Malassezia and Mucor [12].

2. Microbiota in Healthy Individuals

The gastrointestinal tract harbors the largest number of microorganisms from the human body, as it offers a favorable habitat and plentiful nutrients for a great diversity of microbial species. Concurrently, the GI represents the site of the most extensive network of communication systems between the commensal flora and the immune system. The acquired and the innate immunity ensure the immune homeostasis and tolerance for the GI flora [5,16,17][5][16][17]. GI flora is represented by five primary bacteria phyla: Firmicutes (synonym Bacilliota) and Bacteroides (synonym Bacteroidota) phylum predominate the microbiome, while Actinobacteria (synonym Actinomycetota), Proteobacteria (synonym Pseudomonadota) and Verrucomicrobia phylum are found in modest proportions, similar in healthy adults, however there are notable changes in the interindividual variation of genus and species, conditioned by genetic and environmental factors [1,18][1][18]. Unlike the human genome, which is inherited from siblings, the human microbiome is something we acquired and changes its composition during one’s existence. For decades it was considered that the uterus is sterile; however, recent studies have proven that the development of the microbiome starts during prenatal life and continues during birth, breastfeeding and throughout senescence [2,3,19,20][2][3][19][20]. Pre- and postnatal microbial stimulation is essential for developing T-helper type 1 (Th1) and regulatory-T cells (Treg) mediated immune responses [21,22,23][21][22][23] The infant’s future microbiome depends on his mother’s gut and urogenital flora, however the mechanisms that ensure the passing of the microbes from mother to fetus are not fully understood. Studies analyzing infants’ meconium, the first stool after birth, were found to have no difference in bacterial composition, regardless of their delivery method. On the contrary, when compared to placental and amniotic fluid, there was an approximately 50% percent matching with meconium microbes, probably as a result of amniotic fluid ingestion during pregnancy and in utero colonization [19]. Babies born naturally through the birth canal have a microbiota similar to their mother’s vaginal and fecal microbiota (Lactobacillus and Bifidobacterium genera), while infants delivered through cesarean section receive germs from their mother’s skin and the surrounding environment (Staphylococcus, Corynebacterium, and Propionibacterium genera). Regarding the time of delivery, preterm infants’ microbiota is characterized by a reduction in Bifidobacterium and Bacteroides species with a secondary increase in the number of potentially pathogenic bacteria [2]. During pregnancy, different factors such as the mother’s diet, antibiotic exposure, stress and health status seem to have a certain influence on the fetuses early colonization and state of well-being [2]. Maternal obesity as well as an inappropriate diet leads to a reduction in infant gut bacteria, with low levels of Bifidobacterium, similar to the microbiota of obese adults [19]. There is an increased risk of overweight, asthma and inflammatory bowel disease (IBD) in childhood linked to an early exposure to antibiotics prenatally and in infancy [2,19,22][2][19][22]. The early administration of antibiotics leads to lower levels of Bifidobacterium and Lactobacillus genera, while pathogens such as Staphylococcus, Streptococcus, Serratia, and Parabacteroides genera increase in number. A decrease of 25% in microbiota diversity has been identified after only 7 days of antibiotic use. Based on their spectrum of antimicrobial intensity, some antibiotics are associated with more than 2 years of disruptive damages in the gut microbial environment: clindamycin decreases Bacteroides diversity, clarithromycin and ciprofloxacin have a similar effect on Actinobacteria and Ruminococcus spp., while vancomycin reduces Bacteroides, Ruminococcus and Faecalibacteria populations [24]. Antibiotics resistance genes, found in the maternal microbiome, were also identified in infant perinatal stool samples. A stress related maternal microbiome, it is associated with higher rates of allergy and gastrointestinal issues in infants and lower rates of Bifidobacterium and Lactobacillus spp. in their gut [19]. Apart from the mother’s influence during pregnancy and early childhood, genetics seem to be responsible for similarities found between family members’ microbiota. As an example, when compared to dizygotic twins, monozygotic twins tend to have more similar features regarding their GI microbiota. Children with siblings are more likely to have more Bifidobacterium than families with a single child [2,4,18][2][4][18]. Feeding practices also play a major role in the development of the infant’s microbiota. Enterococcus, Enterobacteriaceae, Bacteroides, Clostridium and Streptococcus genera are dominating the flora of formula-fed infants. Breast milk, through its nutrients and bioactive compounds, promotes the growth of beneficial bacteria like lactobacilli and bifidobacteria, encouraging healthy immune function as an important supporter of the child’s health condition. When shifting from milk to solid foods, a toddler’s microbiota becomes enriched, with Bacteroidota and Bacilliota phylum dominating the gut [2,24][2][24]. In children between 2–5 years of age, it is observed that a stable adult-like microbiota is achieved, although the microbial composition continues to gradually enrich its diversity until the age of 7–12 years, with Bacilliota and Actinomycetota phylum in greater proportion than that found in adult microbiota. As children age, their microbiota diversifies, gradually achieving a the status similar to adult microbiota [4]. Geographical distribution, with its locally inclined food consumption cultures and preferences, dietary habits such as high levels of saturated fat, sugar and a low fiber intake have been linked to a pro-inflammatory microbiota with reduced diversities. Alcohol and tobacco use and a sedentary lifestyle negatively influence the GI microbiota. Socioeconomic status, pollution and household pets also interfere with normal microbiome composition [4,18,25][4][18][25].

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