**2. The function of the intestinal microbiota**

The microbiome is considered as an active organ because of manufacturing intrinsic signals for shifting postnatal development, inspiration of tolerance

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*Probiotic Bacteria in Microbiome against Allergy DOI: http://dx.doi.org/10.5772/intechopen.93385*

pathogens [38–42].

substances [44].

mechanisms and immunogenicity reduction, and resistance against invasive

Consuming substrates of the microbiota containing fibers and mucins provides additional energy for the host as fatty acids [43]. Amines, sulfides, and ammonia are the products of them, which are detrimental metabolites for the human.

The protective barrier function against the invasive microbes by their colonization in the intestine is another potential of the microbiota. Different mechanisms for the resistance colonization of the microbiota are considered, such as competition for nutrients and connection to the binding sites and secretion of the antimicrobial

Stimulation of the innate signaling pathways through the straight cell-to-cell communications or secretion of short-chain fatty acids (SCFA) are the other regulatory actions of the microbiota. SCFAs produced by the microbiota can direct

The role of maternal microbiota in the process of preventing allergy has been proven. Infants from allergic parents are at least twice more likely to the risk of developing allergic diseases than nonallergic parents. Microbiota diversity exists between allergic and nonallergic persons. Reduction in the fecal diversity of the bacteroidetes in pregnancy is connected with the prevalence of atopic eczema in their young children [49]. The microbiota of healthy infants with nonallergic parents frequently consists of healthy lactobacilli, representing the role of maternal microbiota in preventing allergic disorders. A decrease in the number of lactobacilli and bifidobacteria and an increase in the colonization of *Staphylococcus aureus* and *Clostridium difficile* are associated with the development of allergic disorders later in life, which shows the abnormality even before the onset of the allergy [50, 51]. Apart from quantitative alterations, qualitative alterations are important in the microbiota. For example, the microbiota of infants suffering from atopic dermatitis (AD) consists of mostly *B. adolescentis* which is mainly forming adult microbiota, whereas *B. bifidum* is the fundamental former of the healthy breastfeeding infants [52, 53]. Bifidobacteria of atopic dermatitis infants encourage the secretion of proinflammatory cytokines, whereas the bifidobacterium of healthy ones encourages the secretion of anti-inflammatory cytokines [54]. Besides, these bifidobacteria have different adhesion behaviors to Caco-2 tissue culture cells [55] and intestinal mucus [56], which seems to be the reason for the reduction in stimulating the immune system. And at last, the metabolic activity of the microbiota composition is different too. Higher levels of butyrate, isovalerate, and caproate in the fecal matter of children with high risk for developing allergy in comparison with normal

The intestine, the largest immune organ of the body, which is the source of the most antibody-producing cells [58] is the target of triggering maturation of the immune system or the restoration of the impaired commensal bacteria. Stimulation of the immune system is one of the most impressive functions of the resident microbiota of the intestine. Probiotic bacteria are considered as a safe solution for modulation of diminished commensal composition and also as influencer of the immune system in preventing allergic disorders [59]. Lactic acid bacteria and

intestinal Treg cells and inhibit pro-inflammatory responses [45–48].

**3. The intestinal microbiota of allergic ones**

children are the confirmation of this claim [57].

**4. Stabilizing intestinal bacterial flora**

*Probiotic Bacteria in Microbiome against Allergy DOI: http://dx.doi.org/10.5772/intechopen.93385*

*Human Microbiome*

sensible now.

autoimmune disease [12, 15–19].

seems to be beneficial to prevent the T helper cell type-2 (Th2)-mediated allergic disease [10]. Th2 phenotype is the dominant one in newborns [11] to prevent rejection in utero. Skewing to Th2 in the immune system leads to the stimulated secretion of IgE by B cells and hence to allergies as seen in germ-free mice with the same condition that results in greater IgE responses to food antigens and failure in producing the proper amount of regulatory T cell (Treg) responses [12–14]. On the other hand, upsurge in the amount of T helper cell type-1 (Th1) also mediates the

Restoring Th1/Th2 is the significant role of the microbiota [20]. The association of microbiota and the immune system is mutual. This engagement results in different signaling pathways through the immune system's molecules that increase immune responses [21]. These regulations are crucial for maintaining the homeostasis of the host and for the prevention of different diseases by inducing secretion of IgA and regulatory T cell (Treg) and stimulation of tolerance in face of common antigens [22]. So the formation, maintenance, and heterogeneity of microbiota are necessary during early life owing to their regulatory and tolerance properties in the immune system [23, 24], as it was confirmed that the lack of microflora during a short time in early life results in defection in immune regulation [15]. The mechanisms of oral tolerance which are necessary to suppress excessive immune reactions to antigens are mediated by Foxp3þ Treg [25] and IgA, which is known as the most abundant immunoglobulin and is vital in establishing the composition of micro-

Although, it is observed that abnormal IgA responses lead to allergy development [28]. So the obligation of equilibrium of the allergy mediators is more

Lack of genetic elements such as Toll-like receptors that cause enterocyte proliferation like TLR4 and CD14, which enhance the detection of bacterial LPS by TLR4, and TLR9, which identify the genetic molecules of the microorganisms, also

As the priority of the microbiome is proven, some factors are mentioned as follows, to support their presence and diversity in the body. Mode of birth; surgical or natural delivery, the process of contacting microflora in the first moment of the presence. Breast or formula feeding; the extension of contact with microflora. Nutritional patterns; the habit of food, based on people's patterns to eat fatty and fast foods or healthy ones like prebiotics which are considered beneficial for even the microbiota of the host. Antibiotics; the matter of using antibiotics at an early age or the trouble of overuse of them in all ages which impair normal flora. Locality; living in urban areas with all of the stresses, less interaction with nature in contrast with living in rural areas results in losing ancient commensal microbiota. Environmental factors; contacting people or animals. Hygiene; the obsession behaviors or normal ones. Lifestyle; the matter of activity or sedentariness in someone's lifestyle.

Natural delivery and breastfeeding are the first two initial and essential exposures when the immune system is not still mature and needs antigens to active oral tolerance [18, 25, 31]. Contravention of these simple factors grounds reformed patterns of early settlement which may result in the incidence of allergy [32]. Food sensitization especially milk allergy and atopic eczema are examples of reduced gut

The microbiome is considered as an active organ because of manufacturing intrinsic signals for shifting postnatal development, inspiration of tolerance

biota [26] and strengthening the mucosal barrier function [27].

increase susceptibility to allergies [29, 30].

**140**

microbial diversity [33–37].

**2. The function of the intestinal microbiota**

mechanisms and immunogenicity reduction, and resistance against invasive pathogens [38–42].

Consuming substrates of the microbiota containing fibers and mucins provides additional energy for the host as fatty acids [43]. Amines, sulfides, and ammonia are the products of them, which are detrimental metabolites for the human.

The protective barrier function against the invasive microbes by their colonization in the intestine is another potential of the microbiota. Different mechanisms for the resistance colonization of the microbiota are considered, such as competition for nutrients and connection to the binding sites and secretion of the antimicrobial substances [44].

Stimulation of the innate signaling pathways through the straight cell-to-cell communications or secretion of short-chain fatty acids (SCFA) are the other regulatory actions of the microbiota. SCFAs produced by the microbiota can direct intestinal Treg cells and inhibit pro-inflammatory responses [45–48].
