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Human Milk and Atopic Disease
Key Points
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The prevalence of allergy is increasing across the world, and asthma is the most common chronic disease in children.
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The exact role of genetics and epigenetics in the development of allergy are being explored with newer research techniques.
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Exclusive breastfeeding does decrease the occurrence of eczema in the first 2 years of life, and a longer duration of breastfeeding decreases wheezing in the first 2 years of life. A longer duration of breastfeeding protects against asthma even up to 5 years of age.
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Food allergies in breastfeeding infants do occur, although the exact timing and mechanism(s) of sensitization are poorly understood. Maternal elimination diets in pregnancy and/or lactation do not prevent atopic disease, but infant avoidance of foods and maternal elimination diet may be useful in infants with diagnosed food allergies and specifically food protein–induced enterocolitis syndrome.
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An expert panel of the American Academy of Pediatrics now recommends early introduction (4 to 6 months of age) of infant-safe forms of peanuts to decrease the risk for peanut allergy in at-risk infants, including description of risk testing and amount and frequency of peanut allergen.
Atopic Disease
Atopic disease includes various clinical manifestations of allergy (atopic dermatitis [AD]/eczema, asthma, food allergy, allergic rhinitis) and multiple mechanisms of allergic reaction. The complexity of atopic disease is extended by the differing phenotypes of allergic disease (age of onset, triggers, “target organs/systems,” clinical manifestations, severity, response to therapy, and natural history), and the contribution of heredity versus exposure to specific allergens. The several different types of hypersensitivity reactions (type I—immunoglobulin E [IgE] antibody mediated; type II—antibodies mediated; type III—antigen-antibody complex mediated; type IV—activated T-cell and cytokines mediated; and types V and VI—combinations of antibody- and cell-mediated reactions) add to the complexity of atopic disease. Given this complexity and the various mechanisms and clinical manifestations of allergic disease, one should not expect a simple relationship between breastfeeding and atopic disease. Nevertheless, there is accumulating evidence that breastfeeding can offer some protection against the development of specific illnesses, AD, wheezing, and asthma. Equally important is the investigation of the active components of human milk and their contribution to the development of the infant’s gastrointestinal tract and immune system and influence on the response to environmental exposures to allergens in infancy. 1 This chapter will attempt to address some of the issues relating breastfeeding to atopic disease ( Box 17.1 ).
Box 17.1
Selected Definitions
From Greer FR, Sicherer SH, Burks AW, et al. The effects of early nutritional interventions on the development of atopic disease in infants and children: the role of maternal dietary restriction, breastfeeding, hydrolyzed formulas, and timing of introduction of allergenic complementary foods. Pediatrics . 2019;143(4):1–11. http://doi:10.1542/peds.2019-0281 .
| Allergy: | A hypersensitivity reaction initiated by immunologic mechanisms. |
| Allergenic foods: | Eight major groups of allergenic foods that account for approximately 90% of all food allergies and must be declared on labels for processed foods in the United States. These include cow milk, eggs, fish, crustacean shellfish, tree nuts, peanuts, wheat, and soybean. More than 170 foods have been described to cause allergic reactions, and additional foods (e.g., sesame) are included in labeling laws in other countries |
| Atopy: | A personal or familial tendency to produce immunoglobulin E (IgE) antibodies in response to low-dose allergens, confirmed by a positive skin-prick test (SPT) result. |
| Atopic disease: | A clinical disease characterized by atopy. Atopic disease typically refers to atopic dermatitis, asthma, allergic rhinitis, and food allergy. |
| Atopic dermatitis (eczema): | A pruritic, chronic, inflammatory skin disease that commonly manifests during early childhood and is often associated with a personal or family history of other atopic diseases. |
| Asthma: | An allergic-mediated response in the bronchial airways that is verified by the variation in lung function (measured by spirometry), either spontaneously or after pharmacologic bronchodilation. |
| Food allergy: | An immunologically mediated hypersensitivity reaction to any food, including IgE-mediated and/or non–IgE-mediated allergic reactions. |
| Allergic rhinitis: | Inflammation of the nasal passages caused by allergic reaction to airborne substances, hypersensitivity reaction initiated by local immunologic mechanisms in the nose. |
| Hypoallergenic: | Reduced allergenicity or reduced ability to stimulate an IgE response and induce IgE-mediated reactions. |
| Complementary foods: | Foods and/or beverages (liquids, semisolids, and solids) other than human milk, infant formula, and cow milk (consumed in the first year of life) provided to an infant or young child to provide micronutrients and macronutrients, including energy. |
| Infants at high risk for developing allergy: | Infants with at least one first-degree relative (parent or sibling) with documented allergic disease. |
Historical Data on Atopic Disease
The association of allergy with cow milk has been documented in the literature for decades. 2 , 3 , 4 The incidence of this allergy in the general population has been noted to increase progressively since the original comments on the subject by Rowe 5 in 1931. The incidence has reportedly increased 10 times in the last 20+ years. This increase has been attributed to increased recognition, increased incidence of exposure to known allergens, and a gradual decrease in infection as a source of morbidity, because the use of antibiotics and immunization revealed an underlying allergic component to chronic symptoms. Glaser 6 attributed the rapid increase in the development of allergic diseases during the 1950s to the abandonment of breastfeeding when safe, pasteurized milk became available. It was noted that 20% of all children had some manifestations of atopic disease by 20 years of age.
Studies of office pediatrics have shown that one-third of the visits are a result of allergy. 7 One-third of all chronic conditions in patients younger than 17 years result from allergy and one-third of lost school days from asthma. In the evaluation of 2000 consecutive, unselected newborns in pediatric practice, 50% had family histories of allergy. Grulee et al. 8 observed, as early as 1934, that eczema was seven times more common in infants fed cow milk than in breastfed infants. The incidence of atopic disease (eczema and food allergy) seemed to increase from 1997 to 2011. 9 A 2019 cross-sectional survey of 10 primary care practices in five US states included 652 children; the estimated prevalence of ever having AD was 24% (95% confidence interval [CI] 21 to 28), ranging from 15% among children under the age of 1 to 38% among those aged 4 to 5 years. The occurrence of asthma was higher among AD participants compared with those with no AD, at 12% and 4%, respectively ( p < 0.001). 10 In industrialized nations, the incidence of AD is reported to have increased two to three times in recent decades. It is estimated to affect 15% to 20% of children and 1% to 3% of adults. 11 AD notably develops early in life; 60% of individuals manifesting symptoms by 1 year of age and 90% by 5 years of age. 12
Asthma: The Most Common Chronic Disease in Childhood
Asthma is the most common chronic disease of childhood, affecting over 6 million children, according to a Centers for Disease Control and Prevention (CDC) report in 2001. 13 , 14 These data indicate that, in the United States, people with asthma (over 32 million) collectively have more than 100 million days of restricted activity and 470,000 hospitalizations annually, with more than 5000 deaths annually. Asthma hospitalization rates have been highest among black adults and children, with mortality rates consistently highest among black individuals ages 15 to 24 years. Asthma costs the American public billions of dollars every year. Worldwide, asthma is reported to affect approximately 334 million people. 15 The prevalence of self-reported asthma in children has continued to increase (10% to 15%) through 2015, with recent declines in admission rates (approximately 2/1000) and mortality rates (<2/1 million) in children. 16 Examining worldwide asthma mortality by country in 5–34 year olds, deaths have declined for 2011–2015 compared to previous years. Most countries exhibit 1–5 asthma deaths per 1 million persons, but large disparities in mortality rates exist between countries. 16 In 2016, asthma in all ages was responsible for 23.7 million Disability Adjusted Life Years (DALYs) worldwide and ranked 28th among the leading causes of burden of disease. 16 Questions remain about the increase in prevalence of asthma and its causes (genetic predisposition, allergens, exposure to smoke and air pollution, antibiotic use, and altered microbiome early in life), although the diminished morbidity and mortality are ascribed to education, treatment programs, and targeted therapies for specific phenotypes and the assessed severity of the disease. 17 , 18 , 19 , 20
Decades of investigation have resulted in conflicting results regarding avoidance of allergenic foods during pregnancy or lactation in prevention of atopic disease. There also have been numerous systematic reviews and meta-analyses trying to resolve the question of prevention and interpret the available data and what it indicates. 21 , 22 In the past, it was concluded that cow milk should be avoided for at least the first 4 months of life in children at risk for allergy. Maternal avoidance of allergens during pregnancy also produced conflicting results, except for the avoidance of cow milk during pregnancy when there was a family history of atopic disease. Maternal avoidance of cow milk resulted in lower levels of mucosal-specific IgA and a lower incidence of cow milk allergy in the infant. 23 The American Academy of Pediatrics (AAP) had previously recommended that cow milk and dairy products should be avoided in at-risk infants for the first year of life. The AAP and others have declared that soy milk has no role in the prevention of allergy. The AAP is very supportive of breastfeeding for at least 6 months and the delay in starting solids until 6 months. Some mothers with a strong history of atopic disease have attempted strict elimination diets in pregnancy and lactation to avoid sensitization of their infants. It is unclear that such elimination diets are effective. Bone turnover is increased when mothers are on elimination diets that include elimination of cow milk, cow milk products, and eggs, even when they are on supplemental calcium. Mothers who were found to have some bone mobilization for 6 months recovered quickly when breastfeeding was discontinued. 24
There are new evidence-based guidelines regarding early nutritional interventions for the prevention of atopic disease in infants and children. 22
Natural History of Food Allergy
Similar to the other atopic diseases in children, food allergy prevalence is reportedly increasing and approaching 10% in children. 25 There is concern that the literature presents an imprecise picture, including self-reporting versus confirmatory diagnosis by oral food challenge, use of selected populations in published studies, and selection bias, which would limit the application of results to the larger population. 26 Over 170 foods have been reported as causing allergic reactions, and there are eight major groups of allergenic foods (cow milk, eggs, fish, crustacean shellfish, tree nuts, peanuts, wheat, and soybean), which supposedly account for 90% of all food allergies. 22 The reported increase over time of food allergy could also be secondary to generalized awareness of the condition leading to increased self-reporting. 27
Salo et al. 28 reported prevalence estimates for sensitization to various foods in 9440 children with serum specific IgEs. In children aged 6 years and older, 44.6% had detectable serum IgEs (sIgEs), whereas 36.2% of children aged 1 to 5 years were sensitized to one or more allergens. In the children aged 1 to 5 years, 6.8% were sensitized to peanut, 21.8% to milk, and 14.2% to egg, and in children aged 6 and over 7.6% were sensitized to peanut, 5.9% to shrimp, 4.8% to milk, and 3.4% to egg. The natural history of food allergy is complicated, requiring information on the onset of clinical allergy and the later persistence or resolution of symptoms with continued exposure. It should also include careful assessment at different time points over the course of the disease by physician-supervised oral food challenge. 25 There are few longitudinal exacting studies that carefully document onset and resolution of allergy symptoms along with careful diagnosis by oral food challenge. Savage and Johns 25 summarized estimates of the age of onset and age of resolution for common food allergens ( Table 17.1 ). In a more recent review led by Savage et al., 26 specific food allergies were considered to have a high rate of resolution in childhood (milk, >50% resolution by 10 years of age; egg, approximately 50% by 9 years of age; wheat, 50% by 7 years of age; and soy, 45% by 6 years of age), and others more consistently persisted into adolescence or later (peanut 20% resolution by 4 years, and approximately 10% resolution by age 10 for tree nuts, seeds, fish, and shellfish). 26
Table 17.1
Proposed Natural History for Common Food Allergens
From Savage J, Johns CB. Food allergy: epidemiology and natural history. Immunol Allergy Clin North Am . 2015;35(1):45–59. http://doi:10.1016/j.iac.2014.09.004 .
| Food | Age of Onset | Age of Resolution |
|---|---|---|
| Egg | Infant/toddler | Early to late childhood |
| Milk | Infant/toddler | Early to late childhood |
| Peanut | Infant/toddler | Early to late childhood—uncommon |
| Adulthood | Unknown | |
| Tree nuts | Toddler/early childhood | Early to late childhood—uncommon |
| Adulthood | Unknown | |
| Soy | Infant/toddler | Early to late childhood |
| Adulthood (rare) | Unknown | |
| Wheat | Infant/toddler | Early to late childhood |
The Question of Heredity
Heredity undoubtedly plays a part in the development of allergic disease, an observation first recorded by Maimonides in his Treatise on Asthma in the 12th century. Most studies in the past 60 years have concurred with the concept of a recessive mode of inheritance. 29
Kern 30 noted that the outstanding etiologic factor in human hypersensitivity is heredity. He stated that few diseases exist in which heredity is so clearly identified and so common.
Hamburger 31 reported that children with two atopic parents had a 47% chance of developing atopic disease. One atopic parent meant a 29% chance of developing atopy, and the risk dropped to 13% with no allergic parent. In a study of asthmatic monozygotic twins, Falliers et al. 32 observed similar serum IgE, blood eosinophil counts, and positive skin tests to allergens in both twins. However, they had dissimilar responses to infection and methacholine. This finding suggests an acquired component to bronchial hyperactivity.
Genetics and Epigenetics of Allergic Disease
New technology is opening the way to studying the genetics and epigenetics of allergic disease. This includes genome-wide association studies, single nucleotide polymorphisms (SNPs), the use of omics (genomics [whole gene sequencing], epigenomics [DNA methylation, histone modification, RNA interference], transcriptomics [microarrays, single-cell RNAseq], and analysis of gene polymorphisms. For asthma, implicated genes include SNPs related to ADAM33, DPP10, PHF11, GPR , and PTGDR genes and the activation or inhibition of the Nrf2-mediated antioxidant response in the lung and genetic variants that alter prostaglandins and leukotriene activity related to nonsteroidal antiinflammatory drug–exacerbated respiratory disease (NERD). 33 , 34 , 35 , 36 Similarly, for genetic determinants of pediatric food allergy, there are a few implicated genes: FLG (filaggrin), HLA-DR and HLA-DQ (major histocompatibility complex), IL10 (interleukin [IL] 10), IL13 (IL 13) and evidence of methylation in genes for the TH1-TH2 pathways (IL1RL1, IL5RA, STAT4, IL4, CCL18) . 37 , 38 For AD (eczema), genetic variants of FLG and POSTN (periostin) may be involved. Obviously the role of the genes related to the innate immune system, skin integrity and immunity, mucosal integrity and mucosal-associated immunity, and antioxidant protection may be important, as are the genetics of T cells (TH2, Treg, and TH1, TH17, and TH22 in the skin) and B cells (IgE- and SIgA-producing cells).
Infants at High Risk for Atopy
To identify infants at high risk for developing atopy, several approaches have been suggested. Cord serum total IgE levels of greater than 100 units/mL are associated with a 5 to 10 times greater risk than lower levels. Eosinophilia and lymphocytes may prove to be markers, but, at present, only the family allergy history and the cord blood IgE have been significantly reliable predictors for recurrent wheezing. 39
Related to potential environmental risk factors for allergy, several hypotheses have been postulated, including microbial exposure (hygiene), allergen avoidance, dual allergen exposure, nutritional immunomodulation, and a variety of other hypotheses (obesity [chronic inflammatory state]; exposure to processed foods, food additives, and genetically modified foods). 40 In the 1930s, Glaser 41 speculated that if a child was at a high risk for developing allergy, prophylaxis should be able to change the outcome. The original work on prophylaxis was done by Glaser and Johnstone 42 in Rochester, New York and reported in 1953. Only 15% of a group of children whose mothers controlled their own diet in pregnancy and the infants’ diets and environments at birth did develop eczema. In contrast, 65% of the sibling controls and 52% of the nonrelated controls who received cow milk developed similar allergic illnesses. Another study was designed and carried out prospectively by Johnstone and Dutton, 43 to investigate dietary prophylaxis of allergic disease. They observed a difference of more than 10 years in the incidence of asthma and perennial allergic rhinitis in those fed soybean milk (18%) and those fed evaporated milk (50%). No infant in this study of 283 children was breastfed, however. A study of 1753 children fed breast milk, soy milk, and cow milk from birth to 6 months of age, who were followed until they were 7 years or older, was published. The children included those with high-risk, low-risk, and no-risk family histories for allergy. No difference in outcome was related to early diet, but a relationship to the family history was seen. 44
In a prospective study to identify the development of reaginic allergy, infants of allergic parents were placed in a study or control group. The study group followed an allergen-avoidance regimen, including breastfeeding. At 6 months and 1 year, the study infants had less eczema than the control infants, as well as lower serum total IgE levels. 3 The discussion of the efficacy of allergen avoidance, delayed introduction of commonly allergenic foods, and breastfeeding (exclusive and/or longer duration) to avoid food allergens and optimize the intestinal microbiome continue to be debated and studied.
Human Milk Contains Foreign Antigens and Antibodies
Human milk has been analyzed and shown to contain maternal dietary proteins. A small study of 29 women analyzed breast milk by solid-phase radioimmunoassay after the women had ingested either cow milk or a raw egg. Beta-lactoglobulin was detected in breast milk from 10 of 19 women, ovalbumin in 13 of 22 women, and ovomucoid protein in 7 of 9 women. Maximum levels of these foreign proteins in breast milk occurred at approximately 4 to 6 hours after ingestion. There was no evidence of immune complexes in the human milk. 45 Subsequent studies looking for beta-lactoglobulin by an enzyme-linked immunosorbent assay in human milk have also demonstrated its presence at baseline and after a challenge with an oral cow milk load (in 75% of women). In a small percentage of women (15%), no beta-lactoglobulin was detected. 46 , 47 In a recent study performed with enhanced detection using proteomics, the protein content of human milk was analyzed. Protein detection included 1577 human proteins and 109 nonhuman peptides. Thirty-seven nonhuman peptides were further analyzed, and 9 of these were repeatedly detected in the different human milk samples. These predominant nonhuman proteins were bovine milk products, including casein (α-S1-, α-S2-; beta-, kappa-caseins) and beta-lactoglobulin in quantities of 1 to 10 ng/μL of milk. 48
Human milk consistently contains antibodies, especially secretory IgA (SIgA), to major food proteins. The levels are influenced by the mother’s own external antigen exposure. Savilahti et al. 49 measured IgG subclass antibodies (1 to 4) and IgE to cow milk and hen’s egg in 45 infants with documented cow milk allergy based on positive oral challenge testing and skin prick test (SPT) compared with 50 children without cow milk allergy. Infants with cow milk allergy had lower IgG4 levels to alpha-casein, and IgE to beta-lactoglobulin was higher. Infants positive for SPT to egg had elevated levels of sIgG to ovalbumin, beta-lactoglobulin, and alpha-casein and IgA to alpha-casein. 49
In a study of 500 babies born to families at a high risk for allergies, one group was deliberately not given cow milk and was fed soy milk by random assignment. 50 No benefit resulted from withholding cow milk, but breastfeeding, even for a short period, was clearly associated with a lower incidence of wheezing, prolonged colds, diarrhea, and vomiting. Smoking and environmental molds were also associated with wheezing. Merrett et al. 50 concluded from this that breastfeeding played a significant role in prophylaxis, although this could be explained simply by protection against infection in the respiratory and gastrointestinal tracts. 50
The effect of breastfeeding on allergic sensitization is proposed to be both direct, through the elimination of nonhuman milk protein as an exposure to antigen, and indirect, by interfering with the absorption of antigen through the intestinal tract. 3
Enteromammary Immune System
Maternal antibodies are transferred to breastfed infants as part of what has been called the enteromammary immune system ( Fig. 17.1 ). 51 The SIgA antibody present in milk is the result of a mother’s enteric immune response to antigens in her gut. SIgA in a mother’s milk provides protection against bacterial, viral, and toxic exposures. There are older prospective studies showing that infants at high risk for atopic illness, from a hereditary standpoint, had significantly less disease when breastfed, especially if reared in a protected environment with delayed use of solid foods ( Table 17.2 ). 52 This was compared with children of similar risk fed cow milk and regular solid foods.
Table 17.2
Prevention of Atopy: Prospective Studies
Modified from Businco L, Marchetti F, Pellegrini G, Cantani A, Perlini R. Prevention of atopic disease in “at-risk newborns” by prolonged breastfeeding. Ann Allergy . 1983;51:296.
| Study | Year Published | No. of Years Followed | No. of Subjects a | Type of Milk/Feeding | Impact on Atopy b |
|---|---|---|---|---|---|
| Johnstone and Dutton | NEJM 1966 | 10 | 235 | Soy, cow | ↓ Asthma, rhinitis |
| Matthew et al. | Lancet 1977 | 1 | 53 (26) | Breast, soy | ↓ Eczema |
| Chandra | Acta Pediatr Scand 1979 | >2 | 134 | Breast | ↓ Eczema, asthma |
| Saarinen et al. | Lancet 1979 | 3 | (256) | Breast | ↓ Eczema, food allergy, asthma |
| Hamburger | Excerpta Medica 1981 | 1 | (300) | Breast | ↓ Eczema, asthma |
| Kaufman and Frick | Ann Allergy 1976, Clin Allergy 1981 | 2 | (94) | Breast | ↓ Asthma |
| Hide and Guyer | Arch Dis Child 1981 | 1 | 843 (266) | Breast <6 mo, soy, cow (maternal diet not controlled) | ↓ Eczema slight, rhinitis |
| Gruskay | Clin Pediatr 1982 | 15 | 908 (328) | Breast 4 mo, soy, cow | ↓ Breast symptoms; soy no effect |
| May et al. | Acta Paediatr Scand 1982 | 1/2 | 67 normal | Soy, cow, modern formula | ↑ Antibodies with no disease symptoms |
| Businco et al. | Ann Allergy 1983 | 2 | (101) | Breast <6 mo; soy, cow | ↓ Asthma, eczema |
| Kajosaari and Saarinen | Acta Paediatr Scand 1983 | 1 | (135) | All breast milk <6 mo; half solid foods early | ↑ Eczema/food intolerance in those fed solids |
| Moore et al. | Arch Dis Child 1985 | 1 | 525 | Study—breastfed 3 mo; control—SMA | Not clear: 74% failed to breastfeed or gave cow milk in study group |
| Zeiger et al. | J Allergy Clin Immunol 1989 | 4 | 288 | Maternal avoidance diet last trimester; controls unrestricted; mother's diet; infants given Nutramigen | ↓ Atopy 16% in restricted infants ↑ Atopy in control infants (to 27%)↓ Urticaria/GI symptoms in restricted group |
| Sigurs et al. | Pediatrics 1992 | 4 | 115 | All breastfed; 65 mothers restricted diet for first 3 mo of lactation; 50 no restrictions | ↓ Atopy/asthma among both groups↓ Greater among restricted group |
GI , Gastrointestinal; SMA , formula by Wyeth (no longer available).
a Number in study; parentheses indicate number at risk for atopy.
b Arrows indicate decrease or increase compared with control group.
Infants with a low incidence of T lymphocytes are at greater risk for developing allergies if fed cow milk rather than breast milk, according to Juto 53 and Juto and Bjorksten. 54 Infants with reduced T-cell fed cow milk also demonstrated higher serum IgE levels and peripheral eosinophil counts. Juto 53 reported that with careful prophylaxis, more than 50% of infants who had both parents with IgE levels greater than 100 mg/mL showed elevated cord and 4-month IgE levels. More than 80% of those infants whose parents had IgE levels less than 100 mg/mL, however, had both low cord blood and low 4-month IgE levels. Such data confirm the genetic effect of both maternal and paternal genes.
Hanson et al. 55 also referred to the enteromammary immune system and the functioning of the breast and infant’s intestine as an immunologic dyad . Antibodies, lymphocytes, and cytokines in breast milk contribute to the infant’s intestinal mucosal barrier, which serves as an enhanced barrier against foreign antigens with less local inflammatory response. At the same time, breast milk constituents facilitate the infant’s intestinal and immunologic development. In particular, SIgA, IgG, and IgE are found in human breast milk against cow milk proteins, which may reflect maternal exposures to potential allergens. 1 , 56 , 57 , 58 Rajani et al. 1 summarize data on immune active factors in human milk and their potential role in the development of atopic disease. Importantly, protein-specific SIgA, cytokines and chemokines are produced by lymphocytes in the breast migrated from the mother’s intestine, based on maternal exposure in her intestine (enteromammary system). Various factors in breast milk are considered in their potential role in protection against atopic disease: soluble CD14/LTR, transforming growth factor-β (TGF-β), cytokines (IL-1β, IL-6, IL-10, IL-13), polyunsaturated fatty acids (PUFAs and specifically omega-3 fatty acids and docosahexaenoic [DHA] and eicosapentaenoic acids [EPAs]), and human milk oligosaccharides. Separately the infant’s microbiome (intestinal, respiratory tract, and skin) is discussed as influenced by breast milk and its effect on the intestinal milieu and infant’s immunologic development during the period of early environmental exposure. 1 The question of how “microbial dysbiosis” in the intestine or the lung might influence the development of atopic disease is an important one to be addressed. 59 The use of “omics” will be important in future studies on the development of atopic disease in infants and the role of breast milk. Type 2 cell-mediated immunity (CMI) (with eosinophils, basophils, mast cells, CD4 + T helper 2 cells, and innate lymphoid cells) contribute directly to chronic allergic diseases (asthma, AD). Along with barrier epithelial cells (ECs) and dendritic cells (DCs) as an early line of defense at mucosal barriers foreign antigens can trigger different responses from the type 2 cell-mediated immunity (CMI), which leads to protection or development of atopic disease. Breast milk plays an important role in barrier function and immunity at mucosal barriers, which certainly plays a role in the development of atopic disease. 60
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