Maternal country of origin, breast milk characteristics and potential influences on immunity in offspring

Holmlund, Ulrika; Amoudruz, Petra; Johansson, Maria A.; Haileselassie, Yeneneh; Ongoïba, Aïssata; Kayentao, Kassoum; Traoré, Broulaye; Doumbo, Safiatou; Schollin, Jens; Doumbo, Ogobara K.; Montgomery, Scott; Sverremark-Ekström, Eva

doi:10.1111/j.1365-2249.2010.04275.x

Cited by 40 publications

(43 citation statements)

References 40 publications

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“…We also observed variation in EGF as a negative function of infant age ( Figure 4B), a result that agrees well with earlier studies (Donovan and Odle 1994). Perhaps importantly, we observed relatively elevated levels of TGF-β 2 in the milk of Aeta women, suggesting a greater exposure to infectious pathogens (Amoudruz et al 2009;Peroni et al 2010); however, median levels in Aeta and Ilocano milks (2,419 and 1,644 pg/ml, respectively) were lower than mean values from Mali (3,727 pg/ml) and Sweden (3,703 pg/ml) (Holmlund et al 2010). Such a difference highlights the potential for global variation in the baseline values of some cytokines (McDade et al 2009).…”

Section: Discussionsupporting

confidence: 79%

Mount Pinatubo, Inflammatory Cytokines, and the Immunological Ecology of Aeta Hunter-Gatherers

Bernstein

Dominy

2013

Human Biology

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Early growth cessation and reproduction are predicted to maximize fitness under conditions of high adult mortality, factors that could explain the pygmy phenotype of many rainforest hunter-gatherers. This lifehistory hypothesis is elegant but contentious in part because it lacks a clear biological mechanism. One mechanism stems from the field of human immunological ecology and the concept of inflammation "memory" across the life cycle and into subsequent generations. Maternal exposures to disease can infl uence immunological cues present in breast milk; because maternal provisioning via lactation occurs during critical periods of development, it is plausible that these cues can also mediate early growth cessation and small body size. Such epigenetic hypotheses are difficult to test, but the concept of developmental programming is attractive because it could explain how the stature of a population can change over time, in terms of both secular increases and rapid intergenerational decreases. Here we explore this concept by focusing on the Aeta, a population of former hunter-gatherers, and the Ilocano, a population of rice farmers. We predicted that Aeta mothers would produce breast milk with higher concentrations of four bioactive factors due to high infectious burdens. Further, we predicted that the concentrations of these factors would be highest in the cohort of women born in the early 1990s, when exposure to infectious disease was acute following the eruption of Mount Pinatubo in June 1991. We analyzed levels of adiponectin, C-reactive protein, and epidermal growth factor in the milk of 24 Aeta and 31 Ilocano women and found no detectable differences, whereas levels of transforming growth factor-β 2 were elevated among the Aeta, particularly as a function of maternal age. We found no difference between cohorts divided by the volcanic eruption (n = 43 born before, n = 12 born after). We discuss the implications of our findings for the terminal investment hypothesis and we suggest that the historical ecology of the Aeta is a promising model system for testing epigenetic hypotheses focused on the evolution of small body size. Abstract Early growth cessation and reproduction are predicted to maximize fitness under conditions of high adult mortality, factors that could explain the pygmy phenotype of many rainforest hunter-gatherers. This life-history hypothesis is elegant but contentious in part because it lacks a clear biological mechanism. One mechanism stems from the field of human immunological ecology and the concept of inflammation "memory" across the life cycle and into subsequent generations. Maternal exposures to disease can infl uence immunological cues present in breast milk; because maternal provisioning via lactation occurs during critical periods of development, it is plausible that these cues can also mediate early growth cessation and small body size. Such epigenetic hypotheses are difficult to test, but the concept of developmental programming is attractive because it could explain how the...

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Section: Discussionsupporting

confidence: 79%

Mount Pinatubo, Inflammatory Cytokines, and the Immunological Ecology of Aeta Hunter-Gatherers

Bernstein

Dominy

2013

Human Biology

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“…Our study indicates that whey from African-American mothers had increased levels of IL-6, IFN-γ, and CXCL8 compared with those of other racial/ethnic groups ( Table 5). Recently, Holmlund et al found that breast milk of women who immigrated to Sweden contained higher levels of TGF-β1 and CXCL8 than milk from native Swedish women (27). Country of origin seems to play a role in the concentration of CXCL8 and TGF-β1 in breast milk, which further supports the idea that race/ethnicity may influence whey cytokine levels.…”

Section: Maternal Characteristics and Other Child's Covariatesmentioning

confidence: 88%

Pre- and perinatal characteristics and breast milk immune markers

et al. 2013

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Background: Maternal allergy and gestational exposures can alter the concentration of type-1/type-2/T-regulatory markers in breast milk. We tested whether maternal risk factors are related to breast milk immune markers. Methods: Expecting mothers were enrolled in [2008][2009][2010] in South Carolina in prenatal clinics and classes. Interferon (IFN)-γ-induced protein 10 (CXCL10), CCL11, interleukin (IL)-1β, IL-4, IL-5, IL-6, CXCL8, IL-10, IL-12(p70), IL-13, transforming growth factor (TGF)-β1, and immunoglobulin (Ig)A in 115 whey samples were measured by immunoassays. Maternal asthma, eczema, rhinitis, smoking, urogenital infections during gestation, pet exposure, education, race/ethnicity, age, body mass, and the child's birth date and sex were ascertained. The effects of these risk factors on immune markers were estimated using general linear models. results: Maternal asthma was linked to higher levels of IL-5, rhinitis to lower levels of IL-5 and INF-γ, and eczema to lower levels of IL-6. Gestational smoking was related to increased concentrations of CXCL8 and IL-6. African-American mothers had markedly higher levels of IL-6, IFN-γ, and CXCL8. Urogenital infections, maternal age, body mass, child's sex, and season of birth contributed to the variation. conclusion: The impact of maternal allergies on immune markers in breast milk was small compared with that of maternal nondisease characteristics. t he prevalence of allergic diseases, including asthma, eczema, and rhinitis, has increased significantly in past decades. Studies have reported that breastfeeding may influence the development of atopic disease (1-3). Breast milk contains a large number of immune-modulating factors (e.g., cytokines, chemokines, immunoglobulins (Ig), enzymes, and hormones) that are thought not only to allow the development of the infant's immune system but also to protect the infant from infection and gut inflammation (2,4,5). Because cytokines and chemokines are significant immune-modulating agents found in breast milk, identification of factors that influence their levels in breast milk is of importance. Knowledge on breast milk immune markers will help to evaluate future disease risks of breastfed infants.Several studies have reported different concentrations of immune constituents in breast milk obtained from atopic vs. nonatopic mothers (2,4,6,7), in addition to that obtained from mothers whose children developed cow's milk allergies compared with mothers having nonallergic children (3,5). Hence, exposures to different levels of immune factors through breast milk are considered to affect the occurrence of childhood allergies. However, relatively few studies have examined factors (e.g., maternal allergy) that may alter breast milk cytokine/ chemokine and IgA levels (2,4,5,8,9). Circumstantial evidence suggests that maternal allergy may be an important factor because a history of maternal asthma, rhinitis, and eczema seems to increase the risk of allergic diseases in infants (10). Studies have reported that mothers with allergic di...

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“…TGF-β1 (30, 31, 35, 50, 68, 72, 75-77, 80, 81, 83, 122, 127, 131, 137, 148, 149, 152, 153) TGF-β2 (30,31,35,50,52,68,72,73,75,77,80,122,125,127,152) TGF-β3 (35) EGF (122) HGF (49,154) inhibitors CST3 (46,47) SERPIN-A1, A3, B1, C1, G1 (46,47) SPINT1 (46,47) Other Coenzyme A (157) β-casomorphin (158) sCD14 (8,31,72,75,77,83,131,148,153) Other factors did not differ. …”

Section: Growth Factorsmentioning

confidence: 99%

Factors affecting breast milk composition and potential consequences for development of the allergic phenotype

Munblit

Boyle

Warner

2015

Clin Experimental Allergy

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There is conflicting evidence on the protective role of breastfeeding in relation to allergic sensitization and disease. The factors in breast milk which influence these processes are still unclear and under investigation. We know that colostrum and breast milk contain a variety of molecules which can influence immune responses in the gut-associated lymphoid tissue of a neonate. This review summarizes the evidence that variations in colostrum and breast milk composition can influence allergic outcomes in the infant, and the evidence that maternal and environmental factors can modify milk composition. Taken together, the data presented support the possibility that maternal dietary interventions may be an effective way to promote infant health through modification of breast milk composition.

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Maternal country of origin, breast milk characteristics and potential influences on immunity in offspring

Cited by 40 publications

References 40 publications

Mount Pinatubo, Inflammatory Cytokines, and the Immunological Ecology of Aeta Hunter-Gatherers

Mount Pinatubo, Inflammatory Cytokines, and the Immunological Ecology of Aeta Hunter-Gatherers

Pre- and perinatal characteristics and breast milk immune markers

Factors affecting breast milk composition and potential consequences for development of the allergic phenotype

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