Prostaglandin Stability in Human Milk and Infant Gastric Fluid

Bedrick, Alan D.; Britton, J. Robert; Johnson, S; Koldovský, Otakar

doi:10.1159/000243122

Cited by 13 publications

(8 citation statements)

References 13 publications

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“…Furthermore, the disconnection between points of maximal PGE 2 synthesis and receptor expression levels suggests that PGE 2 may perform distinct functions at different stages of mammary development. PGE 2 via the actions of EP2/EP4 may regulate mammaryspecific cellular functions during pregnancy, whereas high amounts of PGE 2 secreted into breast milk may modulate infant physiology or immune responses (52,53). Specifically, PGE 2 may promote intestinal maturation or motility in the infant (54,55) or be cytoprotective during postnatal development of the intestinal mucosa.…”

Section: Discussionmentioning

confidence: 99%

Coupling of COX-1 to mPGES1 for prostaglandin E2 biosynthesis in the murine mammary gland

Chandrasekharan

Foley

Jania

et al. 2005

Journal of Lipid Research

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The mammary gland, like most tissues, produces measurable amounts of prostaglandin E 2 (PGE 2 ), a metabolite of arachidonic acid produced by sequential actions of two cyclooxygenases (COX-1 and COX-2) and three terminal PGE synthases: microsomal prostaglandin E 2 synthase-1 (mPGES1), mPGES2, and cytosolic prostaglandin E 2 synthase (cPGES). High PGE 2 levels and COX-2 overexpression are frequently detected in mammary tumors and cell lines. However, less is known about PGE 2 metabolic enzymes in the context of normal mammary development. Additionally, the primary COX partnerships of terminal PGE synthases and their contribution to normal mammary PGE 2 biosynthesis are poorly understood. We demonstrate that expression of COX-1, generally considered constitutive, increases dramatically with lactogenic differentiation of the murine mammary gland. Concordantly, total PGE 2 levels increase throughout mammary development, with highest levels measured in lactating tissue and breast milk. In contrast, COX-2 expression is extremely low, with only a modest increase detected during mammary involution. Expression of the G s -coupled PGE 2 receptors, EP2 and EP4, is also temporally regulated, with highest levels detected at stages of maximal proliferation. PGE 2 production is dependent on COX-1, as PGE 2 levels are nearly undetectable in COX-1 -deficient mammary glands. Interestingly, PGE 2 levels are similarly reduced in lactating glands of mPGES1 -deficient mice, indicating that PGE 2 biosynthesis results from the coordinated activity of COX-1 and mPGES1. We thus provide evidence for the first time of functional coupling between COX-1 and mPGES1 in the murine mammary gland in vivo.

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Section: Discussionmentioning

confidence: 99%

Coupling of COX-1 to mPGES1 for prostaglandin E2 biosynthesis in the murine mammary gland

Chandrasekharan

Foley

Jania

et al. 2005

Journal of Lipid Research

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“…Prostaglandins, 86 , 87 in addition to AT, are also present in significant quantities in breast milk and both are powerful stimulants of mast cell secretion of histamine. Histamine acting via the H 2 receptors is known to induce immunosuppression at high concentrations and immune stimulation at low concentrations.…”

Section: Possible Roles and Functions Of Mucosal Complementmentioning

confidence: 99%

Role and significance of the complement system in mucosal immunity: Particular reference to the human breast milk complement

Ogundele

2001

Immunol Cell Biol

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SummaryThe complement system plays an important role in a host's defence mechanisms, such as in immune bacteriolysis, neutralization of viruses, immune adherence, immunoconglutination and in enhancement of phagocytosis. The possible role of this important biological system in biological fluids on the mucosal surfaces, including breast milk, has however been largely neglected. Its contribution to the 'common' mucosal immunity is still enigmatic and largely speculative. Assessment of the complement system in human breast milk, which has so far largely been limited to different assays of the individual component proteins, is reviewed. A brief review of the classical and the alternative pathways of complement activation is presented. The potential physiological roles of various complement components and their activation fragments in human milk in particular, and other mucosal surfaces in general, are also presented. It was concluded that the complement system might play a complementary role to other immunological and non-immunological protective mechanisms on the mucosal surfaces.

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“…The neonatal spleen contains suppressor cells [26] that can depress the normally high response of adult lymphocytes. Additionally, prostaglandins, present in milk, appear to play a role in this suppression [27].…”

Section: Discussionmentioning

confidence: 99%

Maternal Selenium Nutrition and Neonatal Immune System Development

2002

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We evaluated the impact of dietary selenium intake on neonatal immune cell differentiation and function. A low selenium intake during pregnancy and lactation produced reductions in maternal plasma selenium (33%, p = 0.0001), milk selenium (36%, p = 0.001), and corresponding neonatal plasma selenium (47%, p = 0.008). Thymocytes from neonates receiving low-selenium milk showed an impaired activation in vitro (p = 0.001). The percentages of CD8 cytotoxic T cells (p = 0.03), CD2 T cells (p = 0.09), panB cells ( = 0.02), and natural killer cells (p = 0.07) were all decreased in neonates nursed by mothers fed a low-selenium diet. The results indicate that maternal selenium intake impacts neonatal selenium status which in turn influences the neonatal immune system development.

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Prostaglandin Stability in Human Milk and Infant Gastric Fluid

Cited by 13 publications

References 13 publications

Coupling of COX-1 to mPGES1 for prostaglandin E2 biosynthesis in the murine mammary gland

Coupling of COX-1 to mPGES1 for prostaglandin E2 biosynthesis in the murine mammary gland

Role and significance of the complement system in mucosal immunity: Particular reference to the human breast milk complement

Maternal Selenium Nutrition and Neonatal Immune System Development

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