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Mammary Gland Development is altered by LPS‐induced Maternal Inflammation
Author(s) -
Valentine Christina J.,
Hodge A E,
Dingess K A,
Heyob K M,
Rogers L K
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.104.8
Subject(s) - inflammation , mammary gland , medicine , endocrinology , saline , population , histology , p38 mitogen activated protein kinases , mapk/erk pathway , kinase , biology , andrology , cancer , microbiology and biotechnology , breast cancer , environmental health
Mothers of preterm infants have difficulty expressing adequate milk volume and often have had an inflammatory insult. We speculated that prenatal inflammation could affect mammary development and influence the MAP‐kinase pathway with a potential effect on the initiation of lactogenesis. We tested the hypothesis that systemic maternal inflammation in a murine model would alter mammary gland development histologically and induce inflammatory pathways. Pregnant C3H/HeN mice were injected with saline or LPS at embryonic day 16 (E16), and at birth the litters were placed in 85% O 2 or RA, with the dams rotated daily between O 2 and RA. The mice were sacrificed at either E19, postnatal day (D3), or day 7 (D7). Mammary glands were formalin fixed and H&E stained. Phosphorylated and total ERK, JNK, and p38 were measured in tissue homogenates by western blot Histology revealed fewer alveoli in the mammary glands and higher ERK concentrations (p=0.038) in the LPS‐treated mice than saline‐treated mice. JNK levels were significantly higher in the saline group at D3 (p=0.0087). This mammary gland model of inflammation describes an altered alveolar development and ERK and JNK pathway changes which could be the basis for the mechanism behind failure of lactogenesis in the preterm population. Funding was by intramural support from the Research Institute.