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Biochem Biophys Res Commun. 2010 Apr 30;395(2):238-43. doi: 10.1016/j.bbrc.2010.03.170. Epub 2010 Apr 1.

The transfer of maternal antigen-specific IgG regulates the development of allergic airway inflammation early in life in an FcRn-dependent manner.

Author information

1
Division of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.

Abstract

Asthma is a chronic inflammatory airway disease characterized by airway hyperreactivity, increased mucus production, and reversible airway contraction. Asthma is a complex genetic trait caused by environmental factors in genetically predisposed individuals. The transportation of maternal antigen-specific IgG via amniotic fluid, placenta and breast milk plays an important role in passive immunity. First, to examine whether maternal passive immunity by the transportation of antigen-specific IgG via FcRn regulates allergic airway inflammation, ovalbumin-immunized FcRn(+/-) female mice were bred with FcRn(-/-) male mice to evaluate the degree of ovalbumin-induced allergic airway inflammation of FcRn(-/-) offspring. Maternal passive immunity regulated allergic airway inflammation in an FcRn-dependent manner. Second, to examine the role of maternal antigen-specific IgG1 injection into mothers, we intravenously injected ovalbumin-specific IgG1 into wild-type or FcRn(+/-) mice immediately after they gave birth. The offspring were sensitized and challenged with ovalbumin. Antigen-specific IgG1 administered to lactating mice reduced allergic airway inflammation in their offspring in an FcRn-dependent manner. Last, to exclude the factor of maternal passive immunity other than ovalbumin-specific IgG1, we administered ovalbumin-specific IgG1 orally to offspring after birth. Oral administration of ovalbumin-specific IgG1 to offspring during the lactating period prevented the development of allergic airway inflammation in an FcRn-dependent manner. These data show that the transfer of maternal antigen-specific IgG regulates the development of allergic airway inflammation early in life in an FcRn-dependent manner.

PMID:
20362552
PMCID:
PMC3990410
DOI:
10.1016/j.bbrc.2010.03.170
[Indexed for MEDLINE]
Free PMC Article

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