The transfer of maternal antigen-specific IgG regulates the development of allergic airway inflammation early in life in an FcRn-dependent manner.
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.
Nakata
Kyosuke
K
Division of Respiratory Medicine, Kobe University Graduate School of Medicine, Kobe 650-0017, Japan.
Kobayashi
Kazuyuki
K
Ishikawa
Yumiko
Y
Yamamoto
Masatsugu
M
Funada
Yasuhiro
Y
Kotani
Yoshikazu
Y
Blumberg
Richard S
RS
Karasuyama
Hajime
H
Yoshida
Masaru
M
Nishimura
Yoshihiro
Y
D000818:Animals; D000941:Antigens / Q000276:immunology*; D001249:Asthma / Q000235:genetics / Q000276:immunology* / Q000517:prevention & control; D005260:Female; D015395:Histocompatibility Antigens Class I / Q000235:genetics / Q000378:metabolism*; D007116:Immunization, Passive; D007074:Immunoglobulin G / Q000008:administration & dosage / Q000276:immunology*; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000517:prevention & control; D007774:Lactation / Q000276:immunology; D008297:Male; D008431:Maternal-Fetal Exchange / Q000276:immunology*; D051379:Mice; D008817:Mice, Mutant Strains; D010047:Ovalbumin / Q000276:immunology; D011247:Pregnancy; D011961:Receptors, Fc / Q000235:genetics / Q000378:metabolism*; D012130:Respiratory Hypersensitivity / Q000235:genetics / Q000276:immunology / Q000517:prevention & control
D000941:Antigens; D015395:Histocompatibility Antigens Class I; D007074:Immunoglobulin G; D011961:Receptors, Fc; D010047:Ovalbumin; C100688:Fc receptor, neonatal