TY - JOUR
T1 - Human lactoferrin induces asthmatic symptoms in NC/Nga mice
AU - Nagaoka, Kenjiro
AU - Ito, Tatsuo
AU - Ogino, Keiki
AU - Eguchi, Eri
AU - Fujikura, Yoshihisa
N1 - Funding Information:
Funding Information This work was supported in part by JSPS/MEXT KAKENHI Grant Number 26670331. We thank R. Zhang at the Control of Innate Immunity Technology Research Association, 2217-16 Hayashi-cho, Takamatsu, Kagawa 761-0301, Japan, for her kind assistance.
Publisher Copyright:
© 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.
PY - 2017/8
Y1 - 2017/8
N2 - Lactoferrin in commercial supplements is known to exert anti-viral and anti-allergic effects. However, this is the first study to evaluate the induction of allergic airway inflammation in NC/Nga mice. Human lactoferrin was administered intraperitoneally with aluminum oxide for sensitization. Five days later, lactoferrin was inoculated intranasally for 5 days, and then on the 12th day, the single inoculation of lactoferrin intranasally was performed as a challenge. On the 13th day, airway hypersensitivity was assessed (AHR), a bronchoalveolar fluid (BALF) cell analysis was conducted, serum IgE and serum lactoferrin-specific IgG and IgE levels as well as the mRNA expression levels of cytokines and chemokines in the lung were measured, and a histopathological analysis of the lung was performed. Human lactoferrin increased AHR, the number of eosinophils in BALF, serum lactoferrin-specific IgG levels, and the mRNA levels of IL-13, eotaxin 1, and eotaxin 2. Moreover, the accumulation of inflammatory cells around the bronchus and the immunohistochemical localization of arginase I and human lactoferrin were detected. Collectively, these results indicate that human lactoferrin induced allergic airway inflammation in mice. Therefore, the commercial use of human lactoferrin in supplements warrants more intensive study.
AB - Lactoferrin in commercial supplements is known to exert anti-viral and anti-allergic effects. However, this is the first study to evaluate the induction of allergic airway inflammation in NC/Nga mice. Human lactoferrin was administered intraperitoneally with aluminum oxide for sensitization. Five days later, lactoferrin was inoculated intranasally for 5 days, and then on the 12th day, the single inoculation of lactoferrin intranasally was performed as a challenge. On the 13th day, airway hypersensitivity was assessed (AHR), a bronchoalveolar fluid (BALF) cell analysis was conducted, serum IgE and serum lactoferrin-specific IgG and IgE levels as well as the mRNA expression levels of cytokines and chemokines in the lung were measured, and a histopathological analysis of the lung was performed. Human lactoferrin increased AHR, the number of eosinophils in BALF, serum lactoferrin-specific IgG levels, and the mRNA levels of IL-13, eotaxin 1, and eotaxin 2. Moreover, the accumulation of inflammatory cells around the bronchus and the immunohistochemical localization of arginase I and human lactoferrin were detected. Collectively, these results indicate that human lactoferrin induced allergic airway inflammation in mice. Therefore, the commercial use of human lactoferrin in supplements warrants more intensive study.
KW - Asthma
KW - bronchus
KW - human lactoferrin
KW - inflammation
KW - lung
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U2 - 10.14814/phy2.13365
DO - 10.14814/phy2.13365
M3 - Article
C2 - 28774951
AN - SCOPUS:85027506149
SN - 2051-817X
VL - 5
JO - Physiological Reports
JF - Physiological Reports
IS - 15
M1 - e13365
ER -