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Lactoferrin Administration into the Nostril Alleviates Murine Allergic Rhinitis and its Mechanisms
Author(s) -
Wang S. B.,
Deng Y. Q.,
Ren J.,
Xiao B. K.,
Chen Z.,
Tao Z. Z.
Publication year - 2013
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12118
Subject(s) - ovalbumin , nasal administration , downregulation and upregulation , lactoferrin , allergic inflammation , endogeny , immunology , mucous membrane of nose , inflammation , medicine , messenger rna , immune system , endocrinology , chemistry , gene , biochemistry
Lactoferrin ( LF ) can downregulate allergic airway inflammation in asthma. However, the in vivo effect of exogenous LF on allergic rhinitis ( AR ), a disease attributed to airway inflammation, has yet to be determined. We investigated the effect of intranasal administration recombinant human (rh) LF and its underlying mechanisms on AR in BALB /c mice. Multiple parameters of allergic responses were evaluated to determine the effect of rhLF. We found that the number of eosinophils and goblet cells, as well as m RNA and protein expression of type 2 helper T (Th2), Th17 and regulatory T ( T reg) cells in the nasal cavity, was significantly upregulated in AR mice compared with the controls, Conversely, administration of rh LF prior to or after intranasal ovalbumin challenge markedly downregulated these same parameters. Th1‐specific m RNA and protein expression in the nasal cavity of the controls was not different from that in AR mice, but expression significantly increased with rh LF treatment. The m RNA and protein expression of endogenous LF in the nasal cavity was significantly downregulated in AR mice compared with the controls. However, after rh LF treatment, endogenous LF mRNA and protein expression was significantly upregulated. Exogenous rh LF inhibited allergic inflammation in AR mice, most likely by promoting the endogenous LF expression and skewing T cells to a Th1, but not a Th2 and Th17 phenotype in the nasal mucosa. Our findings suggest that rh LF treatment may be a novel therapeutic approach for prevention and treatment AR .