title: Dietary lactoferrin alleviates age-related lacrimal gland dysfunction in mice.
abstract: BACKGROUND
  Decrease in lacrimal gland secretory function is related to age-induced dry eye disease. Lactoferrin, the main glycoprotein component of tears, has multiple functions, including anti-inflammatory effects and the promotion of cell growth. We investigated how oral administration of lactoferrin affects age-related lacrimal dysfunction.
  
  
  RESULTS
  Twelve-month-old male C57BL/6Cr Slc mice were randomly divided into a control fed group and an oral lactoferrin treatment group. Tear function was measured at a 6-month time-point. After euthanasia, the lacrimal glands were subjected to histological examination with 8-hydroxy-2'-deoxyguanosine (8-OHdG) antibodies, and serum concentrations of 8-OHdG and hexanoyl-lysine adduct (HEL) were evaluated. Additionally, monocyte chemotactic protein-1(MCP-1) and tumor necrosis factor-α (TNF-α) gene expression levels were determined by real-time PCR. The volume of tear secretion was significantly larger in the treated group than in the control. Lactoferrin administration reduced inflammatory cell infiltration and the MCP-1 and TNF-α expression levels. Serum concentrations of 8-OHdG and HEL in the lactoferrin group were lower than those in the control group and were associated with attenuated 8-OHdG immunostaining of the lacrimal glands.
  
  
  CONCLUSIONS
  Oral lactoferrin administration preserves lacrimal gland function in aged mice by attenuating oxidative damage and suppressing subsequent gland inflammation.
authors.affiliation: Department of Ophthalmology, Keio University School of Medicine, Tokyo, Japan. motoko-k@a3.keio.jp
authors.forename: Motoko
authors.initials: M
authors.lastname: Kawashima
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Kawakita
authors.forename: Takaaki
authors.initials: T
authors.lastname: Inaba
authors.forename: Naoko
authors.initials: N
authors.lastname: Okada
authors.forename: Masataka
authors.initials: M
authors.lastname: Ito
authors.forename: Shigeto
authors.initials: S
authors.lastname: Shimmura
authors.forename: Mitsuhiro
authors.initials: M
authors.lastname: Watanabe
authors.forename: Ken
authors.initials: K
authors.lastname: Shinmura
authors.forename: Kazuo
authors.initials: K
authors.lastname: Tsubota
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000284:Administration, Oral; D000375:Aging; D000818:Animals; D000890:Anti-Infective Agents / Q000008:administration & dosage / Q000494:pharmacology; D018932:Chemokine CCL2 / Q000235:genetics; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000097:blood / Q000378:metabolism; D019587:Dietary Supplements; D015870:Gene Expression / Q000187:drug effects; D007150:Immunohistochemistry; D007765:Lacrimal Apparatus / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D007766:Lacrimal Apparatus Diseases / Q000473:pathology / Q000503:physiopathology / Q000517:prevention & control*; D007781:Lactoferrin / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D046529:Microscopy, Electron, Transmission; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D013666:Tears / Q000187:drug effects / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics
chemical_list: D000890:Anti-Infective Agents; D018932:Chemokine CCL2; D014409:Tumor Necrosis Factor-alpha; D000080242:8-Hydroxy-2'-Deoxyguanosine; D007781:Lactoferrin; D003849:Deoxyguanosine