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The role of titanium in the altered endotoxin‐induced nitric oxide synthase expression in alveolar macrophages from titanium‐alloy‐implanted rats
Author(s) -
Yang RongSen,
Chen YiHung,
LinShiau ShoeiYn,
Liu TangKue,
Liu ShingHwa
Publication year - 2003
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.10049
Subject(s) - nitric oxide synthase , nitric oxide , phosphorylation , tyrosine phosphorylation , lipopolysaccharide , tyrosine , microbiology and biotechnology , chemistry , biochemistry , medicine , materials science , endocrinology , biology
We have found that the concentration of titanium (Ti) in the blood of patients with loosened Ti‐alloy prostheses is elevated. An increase in the levels of elemental Ti in the blood and lung tissues of rats with an alloyed‐Ti implant also has been found. The cellular reaction to elevated elemental Ti in the circulation remains unclear. We further performed experiments to examine the changes of inducible nitric oxide synthase (iNOS) expression in alveolar macrophages from alloyed‐Ti‐implanted rats. The elevation of nitrite and iNOS expression induced by lipopolysaccharide (LPS) was suppressed. The in vitro effect of a soluble form of Ti was further investigated. Ti (0.01–0.06 m M ) inhibited the LPS‐induced nitrite production and iNOS expression in alveolar macrophages from normal rats without any cytotoxic effects. LPS induced protein tyrosine phosphorylation, tyrosine‐phosphorylation of lyn (a CD14‐receptor‐associated‐tyrosine kinase), and degradation of IκB‐α protein (inhibitor of NF‐κB) in alveolar macrophages. These events were inhibited by co‐incubation with Ti. These results indicate that elemental Ti may impair iNOS expression in alveolar macrophages through the alteration of protein tyrosine phosphorylation and NF‐κB activation. The inhibitory action of Ti on cellular responses of alveolar macrophages may be anti‐inflammatory and thus may depress local defense mechanisms related to microbial killing. © 2003 Wiley Periodicals, Inc. J Biomed Mater Res 66A: 802–810, 2003