title: Cystine improves survival rates in a LPS-induced sepsis mouse model.
abstract: OBJECTIVE
  The control of inflammation is important for suppressing severe sepsis. Oral administration of cystine and theanine have been shown to suppress inflammatory responses due to invasion. Furthermore, the uptake of cystine into monocytes is promoted by exposure to lipopolysaccharide (LPS). In the present study, the effects of cystine were examined in the context of inflammatory responses.
  
  
  METHODS
  Cystine was orally administered to mice, and the levels of interleukin (IL)-6 in the blood and spleen and the survival rates were calculated after the administration of LPS. The effects of cystine as well as neutralising anti-IL-10 antibodies on the LPS-induced production of IL-6 and IL-10 were examined in a monocyte cell line.
  
  
  RESULTS
  The oral administration of cystine reduced IL-6 levels in the blood and spleen after LPS stimulation and improved survival rates. The addition of cystine to monocytes suppressed LPS-induced IL-6 production but enhanced IL-10 production. A neutralising anti-IL-10 antibody eliminated the inhibitory effects of cystine on the LPS-induced production of IL-6.
  
  
  CONCLUSIONS
  The oral administration of cystine suppressed IL-6 production following LPS stimulation and improved survival rates in mice with LPS-induced sepsis. The enhanced production of IL-10 by monocytes may be involved in this anti-inflammatory response.
authors.affiliation: Institute for Innovation, Ajinomoto Co., Inc., Japan. Electronic address: kenji_tanaka@ajinomoto.com.
authors.forename: Kenji A K
authors.initials: KA
authors.lastname: Tanaka
authors.affiliation: Institute for Innovation, Ajinomoto Co., Inc., Japan. Electronic address: shigekazu_kurihara@ajinomoto.com.
authors.forename: Shigekazu
authors.initials: S
authors.lastname: Kurihara
authors.affiliation: Institute for Innovation, Ajinomoto Co., Inc., Japan. Electronic address: tetsuro_shibakusa@ajinomoto.com.
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Shibakusa
authors.affiliation: Nutrition Care Department, Ajinomoto Co., Inc., Japan. Electronic address: yasumasa_chiba@ajinomoto.com.
authors.forename: Yasumasa
authors.initials: Y
authors.lastname: Chiba
authors.affiliation: Research Institute for Bioscience Products & Fine Chemicals, Ajinomoto Co., Inc., Japan. Electronic address: takashi_mikami@ajinomoto.com.
authors.forename: Takashi
authors.initials: T
authors.lastname: Mikami
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D003553:Cystine / Q000494:pharmacology*; D004195:Disease Models, Animal; D005971:Glutamates / Q000494:pharmacology; D006801:Humans; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides; D051379:Mice; D009000:Monocytes / Q000187:drug effects / Q000378:metabolism; D018805:Sepsis / Q000139:chemically induced / Q000188:drug therapy*; D013154:Spleen / Q000187:drug effects / Q000378:metabolism; D015996:Survival Rate
chemical_list: D000893:Anti-Inflammatory Agents; D005971:Glutamates; D015850:Interleukin-6; D008070:Lipopolysaccharides; D016753:Interleukin-10; D003553:Cystine; C026166:theanine
keywords: Anti-inflammatory; Cystine; IL-10; IL-6; Sepsis