Role of serum factors in epithelial cell responses to Helicobacter pylori infection in vitro.
BACKGROUND
Gastric epithelial cell lines have been utilized extensively as tools to define aspects of the interactions between Helicobacter pylori and host epithelial cells. Fetal calf serum (FCS) is employed as a growth stimulant, but it is unclear whether this agent may in itself alter host responses.


METHODS
Two gastric epithelial cell lines were utilized to ascertain the effects of varying FCS concentration on cellular responses following H. pylori infection. Media containing 0%, 5% or 10% FCS was added to cell lines prior to infection with H. pylori of defined genotype. Cellular interleukin (IL)-8 production was measured as a marker of cellular response. Effects of altered FCS upon cell viability were also determined by trypan blue exclusion.


RESULTS
Interleukin-8 production by AGS cells following H. pylori infection was not altered by variation of media FCS concentration. However, KATO-III cells produced greater amounts of IL-8 when media was FCS-free than at 5% or 10% FCS. Although cellular viability was not altered in AGS cells exposed to varied concentrations of FCS, viability was decreased in serum-free KATO-III cells, but not when cells were kept at 5% FCS.


CONCLUSIONS
Serum-derived factors alter cellular responses to H. pylori infection in a cell-line-dependent manner and impaired cellular viability may relate to this effect. However, the mechanisms for these observations are unclear and further work is now required to determine the nature of these important interactions.
Sieveking
Daniel
D
School of Biotechnology, University of New South Wales, Sydney, New South Wales, Australia.
Leach
Steven T
ST
Mitchell
Hazel M
HM
Day
Andrew S
AS
D000818:Animals; D002417:Cattle / Q000097:blood* / Q000196:embryology*; D045744:Cell Line, Tumor; D002470:Cell Survival; D005312:Fetal Blood; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology* / Q000503:physiopathology*; D016481:Helicobacter Infections / Q000378:metabolism / Q000503:physiopathology*; D016480:Helicobacter pylori; D006801:Humans; D016209:Interleukin-8 / Q000096:biosynthesis
D016209:Interleukin-8