Transmembrane Cascade In Host Cells During EPEC Adhension

Enteropathogenic Escherichia coli (EPEC), a fecal-mouth transmission pathogen leads multiple infections in human beings, including severe diarrhea in infants, enteric and urinary tract infections in adults. Since 1970's, EPEC functions as an active cause in nosocomical infecions. The process by which EPEC infect host cells in intestinal tract observed as initial attachment →invasion and internalization→tissue damage. Recently, it has been demonstrated that EPEC can trigger off a cascade of host cell signals which fascilitates the intimate attachment and invasion of bacteria.Our research reported here showed:1 GTP analogue guanosine-5'-o-(3-[³⁵S]thio) triphosphate ([³⁵S]GTP γ S) binding test demonstrated that adherence of EPEC improved the binding of host cell membrane to GTP . E7, a piliated EPEC strain had a markedly stronger effect than H511, a non-piliated EPEC strain. The results suggested that receptors for bacterial binding could be a G protein coupled structure.2 Free calcium in cytoplasm was sharply increased by EPEC adhesion as shown by the pictures shot in the laser confocal microscope in which Fluo-3/AM, a membrane-permeate Ca²⁺ probe was used to bind and label calcium molecules in cytoplasm. Both E7 and H511 had the Ca²⁺-increasing effect though the later had a meager function.3 When Staph. aureus and a-hemolytic streptococcus, the Gram positive bacteria , which without outer membrane structure were tested in our system by the incubation of bacteria with host cells, neither GTP γ S binding nor calcium accumulation were found. However, the intact outer membrane isolated from EPEC could mimic the function of the bacteria cells in the improvement of GTPγS binding as well as Calcium accumulation in host cell.4 Ca2* increase in host cells as well as a result of EPEC binding was partially inhibited by either Dantrolene, a Ca2* release inhibitor or carrying out the experiment in Ca2* -free medium. The result suggested that Ca2* increased in host cells by both cytoplasmic Ca2* store release and Ca2* influx.