Induction of heat shock gene expression in colonic epithelial cells after incubation with Escherichia coli or endotoxin

OBJECTIVE: The universal cellular response to stress is the expression of a family of genes known as heat shock or stress proteins. We investigated whether bacteria or bacterial products (endotoxin) can induce heat shock protein expression in human enterocytes. DESIGN: Controlled, in vitro study. SETTING: Cell culture laboratory. SUBJECTS: Human Caco-2 enterocyte cell line. MEASUREMENTS AND MAIN RESULTS: Incubation of confluent monolayers of Caco-2 cells with Escherichia coli C25 (1 x 10(9) bacteria/mL) for 1 hr at 37 degrees C was found to induce the expression of the 72-kilodalton molecular weight heat shock protein gene (heat shock protein-72), the major inducible form of the 70-kilodalton molecular weight heat shock protein family of stress proteins, as detected by Western blot analysis. The level of heat shock protein-72 induction after incubation with E. coli was similar to the response of Caco-2 cells to heat shock at 43 degrees C for 1 hr. The induction of heat shock protein-72 gene expression by E. coli was not purely due to the process of phagocytosis, since incubation of Caco-2 cells with latex beads (1 micron) failed to induce heat shock gene expression. To elucidate the possible mechanism of heat shock protein-72 induction mediated by bacteria, Caco-2 cells were incubated with E. coli endotoxin (200 micrograms/mL) for 1 hr at 37 degrees C. Such treatment was also found to induce the synthesis of heat shock protein-72. CONCLUSIONS: These results demonstrate that bacteria and/or bacterial products induce the heat shock gene expression in Caco-2 cells. Since intestinal epithelial cells are constantly in contact with bacteria and bacterial products, we speculate that the heat shock gene expression may be part of the natural mechanism of protection for these cells in the potentially harmful environment that may be present in the intestinal tract.     

Mitochondrial RNase P: the RNA family grows

Recent results of biochemical approaches and genome sequencing approaches has extended the members of the family of mitochondrial RNase P RNA genes. So far all of them are AU rich, and most of their secondary structures are easier to predict than was the structure of the first mitochondrial RNase P RNA from S. cerevisiae. The recently sequenced protozoan R. americana mitochondrial gene displays many of the evolutionarily conserved primary sequence and secondary structure attributes of the well characterized bacterial RNase P RNAs. Continued addition of RNAs to this data base should allow increasingly informative alignments and an understanding of what structural elements are dispensable in the smallest mitochondrial RNAs. The only protein subunits identified to date are Rpm2p from S.cerevisiae and the homologous protein from S. douglasii.     

Oxygen uptake and cardiac output during progressive and constant load work in patients after acute myocardial infarction

PURPOSE: Simultaneously measured oxygen uptake (VO2) and Doppler echocardiography could verify if an alteration in the VO2 response to progressive and constant load work is due to reduced cardiac output. METHODS: The study group consisted of nine patients after acute myocardial infarction (MI), five age-matched healthy subjects (HE), and five young well-trained subjects (WT). Each subject performed a progressive exercise test and two bouts of constant load work at power outputs equated to 10% below (W1) and 10% above (W2) their ventilatory thresholds. VO2 and cardiac output were measured continuously and simultaneously during the tests. RESULTS: VO2 was significantly reduced for the MI group during the initial stages of the progressive exercise test (P < .02) and remained lower throughout the entire test. During the first 60 seconds of constant load work (W2), VO2 was lower for MI (P < .05). At steady state exercise during W2, cardiac output was significantly less for MI (P < .05). VO2 for the MI group was more reliant on cardiac output during lower power outputs and differences in the arterial and venous O2 content (a-VO2 difference) during greater power outputs. CONCLUSIONS: Cardiac rehabilitation programs must be aware of this delayed VO2 and cardiac output response when setting training workloads or selecting the magnitude of the workload increments during progressive exercise tests.