Given our findings that TLR3, TLR7, or TLR7/8 activation was sufficient to produce pregnancy-dependent hypertension and endothelial dysfunction in mice, we hypothesize that excessive TLR3/7/8 activation initiates the symptoms of PE in women, however prospective studies and earlier measures are needed. Our results suggest that TLR3, TLR7, and TLR8 play a significant role in the development of PE and may be potential therapeutic targets to diminish the severity of PE symptoms in women. Avian pathogenic Escherichia coli, a gram-negative, facultative anaerobic bacterium, causes intestinal and extraintestinal infections, septicemia, and mortality in broiler chickens. The most common infectious bacterial disease in poultry, APEC-induced colibacillosis reduces growth and egg production, thereby causing significant economic losses, as well as potentially contaminating poultry products, which generatess a risk for human health. The APEC-O1, O2, O78 serotypes of the O serogroup represent at least half of the total number of isolates, and are responsible for over 80% of human septicemia cases world wide. Except for the control of environmental conditions, such as humidity and ventilation, prevention of APEC infection usually relies on antibiotic therapy or vaccine administration. However, vaccines are not fully effective against heterologous APEC strains and there is consumer pressure to reduce the use of antibiotics in food animal production. Elucidating the host resistance mechanisms against APEC infection is a foundational step in developing sustainable strategies to enhance resistance to APEC through development of more effective vaccines and through genetic selection of poultry populations for enhanced innate resistance to APEC. Until now, the major focus in study of the host:pathogen interaction with APEC has been on the bacteria itself. Some virulence factors or genes responsible for pathogenesis or invasion capacities have been discovered in various APEC strains. With two-dimensional gel electrophoresis, one differentially expressed protein of OmpA was isolated from serum and proposed to be involved in APEC resistance. ExPEC adhesin I has been shown to play a significant role during APEC infection in chickens, as its deletion leads to reduced colonization ability and, moreover, Wortmannin complementation of the adhesin gene restored this ability. By microarray investigation and mutational analysis for confirmation, some upregulated APEC genes have been identified in APEC cultured in APEC-treated chicken serum, and these genes are predicted to contribute to APEC virulence. In addition, some other genes, such as APEC autotransporter adhesin A and ibeA have also been reported to affect APEC infection. Investigations on the host genomic response is also important, so as to reveal the molecular mechanisms of response to APEC infection. With the sequencing of chicken genome, the identification of causative genes and markers for APEC susceptibility or resistance at whole genomic or transcriptomic level is practicable and advantageous for genetic selection of poultry with enhanced resistance capabilities. Gene expression profiling by using an avian macrophage microarray revealed 981 differentially expressed chicken ESTs during phagocytosis of Escherichia coli. A similar study identified 146 common elements modulated by both APEC and M. synoviae and exposure to APEC induced higher expression of cytokine genes and genes involved in oxidative burst than M. synoviae did. Until now, very few studies at the whole transcriptome level have been reported in response to APEC infection in chicken.