Abstract
Escherichia coli strains may be beneficial or pathogenic. Many E. coli strains that cause human disease, especially those responsible for bacteremia and sepsis, express virulence factors that impart resistance to the complement system. The bacterial amyloid curli functions in bacterial adherence and enhances the formation of biofilms. Survival of curli-producing parental and curli-deficient mutant E. coli in the context of a human complement response was evaluated using an in vivo murine model of bacteremia. Results showed that curli production enhanced E. coli survival, which suggests that curli defends against complement-mediated killing. This observation was supported by the results of in vitro assays comparing bacterial survival in human serum. Experiments in which the classical or alternative complement pathways were blocked indicated that the classical pathway is the major contributor to complement activation and that curli inhibits this activity. Our analyses indicate that curli does not appear to play a role in protecting E. coli against alternative pathway complement activation. We found that curli increases binding of E. coli cells to complement component Complement component 1q (C1q) but does not affect Complement component 3b (C3b) binding. We conclude that curli defends E. coli against complement-mediated killing via inhibition of the classical complement pathway.
Highlights
Due to its ability to adhere to biotic and abiotic surfaces, Escherichia coli is capable of successfully inhabiting varied niches including the gastrointestinal tract of vertebrates, plant surfaces, plastic, and steel [1,2]
LSR13 was cleared from the serum after a 120-min, whereas viability of MC4100 was only partially affected (Figure 4B). These results suggest that complement-mediated killing of E. coli is dependent upon the activity of the classical pathway and that curli inhibits this pathway
The protein affect Complement component 3b (C3b) is important in both the lytic complement pathway and opsonophagocytosis [43]; we evaluated binding of C3b to the bacterial cell surface
Summary
Due to its ability to adhere to biotic and abiotic surfaces, Escherichia coli is capable of successfully inhabiting varied niches including the gastrointestinal tract of vertebrates, plant surfaces, plastic, and steel [1,2]. Commensal E. coli resides within the intestine where it provides the human host with nutrients and protection against pathogenic organisms [3,4,5,6]. When coupled with risk factors such as disruption of the intestinal epithelial barrier in patients with diseases like inflammatory bowel disease and acquired immune deficiency syndrome, commensal E. coli may cross the intestinal epithelial barrier and cause systemic disease. A systemic bacterial infection may progress to septic shock, which involves a hyper-inflammatory response that can result in death [7,8]. Expression of various virulence genes by E. coli contributes to a number of pathologic conditions such as infections of the gastrointestinal tract, urinary tract, central nervous system, and bloodstream [9,10]. In the United States alone, over 6.5 million people acquire extra-intestinal E. coli infections every year; more than 100,000 cases of E. coli infection lead to sepsis [11]
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