Abstract
Enteroaggregative Escherichia coli (EAEC) is emerging as a significant diarrheal pathogen in multiple population groups. Like any other enteropathogen, EAEC may encounter life-threatening levels of inorganic acids (H+) during their natural route of infection. In this study, we showed that EAEC orchestrates acid tolerance by modulating the levels of acid-induced outer membrane proteins (OMP). EAEC (T8) was grown in vitro by mimicking in vivo pH conditions of both in stomach and intestine. The lowest pH where EAEC showed growth was 4.0 in Luria Bertani (LB) media, and surprisingly during log phase two de novo OMP of sizes 41 kDa and 48 kDa were exclusively observed at this pH. Further, acid-induced proteins at pH 4.0 were identified by 2D gel electrophoresis and Matrix Assisted Laser Desorption Ionization-Time of Flight (MALDI-TOF). The role of the most notable acid/pH response regulator rpoS in ASP expression was determined by gene knockout in the clinical strain EAEC (T8). Mutation of rpoS gene suppressed growth and downregulated the expression of ASP in EAEC (T8) at pH 4.0 confirming probable role of rpoS in EAEC.
Highlights
Gastric juice is the first line of bactericidal barrier, but in our study Enteroaggregative Escherichia coli (EAEC) (T8) has shown survival in vitro at pH 4.0, which is comparatively higher than the gastric pH
During infection in the stomach, the bacteria are already in the stationary phase and it is well reported that the survival potential of stationary phase or acid-adapted cells is greater than that of exponentially growing cells over the initial period of acid challenge
Our results showed the expression of acid-induced outer membrane proteins (OMP), which could provide a protective effect increases at pH 4.0
Summary
It has been shown that EAEC can induce growth impairment and malnutrition among children even without diarrhea (Nataro et al, 1998). The defining feature of EAEC is its ability to elicit characteristic “stacked brick” like aggregative adherence (AA) to HEp-2 cells. EAEC infections are mediated by 60MDa plasmid (pAA) encoding aggregative adherence fimbriae (AAF) for AA phenotype to human erythrocytes, and clump and biofilm formation (Bhardwaj et al, 2006). EAEC isolates express chromosome-encoded virulence markers such as the 116 kDa secreted mucinase, Pic (a protein involved in intestinal colonization) (Henderson et al, 1999). EAEC pathogenesis involves production of mucus-containing biofilm, which leads to mucoid stools and persistent colonization. EAEC leads to an inflammatory response with cytokine release, mucosal toxicity and intestinal fluid secretion by enterotoxins (Fagundes-Neto et al, 2000)
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