Abstract
Pathogenic strains of E. coli including enteropathogenic E. coli (EPEC), enterohemorrhagic E. coli (EHEC), enterotoxigenic E. coli (ETEC) are principle causes for diarrhoea in many parts of the globe. Citrobacter rodentium (C. rodentium), a gram negative bacterium, is a murine pathogen that also utilizes type III secretion system and similar virulence factors to EPEC and EHEC and forms comparable attaching/effacing lesions in the intestines as EPEC and EHEC. The infection caused by C. rodentium in mice is usually self-limiting and results in only minor systemic effects with higher mortality in some susceptible mouse strains. All these characteristics have made the bacteria a commonly used model to study host immune responses to pathogenic E. coli infection. In this review, we focus on the impact of virulence factors of the pathogen; different immune components involved in the immune response and summarize their role during C. rodentium infection.
Highlights
We focus on the impact of virulence factors of the pathogen; different immune components involved in the immune response and summarize their role during C. rodentium infection
Collins et al demonstrated that probiotics such as Lactobacillus acidophilus, L. rhamnosus, and Lactobacillus helveticus administered daily in the form of fermented dairy products (FDPs) lessened C. rodentium induced colonic hyperplasia and stopped the loss of significant bacterial genera that might lead to disease pathology
As a result of this association with other important inflammatory diseases, and that there are cases of more than a million deaths each year from enteropathogenic E. coli (EPEC) and enterohemorrhagic E. coli (EHEC), the knowledge about the pathophysiology of C. rodentium infections and following infection how the host immune system responds to it is of immense significance to understand its subsequent function during these inflammatory diseases
Summary
Mice lacking the signalling adaptor MYD88, a myeloid differentiation primary response protein 88, which is essential for signalling by the majority of TLRs [76] [77] had greater bacterial loads both in the colon and in peripheral tissues as the bacteria penetrated deeply into colonic crypts compared to WT mice They suffered from severe colitis and death after infection. A continued bacterial load was reported in mice deficient in p38α, a mitogen-activated protein kinase (MAPK) in intestinal epithelial cells [84] These animals exhibited no apparent histological lesions, failed to recruit CD4+ T cells and had impaired chemokines expression.
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