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. Author manuscript; available in PMC: 2018 Jan 29.
Published in final edited form as: Mucosal Immunol. 2016 Aug 24;10(1):18–26. doi: 10.1038/mi.2016.75

Table 1.

Enterobacterial blooms in human diseases and mouse disease models

Species Source of inflammation Impact of Blooms References
Mucosa-associated symbiotic E. coli strains Patients with inflammatory bowel disease Monocolonization increased incidence of invasive carcinoma in the IL-10-deficient colorectal cancer mouse model 27
Symbiotic E. coli C. jejuni-colonized infant mice Reduced colonization resistance against C. jejuni 35
Enterobacterial species Mouse oral C. rodentium infection Unknown 34
Proteobacterial species Toll-like receptor 5-deficient mice Transient instability of the gut microbiota 28
Adherent and invasive E. coli (AIEC) Ileitis in patients with Crohn’s disease Unknown 30
E. coli isolates with heightened virulence Isolated from patients with Crohn’s disease or ulcerative colitis In vitro, enhanced capability to activate NLRP3 inflammation and resistance to macrophage killing. 42
Blooms of Klebsiella pneumoniae and Proteus mirabilis T-bet−/− ×Rag2−/−ulcerative colitis (TRUC) mouse model Oral infection with these strains elicited colitis in Rag2/ and WT adult mice 41
Salmonella and E. coli Mouse oral Salmonella model High densities of Salmonella and E. coli lead to horizontal gene transfer of the colicin-plasmid p2 from Salmonella to E. coli 98
E. coli pathobiont Ampicillin and neomycin-treated mice Multidrug-resistant E. coli capable of inducing lethal NAIP5–NLRC4 inflammasome in systemic infection 36
Enterobacterial species Clindamycin-treated mice Enhanced susceptibility to Clostridium difficile-induced colitis 29

Abbrevations: C. jejuni, Campylobacter jejuni; E. coli, Escherichia coli; IL-10, interleukin-10; WT, wild type.