scholarly journals The impact of vitamin D on the innate immune response to uropathogenic Escherichia coli during pregnancy

2015 ◽  
Vol 21 (5) ◽  
pp. 482.e1-482.e7 ◽  
Author(s):  
N.L. Ramos ◽  
M. Sekikubo ◽  
F. Kironde ◽  
F. Mirembe ◽  
M. Sääf ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Vitamin D ◽  
Immune Response ◽  
Innate Immune Response ◽  
Uropathogenic Escherichia Coli ◽  
Innate Immune ◽  
The Impact

Tu1727 Inflammatory and Innate Immune Response Activated by Adherent-Invasive Escherichia coli Strains Isolated From Crohn's Disease Patients

2013 ◽  
Vol 144 (5) ◽  
pp. S-832 ◽  
Author(s):  
Rodrigo Quera ◽  
Marjorie De La Fuente ◽  
David Díaz-Jiménez ◽  
Roberto Vidal ◽  
Francisco López-Kostner ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Crohn’S Disease ◽  
Crohn's Disease ◽  
Innate Immune Response ◽  
Innate Immune

scholarly journals Innate Immune Response of Human Embryonic Stem Cell-Derived Fibroblasts and Mesenchymal Stem Cells to Periodontopathogens

2016 ◽  
Vol 2016 ◽  
pp. 1-15 ◽  
Author(s):  
Gopu Sriram ◽  
Vaishali Prakash Natu ◽  
Intekhab Islam ◽  
Xin Fu ◽  
Chaminda Jayampath Seneviratne ◽  
...  
Keyword(s):  
Stem Cells ◽  
Immune Response ◽  
Mesenchymal Stem Cells ◽  
Innate Immune Response ◽  
Embryonic Stem ◽  
Innate Immune ◽  
Microbial Pathogens ◽  
Multipotent Stem Cells ◽  
Cytokine Expression Profile ◽  
The Impact

Periodontitis involves complex interplay of bacteria and host immune response resulting in destruction of supporting tissues of the tooth. Toll-like receptors (TLRs) play a role in recognizing microbial pathogens and eliciting an innate immune response. Recently, the potential application of multipotent stem cells and pluripotent stem cells including human embryonic stem cells (hESCs) in periodontal regenerative therapy has been proposed. However, little is known about the impact of periodontopathogens on hESC-derived progenies. This study investigates the effects of heat-killed periodontopathogens, namely,Porphyromonas gingivalisandAggregatibacter actinomycetemcomitans, on TLR and cytokine expression profile of hESC-derived progenies, namely, fibroblasts (hESC-Fib) and mesenchymal stem cells (hESC-MSCs). Additionally, the serotype-dependent effect ofA. actinomycetemcomitanson hESC-derived progenies was explored. Both hESC-Fib and hESC-MSCs constitutively expressedTLR-2andTLR-4. hESC-Fib upon exposure to periodontopathogens displayed upregulation of TLRs and release of cytokines (IL-1β, IL-6, and IL-8). In contrast, hESC-MSCs were largely nonresponsive to bacterial challenge, especially in terms of cytokine production. Further, exposure of hESC-Fib toA. actinomycetemcomitansserotype c was associated with higher IL-8 production than serotype b. In contrast, the hESC-MSCs displayed no serotype-dependent response. Differential response of the two hESC progenies implies a phenotype-dependent response to periodontopathogens and supports the concept of immunomodulatory properties of MSCs.

scholarly journals Molecular Basis of Uropathogenic Escherichia coli Evasion of the Innate Immune Response in the Bladder

2008 ◽  
Vol 76 (9) ◽  
pp. 3891-3900 ◽  
Author(s):  
Benjamin K. Billips ◽  
Anthony J. Schaeffer ◽  
David J. Klumpp
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Urinary Tract Infection ◽  
Urinary Tract ◽  
Tract Infection ◽  
Innate Immune Response ◽  
Molecular Basis ◽  
Neutrophil Recruitment ◽  
Innate Immune ◽  
Cytokine Secretion

ABSTRACT In the urinary tract, the innate immune system detects conserved bacterial components and responds to infection by activating the proinflammatory transcription factor NF-κB, resulting in cytokine secretion and neutrophil recruitment. Uropathogenic Escherichia coli (UPEC), however, has been shown to evade the host innate immune response by suppressing NF-κB activation in urothelial cells, which results in decreased cytokine secretion and increased urothelial apoptosis. To understand the molecular basis of UPEC modulation of inflammation, we performed a genetic screen with UPEC strain NU14 to identify genes which are required for modulation of urothelial cytokine secretion. Disruption of ampG (peptidoglycan permease), waaL (lipopolysaccharide O antigen ligase), or alr (alanine racemase) resulted in increased urothelial interleukin-8 (IL-8) and IL-6 release from urothelial cell cultures. Targeted deletion of these genes also resulted in elevated urothelial cytokine production during UPEC infection. Conditioned media from bacterial cultures of NU14 ΔampG and NU14 ΔwaaL contained a heat-stable factor(s) which stimulated greater urothelial IL-8 secretion than that in NU14-conditioned medium. In a mouse model of urinary tract infection, NU14 ΔampG, NU14 ΔwaaL, and NU14 Δalr were attenuated compared to wild-type NU14 and showed reduced fitness in competition experiments. Instillation of NU14 ΔampG or NU14 ΔwaaL increased bladder neutrophil recruitment, indicating that enhanced urothelial cytokine secretion during urinary tract infection results in an altered host response. Thus, UPEC evasion of innate immune detection of bacterial components, such as lipopolysaccharide and peptidoglycan fragments, is likely an important factor in the ability of UPEC to colonize the urinary tract.

scholarly journals Modulation of Host Innate Immune Response in the Bladder by Uropathogenic Escherichia coli

2007 ◽  
Vol 75 (11) ◽  
pp. 5353-5360 ◽  
Author(s):  
Benjamin K. Billips ◽  
Sarah G. Forrestal ◽  
Matthew T. Rycyk ◽  
James R. Johnson ◽  
David J. Klumpp ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Urinary Tract ◽  
Innate Immune Response ◽  
Bacterial Colonization ◽  
Innate Immune ◽  
Upec Strain ◽  
Chemokine Production ◽  
E Coli ◽  
K 12

ABSTRACT Uropathogenic Escherichia coli (UPEC), the most frequent cause of urinary tract infection (UTI), is associated with an inflammatory response which includes the induction of cytokine/chemokine secretion by urothelial cells and neutrophil recruitment to the bladder. Recent studies indicate, however, that UPEC can evade the early activation of urothelial innate immune response in vitro. In this study, we report that infection with the prototypic UPEC strain NU14 suppresses tumor necrosis factor alpha (TNF-α)-mediated interleukin-8 (CXCL-8) and interleukin-6 (CXCL-6) secretion from urothelial cell cultures compared to infection with a type 1 piliated E. coli K-12 strain. Furthermore, examination of a panel of clinical E. coli isolates revealed that 15 of 17 strains also possessed the ability to suppress cytokine secretion. In a murine model of UTI, NU14 infection resulted in diminished levels of mRNAs encoding keratinocyte-derived chemokine, macrophage inflammatory peptide 2, and CXCL-6 in the bladder relative to infection with an E. coli K-12 strain. Furthermore, reduced stimulation of inflammatory chemokine production during NU14 infection correlated with decreased levels of bladder and urine myeloperoxidase and increased bacterial colonization. These data indicate that a broad phylogenetic range of clinical E. coli isolates, including UPEC, may evade the activation of innate immune response in the urinary tract, thereby providing a pathogenic advantage.

scholarly journals Increase of Escherichia coli Inoculum Doses Induces Faster Innate Immune Response in Primiparous Cows

2004 ◽  
Vol 87 (12) ◽  
pp. 4132-4144 ◽  
Author(s):  
F. Vangroenweghe ◽  
P. Rainard ◽  
M. Paape ◽  
L. Duchateau ◽  
C. Burvenich
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune
Sign in / Sign up

Export Citation Format

Share Document