scholarly journals Molecular Cloning, Characterization, and Anti-avian Pathogenic Escherichia coli Innate Immune Response of the Cherry Valley Duck CIITA Gene

2017 ◽  
Vol 8 ◽  
Author(s):  
Rong Li ◽  
Mengjiao Guo ◽  
Jing Lin ◽  
Tongjie Chai ◽  
Liangmeng Wei
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Molecular Cloning ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Avian Pathogenic Escherichia Coli ◽  
Pathogenic Escherichia Coli ◽  
Cherry Valley Duck

scholarly journals Cloning, Analysis and Anti-Duck Tembusu Virus Innate Immune Response of Cherry Valley Duck TRIM32

2021 ◽  
pp. 101048
Author(s):  
Tianxu Li ◽  
Xiaofang Hu ◽  
Tingting Zhang ◽  
Xingdong Song ◽  
Huihui Zhang ◽  
...  
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Duck Tembusu Virus ◽  
Cherry Valley Duck ◽  
Tembusu Virus

scholarly journals Autophagy—A Story of Bacteria Interfering with the Host Cell Degradation Machinery

Pathogens ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 110
Author(s):  
Anna K. Riebisch ◽  
Sabrina Mühlen ◽  
Yan Yan Beer ◽  
Ingo Schmitz
Keyword(s):  
Escherichia Coli ◽  
Staphylococcus Aureus ◽  
Immune Response ◽  
Mycobacterium Tuberculosis ◽  
Listeria Monocytogenes ◽  
Salmonella Typhimurium ◽  
Innate Immune ◽  
Intracellular Pathogens ◽  
Response Mechanism ◽  
Pathogenic Escherichia Coli

Autophagy is a highly conserved and fundamental cellular process to maintain cellular homeostasis through recycling of defective organelles or proteins. In a response to intracellular pathogens, autophagy further acts as an innate immune response mechanism to eliminate pathogens. This review will discuss recent findings on autophagy as a reaction to intracellular pathogens, such as Salmonella typhimurium, Listeria monocytogenes, Mycobacterium tuberculosis, Staphylococcus aureus, and pathogenic Escherichia coli. Interestingly, while some of these bacteria have developed methods to use autophagy for their own benefit within the cell, others have developed fascinating mechanisms to evade recognition, to subvert the autophagic pathway, or to escape from autophagy.

Molecular cloning of a C-type lectin from Portunus trituberculatus, which might be involved in the innate immune response

2018 ◽  
Vol 76 ◽  
pp. 216-223 ◽  
Author(s):  
Xiaona Zhang ◽  
Junkai Lu ◽  
Changkao Mu ◽  
Ronghua Li ◽  
Weiwei Song ◽  
...  
Keyword(s):  
Immune Response ◽  
Molecular Cloning ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Portunus Trituberculatus

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 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
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