scholarly journals Pediococcus acidilactici P25 Protected Caenorhabditis elegans against Enterotoxigenic Escherichia coli K88 Infection and Transcriptomic Analysis of Its Potential Mechanisms

2020 ◽  
Vol 2020 ◽  
pp. 1-17 ◽  
Author(s):  
Keqin Tan ◽  
Dun Deng ◽  
Xianyong Ma ◽  
Yiyan Cui ◽  
Zhimei Tian
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Caenorhabditis Elegans ◽  
Bile Salt ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Enterotoxigenic Escherichia Coli ◽  
Pediococcus Acidilactici ◽  
Enterotoxin Genes

Enterotoxigenic Escherichia coli (ETEC) K88 is a zoonotic pathogen. Previous studies have shown that lactic acid bacteria (LAB) have great potential in promoting health and resisting pathogenic infections; however, relatively little research has been done on the Pediococcus genus of LAB. This study is aimed at exploring the mechanisms imparted by Pediococcus acidilactici P25 against ETEC K88 in Caenorhabditis elegans. The probiotic performance of P25 was investigated in vitro. Colonization of K88 in the intestinal tract of C. elegans and abundance of enterotoxin genes were measured. In addition, the transcriptome of C. elegans infected by K88 was analyzed. The result showed that P25 possessed the ability to produce acid, as well as high tolerances to acidic and high bile salt concentrations. Coculture revealed that the growth of ETEC K88 was significantly inhibited by the presence of P25. The median survival of C. elegans fed P25 was 2 days longer than the group infected with K88 alone (P<0.01). At the same time, the number of colonizing K88 and the abundances of estB and elt were reduced by up to 71.70% and 2.17 times, respectively, by P25. Transcriptome data indicated that P25 affected expression of genes relative to innate immune response and upregulated the abundance of genes in multiple pathways of C. elegans, including peroxisome, longevity, and mitogen-activated protein kinase (MAPK) pathways. These results demonstrated that in the presence of P25, K88 colonization and their expression of enterotoxin genes were reduced. This was accomplished through the alteration of environmental parameters (pH and bile salt) as well as through the promotion of the innate immune response processes, increased longevity, and increased antipathogenic bacteria-related pathways. This work highlights the potential application of P. acidilactici P25 as a probiotic resistant to ETEC K88.

Early supplementation with Lactobacillus plantarum in liquid diet modulates intestinal innate immunity through TLR4-mediated mitogen-activated protein kinase signaling pathways in young piglets challenged with Escherichia coli K88

2021 ◽  
Author(s):  
K M Yang ◽  
C Zhu ◽  
S T Cao ◽  
X F Yang ◽  
K G Gao ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Immune Response ◽  
Innate Immunity ◽  
Protein Kinase ◽  
Innate Immune Response ◽  
Liquid Diet ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Jejunal Mucosa ◽  
Mitogen Activated Protein

Abstract This study was conducted to investigate the effects of early supplementation during 4-18 day of age with Lactobacillus plantarum (LP) in liquid diets on intestinal innate immune response in young piglets infected with enterotoxigenic Escherichia coli K88 (ETEC K88). Seventy-two barrow piglets at 4-day-old were assigned to basal or LP supplemented liquid diet (5 × 10 10 CFU·kg -1). On d 15, piglets from each group orally challenged with either ETEC K88 (1 × 10 8 CFU·kg -1) or same amount of PBS. The intestinal mucosa, mesenteric lymph node (MLN), and spleen samples were collected on d 18. Here, we found that LP pretreatment significantly decreased mRNA relative expression of inflammatory cytokines (interleukin-1β [IL-1β], interleukin-8 [IL-8], and tumor necrosis factor-α [TNF-α]), β-defensin 2 (pBD-2), and mucins (MUC1 and MUC4) in jejunal mucosa in piglets challenged with ETEC K88 (P &lt; 0.05). Moreover, LP significantly decreased the ileal mucosa mRNA relative expression of IL-8 and MUC4 in young piglets challenged with ETEC K88 (P &lt; 0.05). Furthermore, the piglets of LP+K88 group had lower protein levels of IL-8, secretary IgA (sIgA), pBD-2 and MUC4 in jejunal mucosa than those challenged with ETEC K88 (P &lt; 0.05). Besides, LP supplementation reduced the percentage of gamma/delta T cells receptor (γδTCR) and CD172a + (SWC3 +) cells in MLN, and the percentage of γδTCR cells in the spleen of young piglets after ETEC K88 challenge. Supplementation with LP in liquid diets prevented the upregulated protein abundance of toll-like receptor 4 (TLR4), phosphorylation-p38 (p-p38) and phosphorylation-extracellular signal-regulated protein kinases (p-ERK) in jejunal mucosa induced by ETEC K88 (P &lt; 0.05). In conclusion, LP supplementation in liquid diet possesses anti-inflammatory activity and modulates the intestinal innate immunity during the early life of young piglets challenged with ETEC K88, which might be attributed to suppression of TLR4-mediated mitogen-activated protein kinase (MAPK) signaling pathways. Early supplementation with LP in liquid diets regulates the innate immune response, representing a promising immunoregulation strategy for maintaining intestinal health in weaned piglets.

Macleaya cordata extract alleviated oxidative stress and altered innate immune response in mice challenged with enterotoxigenic Escherichia coli

2019 ◽  
Vol 62 (8) ◽  
pp. 1019-1027 ◽  
Author(s):  
Guiping Guan ◽  
Sujuan Ding ◽  
Yulong Yin ◽  
Veeramuthu Duraipandiyan ◽  
Naif Abdullah Al-Dhabi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Escherichia Coli ◽  
Immune Response ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Enterotoxigenic Escherichia Coli ◽  
Macleaya Cordata

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.

Loss of DNase II function in the gonad is associated with a higher expression of antimicrobial genes in Caenorhabditis elegans

2015 ◽  
Vol 470 (1) ◽  
pp. 145-154 ◽  
Author(s):  
Hsiang Yu ◽  
Huey-Jen Lai ◽  
Tai-Wei Lin ◽  
Chang-Shi Chen ◽  
Szecheng J. Lo
Keyword(s):  
Immune Response ◽  
Innate Immunity ◽  
Caenorhabditis Elegans ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Dnase Ii ◽  
C Elegans ◽  
Elevated Expression

This study uncovered NUC-1 and CRN-7 function in germline apoptosis. Mutations of nuc-1 and crn-7 led to elevated expression of five innate-immunity-related genes and demonstrated that DNase II activity is associated with an innate immune response in C. elegans.

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

scholarly journals Exogenous Gamma and Alpha/Beta Interferon Rescues Human Macrophages from Cell Death Induced by Bacillus anthracis

2004 ◽  
Vol 72 (3) ◽  
pp. 1291-1297 ◽  
Author(s):  
Jeffrey A. Gold ◽  
Yoshihiko Hoshino ◽  
Satomi Hoshino ◽  
Marcus B. Jones ◽  
Anna Nolan ◽  
...  
Keyword(s):  
Immune Response ◽  
Bacillus Anthracis ◽  
Innate Immune Response ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Human Macrophages ◽  
Mitogen Activated Protein ◽  
Host Innate Immune Response ◽  
Alpha Beta ◽  
Early Effects

ABSTRACT During the recent bioterrorism-related outbreaks, inhalational anthrax had a 45% mortality in spite of appropriate antimicrobial therapy, underscoring the need for better adjuvant therapies. The variable latency between exposure and development of disease suggests an important role for the host's innate immune response. Alveolar macrophages are likely the first immune cells exposed to inhalational anthrax, and the interferon (IFN) response of these cells comprises an important arm of the host innate immune response to intracellular infection with Bacillus anthracis. Furthermore, IFNs have been used as immunoadjuvants for treatment of another intracellular pathogen, Mycobacterium tuberculosis. We established a model of B. anthracis infection with the Sterne strain (34F2) which contains lethal toxin (LeTx). 34F2 was lethal to murine and human macrophages. Treatment with IFNs significantly improved cell viability and reduced the number of germinated intracellular spores. Infection with 34F2 failed to induce the latent transcription factors signal transducer and activators of transcription 1 (STAT1) and ISGF-3, which are central to the IFN response. Furthermore, 34F2 reduced STAT1 activation in response to exogenous alpha/beta IFN, suggesting direct inhibition of IFN signaling. Even though 34F2 has LeTx, there was no mitogen-activated protein kinase kinase 3 cleavage and p38 was normally induced, suggesting that these early effects of B. anthracis infection in macrophages are independent of LeTx. These data suggest an important role for both IFNs in the control of B. anthracis and the potential benefit of using exogenous IFN as an immunoadjuvant therapy.

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