scholarly journals Absence of Nucleotide-Oligomerization-Domain-2 Is Associated with Less Distinct Disease in Campylobacter jejuni Infected Secondary Abiotic IL-10 Deficient Mice

2017 ◽  
Vol 7 ◽  
Author(s):  
Markus M. Heimesaat ◽  
Ursula Grundmann ◽  
Marie E. Alutis ◽  
André Fischer ◽  
Stefan Bereswill
Keyword(s):  
Campylobacter Jejuni ◽  
Distinct Disease ◽  
Nucleotide Oligomerization ◽  
Deficient Mice ◽  
Nucleotide Oligomerization Domain ◽  
Oligomerization Domain

scholarly journals Campylobacter jejuni infection of conventionally colonized mice lacking nucleotide-oligomerization-domain-2

Gut Pathogens ◽  
2017 ◽  
Vol 9 (1) ◽  
Author(s):  
Stefan Bereswill ◽  
Ursula Grundmann ◽  
Marie E. Alutis ◽  
André Fischer ◽  
Markus M. Heimesaat
Keyword(s):  
Campylobacter Jejuni ◽  
Nucleotide Oligomerization ◽  
Nucleotide Oligomerization Domain ◽  
Oligomerization Domain

scholarly journals Immune responses upon Campylobacter jejuni infection of secondary abiotic mice lacking nucleotide-oligomerization-domain-2

Gut Pathogens ◽  
2017 ◽  
Vol 9 (1) ◽  
Author(s):  
Stefan Bereswill ◽  
Ursula Grundmann ◽  
Marie E. Alutis ◽  
André Fischer ◽  
Anja A. Kühl ◽  
...  
Keyword(s):  
Immune Responses ◽  
Campylobacter Jejuni ◽  
Nucleotide Oligomerization ◽  
Nucleotide Oligomerization Domain ◽  
Oligomerization Domain

scholarly journals Nod2 Protects the Gut From Experimental Colitis Spreading to Small Intestine

2019 ◽  
Vol 14 (5) ◽  
pp. 669-679 ◽  
Author(s):  
Ziad Al Nabhani ◽  
Dominique Berrebi ◽  
Christine Martinez-Vinson ◽  
Nicolas Montcuquet ◽  
Chrystele Madre ◽  
...  
Keyword(s):  
Small Intestine ◽  
Experimental Colitis ◽  
Rectal Injury ◽  
Intestinal Epithelial ◽  
Innate And Adaptive Immunity ◽  
Nucleotide Oligomerization ◽  
Deficient Mice ◽  
Nucleotide Oligomerization Domain ◽  
Trinitrobenzene Sulphonic Acid ◽  
Oligomerization Domain

Abstract Background and Aims Nucleotide oligomerization domain 2 [NOD2] mutations are key risk factors for Crohn’s disease [CD]. NOD2 contributes to intestinal homeostasis by regulating innate and adaptive immunity together with intestinal epithelial function. However, the exact roles of NOD2 in CD and other NOD2-associated disorders remain poorly known. Methods We initially observed that NOD2 expression was increased in epithelial cells away from inflamed areas in CD patients. To explore this finding, Nod2 mRNA expression, inflammation, and cytokines expression were examined in the small bowel of wild-type [WT], Nod2 knockout and Nod2 mutant mice after rectal instillation of 2,4,6-trinitrobenzene sulphonic acid [TNBS]. Results In WT mice, Nod2 upregulation upstream to rectal injury was associated with pro-inflammatory cytokine expression but no overt histological inflammatory lesions. Conversely, in Nod2-deficient mice the inflammation spread from colitis to ileum and duodenum. Conclusions Nod2 protects the gut from colitis spreading to small intestine.

scholarly journals Stimulation of Nucleotide Oligomerization Domain and Toll-Like Receptors 2 to Enhance the Effect of Bacillus Calmette Guerin Immunization for Prevention of Mycobacterium Tuberculosis Infection: Protocol for a Series of Preclinical Randomized Controlled Trials (Preprint)

2018 ◽  
Author(s):  
Michael Eisenhut
Keyword(s):  
Innate Immunity ◽  
Mycobacterium Tuberculosis ◽  
Bacillus Calmette Guerin ◽  
Infection Rates ◽  
Ifn Gamma ◽  
Prevention Of Infection ◽  
Nucleotide Oligomerization ◽  
Stimulation Of ◽  
Nucleotide Oligomerization Domain ◽  
Oligomerization Domain

BACKGROUND Bacillus calmette guerin (BCG) immunization has been associated with a reduction in Mycobacterium tuberculosis (MTB) infection. BCG immunization has been shown to enhance innate immunity. This effect of BCG can be explained by an enhancing effect on innate immunity. OBJECTIVE This study aimed to test the following hypotheses: (1) BCG immunization can prevent infection with MTB, (2) prevention of infection occurs via stimulation of NOD2 (nucleotide oligomerization domain) and toll-like receptors 2 (TLR2), and (3) the effect of BCG immunization on prevention of infection with MTB can be enhanced by giving stimulators of NOD2 and TLR2. METHODS To detect the influence of immunization on infection rates, the ultralow dose (ULD) infection model is used. The infection rate of mice vaccinated with BCG and exposed after 6 weeks to ULD of MTB and unvaccinated mice are compared via cultures of lung homogenates and interferon (IFN) gamma release assay. If a reduced infection rate by BCG immunization is confirmed, the experiment is repeated by giving BCG combined simultaneously or in time sequence with the enhancers of innate immunity murabutide or beta-glycan. The influence of murabutide or beta-glycan alone on infection rates is investigated. To quantify the contribution of innate immunity levels of tumor necrosis factor, IFN gamma expression, histone H3 K4me3 trimethylation, and concentrations of monocytes with features of activation of innate immunity as defined by the Ly6Chigh as well as CD11b positive phenotype in immunized versus unimmunized infected and uninfected mice in the various immunization protocols is compared. The experiments will be repeated with prior application of the inhibitors of epigenetic programming of innate immunity histone methyltransferase inhibitor 5’-deoxy-5’-methylthio-adenosine and histone acetyl transferase inhibitor epigallocatechin-3-gallate. The influence of BCG on innate immunity is further corroborated by a prospective observational study in human infants. RESULTS Investigations of derivatives of muramyl dipeptide (MDP) to enhance early immunity in the C57BL/6 mouse strain (mice aged 7 weeks) by another group used 300 micrograms per mouse of oil-associated 6-0-mycoloyl-N-acetylmuramyl-L-alanyl-D-isoglutamine (mycol-MDP) 50/50 mixed with Freund’s incomplete adjuvant. Comparison of colony-forming unit (CFU) count in the lungs 3 weeks after aerosol challenge with Mycobacterium bovis of groups (n=5) between groups receiving mycol-MDP in oil emulsion (see above) versus controls (n=5) showed a significantly lower CFU count of 94.5 x106 (SD 22.0) in cases versus controls with 204.0 X 106 (SD 77.6). It is important to note that after elimination of T-cells in this model, a reduction of CFU in lungs of mice treated with mycol-MDP persisted albeit without statistical significance, which was possibly related to the small number of animals used. CONCLUSIONS Demonstration of a reduction of MTB infection by enhancement of innate immunity could show a new approach to improving vaccine efficacy against this pathogen. INTERNATIONAL REGISTERED REPOR PRR1-10.2196/13045

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