scholarly journals Pre- and Neonatal Imprinting on Immunological Homeostasis and Epithelial Barrier Integrity by Escherichia coli Nissle 1917 Prevents Allergic Poly-Sensitization in Mice

2021 ◽  
Vol 11 ◽  
Author(s):  
Priya J. Sarate ◽  
Dagmar Srutkova ◽  
Nora Geissler ◽  
Martin Schwarzer ◽  
Irma Schabussova ◽  
...  
Keyword(s):  
Escherichia Coli ◽  
Grass Pollen ◽  
Allergic Airway Inflammation ◽  
Experimental Models ◽  
Lung Epithelial Cells ◽  
Probiotic Bacteria ◽  
Allergy Prevention ◽  
Lactation Period ◽  
Gnotobiotic Mice ◽  
Immunological Homeostasis

A steady rise in the number of poly-sensitized patients has increased the demand for effective prophylactic strategies against multi-sensitivities. Probiotic bacteria have been successfully used in clinics and experimental models to prevent allergic mono-sensitization. In the present study, we have investigated whether probiotic bacteria could prevent poly-sensitization by imprinting on the immune system early in life. We used two recombinant variants of probiotic Escherichia coli Nissle 1917 (EcN): i) EcN expressing birch and grass pollen, poly-allergen chimera construct (EcN-Chim), and ii) an “empty” EcN without allergen expression (EcN-Ctrl). Conventional mice (CV) were treated with either EcN-Chim or EcN-Ctrl in the last week of the gestation and lactation period. Gnotobiotic mice received one oral dose of either EcN-Chim or EcN-Ctrl before mating. The offspring from both models underwent systemic allergic poly-sensitization and intranasal challenge with recombinant birch and grass pollen allergens (rBet v 1, rPhl p 1, and rPhl p 5). In the CV setting, the colonization of offspring via treatment of mothers reduced allergic airway inflammation (AAI) in offspring compared to poly-sensitized controls. Similarly, in a gnotobiotic model, AAI was reduced in EcN-Chim and EcN-Ctrl mono-colonized offspring. However, allergy prevention was more pronounced in the EcN-Ctrl mono-colonized offspring as compared to EcN-Chim. Mono-colonization with EcN-Ctrl was associated with a shift toward mixed Th1/Treg immune responses, increased expression of TLR2 and TLR4 in the lung, and maintained levels of zonulin-1 in lung epithelial cells as compared to GF poly-sensitized and EcN-Chim mono-colonized mice. This study is the first one to establish the model of allergic poly-sensitization in gnotobiotic mice. Using two different settings, gnotobiotic and conventional mice, we demonstrated that an early life intervention with the EcN without expressing an allergen is a powerful strategy to prevent poly-sensitization later in life.

Inhibition of Escherichia coli Translocation from the Gastrointestinal Tract by Normal Cecal Flora in Gnotobiotic or Antibiotic-Decontaminated Mice

1980 ◽  
Vol 29 (3) ◽  
pp. 1073-1081
Author(s):  
Rodney D. Berg
Keyword(s):  
Escherichia Coli ◽  
Gastrointestinal Tract ◽  
Lymph Nodes ◽  
Bacterial Flora ◽  
Specific Pathogen Free ◽  
Mesenteric Lymph Nodes ◽  
E Coli ◽  
Mesenteric Lymph ◽  
Specific Pathogen ◽  
Gnotobiotic Mice

Escherichia coli C25 maintained population levels of 10 9 to 10 10 per g of cecum and translocated to 100% of the middle mesenteric lymph nodes in gnotobiotic mice monoassociated with E. coli C25. Intragastric inoculation of these mice with the cecal contents from specific-pathogen-free mice reduced the population levels of E. coli C25 to 10 6 per g of cecum and completely inhibited translocation to the mesenteric lymph nodes. Intragastric inoculation with heat-treated, Formalintreated, or filtered cecal contents did not reduce the population levels of E. coli C25 or reduce the incidence of translocation of E. coli C25 to the mesenteric lymph nodes. Thus, viable bacteria apparently are required in the cecal contents inocula to reduce the population levels and the incidence of translocation of E. coli C25. Treatment with streptomycin plus bacitracin decreased the anaerobic bacterial levels in these gnotobiotic mice, allowing increased population levels of E. coli C25 and increased translocation to the mesenteric lymph nodes. E. coli C25 also translocated to the mesenteric lymph nodes of specific-pathogen-free mice treated with streptomycin and bacitracin before colonization with E. coli C25. The high cecal population levels of E. coli C25 in these antibiotic-decontaminated specific-pathogen-free mice apparently overwhelm any barrier to translocation exerted by the immunologically developed lamina propria of the specific-pathogen-free mice. Inoculation of gnotobiotic mice with a cecal flora also reduced the population levels of an indigenous strain of E. coli with a concomitant inhibition of translocation of the indigenous E. coli to the mesenteric lymph nodes. Thus, bacterial antagonism of the gastrointestinal population levels of certain indigenous bacteria, such as E. coli , by other members of the normal bacterial flora appears to be an important defense mechanism confining bacteria to the gastrointestinal tract.

scholarly journals IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models

2017 ◽  
Vol 214 (10) ◽  
pp. 3037-3050 ◽  
Author(s):  
Takashi Ito ◽  
Koichi Hirose ◽  
Aiko Saku ◽  
Kenta Kono ◽  
Hiroaki Takatori ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Airway Inflammation ◽  
House Dust ◽  
House Dust Mite ◽  
Cytokine Production ◽  
Allergic Airway Inflammation ◽  
Lung Epithelial Cells ◽  
Intratracheal Administration ◽  
Lung Epithelial ◽  
Dust Mite

Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells.

scholarly journals Incidence of Escherichia coli  - Glucuronidase Positive on Goat Milk

2016 ◽  
Vol 73 (2) ◽  
pp. 359
Author(s):  
Zorica Voşgan ◽  
Anca Domuţa ◽  
Stela Jelea ◽  
Lucia Mihălescu ◽  
Flavia Pop
Keyword(s):  
Escherichia Coli ◽  
Food Poisoning ◽  
Goat Milk ◽  
Lactation Period ◽  
Health Indicator ◽  
Pathogenic Factor ◽  
E Coli ◽  
Higher Temperature ◽  
Hot Weather

Papers on beta- glucuronidase sensitivity and specificity for identifying Escherichia coli in sources of environment, food, water, etc. have been published since 1976. In this study we conducted a review of the incidence of E. coli β- glucuronidase -positive in goat milk, obtained by hand milking throughout the lactation: spring, summer, autumn. The presence of E. coli in milk is considered both as a health indicator and a pathogenic factor capable of causing food poisoning. The determination of the E. coli β-glucuronidase-positive was carried using TBX medium by cultivating colonies typical blue at 440C. The absence of E. coli in milk yielded during the spring, when the animal milking is done three times a day, was found in the performed analyses; the same was observed during fall, when the milk production is lower and the milking is done once a day. The load of E. coli β-glucuronidase-positive was averaging 66.67 CFU/ml of goat milk, during the middle lactation period (July-August), in conditions of higher temperature. During this period, milking is done in the mountain zone, where the transhumance of animals takes place in summer. The presence of the species E. coli was also confirmed by microscopic examination. Attention should be paid to hygiene and milk should be immediately cooled, during hot weather, as E. coli can be a source of food poisoning.  

scholarly journals Improvement of the Enterotoxigenic Escherichia coli Infection Model for Post-Weaning Diarrhea by Controlling for Bacterial Adhesion, Pig Breed and MUC4 Genotype

2020 ◽  
Vol 7 (3) ◽  
pp. 106
Author(s):  
Hiroki Matsumoto ◽  
Masashi Miyagawa ◽  
Sayaka Takahashi ◽  
Ryouichi Shima ◽  
Takayuki Oosumi
Keyword(s):  
Escherichia Coli ◽  
Experimental Infection ◽  
Antibacterial Agents ◽  
Experimental Models ◽  
Enterotoxigenic Escherichia Coli ◽  
Infection Model ◽  
Swine Industry ◽  
Pig Breeds ◽  
Adhesion Ability ◽  
Escherichia Coli Infection

Enterotoxigenic Escherichia coli (ETEC) is a major cause of post-weaning diarrhea (PWD) in pigs and causes significant damage to the swine industry worldwide. In recent years, there has been increased regulation against the use of antibacterial agents in swine due to their health risks. Utilizing experimental models that consistently recapitulate PWD is important for the development of non-antibacterial agents against PWD in pigs. In this study, we established a highly reproducible PWD infection model by examining differences in adhesion of ETEC to the intestinal tissue as well as the association between MUC4 polymorphisms and sensitivity to PWD. Post-weaning diarrhea differences between pig breeds were also examined. The adhesion to enterocytes varied from 104.0 to 106.4 CFU/mL even among the F4 ETEC strains. Experimental infection revealed that PWD can be induced in all MUC4 genotypes after infection with 1010 CFU/pig of highly adherent ETEC, although there were variable sensitivities between the genotypes. Lowly adherent ETEC did not cause PWD as efficiently as did highly adherent ETEC. The incidence of PWD was confirmed for all pigs with the ETEC-susceptible MUC4 genotypes in all of the breeds. These results indicate that high-precision and reproducible experimental infection is possible regardless of pig breeds by controlling factors on the pig-end (MUC4 genotype) and the bacterial-end (adhesion ability).

The spectrum of Escherichia coli – Bacteroides fragilis pathogenic synergy in an intraabdominal infection model

1988 ◽  
Vol 34 (3) ◽  
pp. 352-357 ◽  
Author(s):  
O. D. Rotstein ◽  
J. Kao
Keyword(s):  
Escherichia Coli ◽  
Bacteroides Fragilis ◽  
Fibrin Clot ◽  
Experimental Models ◽  
Abscess Formation ◽  
Intraabdominal Infection ◽  
Infection Model ◽  
E Coli ◽  
Mixed Inocula ◽  
Number Of Bacteria

Pathogenic synergy between Escherichia coli and Bacteroides fragilis was investigated in an intraabdominal infection model. Defined inocula of E. coli and B. fragilis, alone or in combination, were enmeshed within a fibrin clot and surgically implanted into the peritoneal cavity of rats. A spectrum of bacterial synergy ranging from synergistic abscess formation to synergistic lethality was demonstrated using this model. The type of synergy exhibited was dependent upon the initial E. coli inoculum. When combined with B. fragilis, high inocula of E. coli (> 108 cfu/clot) produced synergistic lethality while low inocula (2 × 102 to 2 × 107 cfu/clot) resulted in synergistic abscess formation. With respect to abscess formation, there was reciprocal synergy between E. coli and B. fragilis. Abscesses resulting from mixed inocula were larger and had significantly higher numbers of E. coli and B. fragilis than abscesses initiated by monomicrobial inocula. These studies define a clinically relevant model of bacterial interactions in the setting of intraabdominal infection and suggest that conclusions drawn from experimental models of bacterial synergy should consider the type of model examined, the strains of bacteria studied, and the number of bacteria inoculated.

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