4 research outputs found

    Species-specific and pathotype-specific binding of bacteria to zymogen granule membrane glycoprotein 2 (GP2)

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    With interest we read the paper by Juste et al 1 proposing the amount of zymogen-granule membrane glycoprotein 2 (GP2) on the surface of intestinal bacteria as a Crohn\u27s disease (CD) marker. Indeed, a decreased GP2 level was found on microbes in patients with CD as compared to those of healthy controls. GP2 is a homologue to the urinary Tamm–Horsefall protein demonstrating an antimicrobial function by binding type 1-fimbriated uropathogenic Escherichia coli (UPEC). Likewise, GP2 seems to interact with intestinal bacteria as a specific receptor of bacterial type-1 fimbriae (FimH) on intestinal microfold cells that are partaking in immune responses against such microbes.2 GP2 is overexpressed in the inflamed intestine of patients with CD and has an immunomodulating role in innate and acquired immune responses.3 ,4Interestingly, GP2 was identified as autoantigen of pancreatic antibodies in CD.4 Altogether, these findings indicate two major GP2 sources (pancreatic/intestinal) and support a role for GP2 in the interaction between the immune system and intestinal microbiota.3 Thus, loss of tolerance to GP2 could play a role in CD\u27s pathophysiology supposed to be exacerbated by preceding intestinal infections. In general, the findings by Juste et al 1 may be explained by a lower pancreatic GP2 secretion, an impaired GP2 binding to bacteria, or by a higher prevalence of bacteria with poor or no GP2 binding in patients with CD

    Effective reduction of Salmonella Enteritidis in broiler chickens using the UPWr_S134 phage cocktail

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    Salmonella is a poultry-associated pathogen that is considered one of the most important zoonotic bacterial agents of contaminated food of animal origin including poultry products. Many efforts are taken to eliminate it from the food chain, and phages are one of the most promising tools to control Salmonella in poultry production. We investigated the usefulness of the UPWr_S134 phage cocktail in reducing Salmonella in broiler chickens. For this purpose, we analyzed the survivability of phages in the harsh environment encountered in the chicken gastrointestinal tract, which has low pH, high temperatures, and digestive activity. Phages in the cocktail UPWr_S134 showed the ability to remain active after storage at temperatures ranging from 4 to 42°C, reflecting temperatures of storage conditions, broiler handling, and the chicken body, and exhibited robust pH stability. We found that although simulated gastric fluids (SGF) caused phage inactivation, the addition of feed to gastric juice allows maintenance of UPWr_S134 phage cocktail activity. Further, we analyzed UPWr_S134 phage cocktail anti-Salmonella activity in live animals such as mice and broilers. In an acute infection model in mice, the application of doses of 107 and 1014 PFU/ml UPWr_S134 phage cocktail resulted in delaying symptoms of intrinsic infection in all analyzed treatment schedules. In Salmonella-infected chickens orally treated with the UPWr_S134 phage cocktail the number of pathogens in internal organs in comparison to untreated birds was significantly lower. Therefore we concluded that the UPWr_S134 phage cocktail could be an effective tool against this pathogen in the poultry industry

    Pre-Growth Culture Conditions Affect Type 1 Fimbriae-Dependent Adhesion of Salmonella

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    Among various fimbrial structures used by Salmonella enterica to colonize host tissues, type 1 fimbriae (T1F) are among the most extensively studied. Although some experiments have shown the importance of T1F in the initial stages of Salmonella infection, their exact role in the infection process is not fully known. We suggested that different outcomes of T1F investigations were due to the use of different pre-infection growth conditions for the induction of the T1F. We utilized qPCR, flow cytometry, and a wide range of adhesion assays to investigate Salmonella Choleraesuis and Salmonella Typhimurium adhesion in the context of T1F expression. We demonstrated that T1F expression was highly dependent on the pre-infection growth conditions. These growth conditions yielded T1F+ and T1F- populations of Salmonella and, therefore, could be a factor influencing Salmonella-host cell interactions. We supported this conclusion by showing that increased levels of T1F expression directly correlated with higher levels of Salmonella adherence to the intestinal epithelial IPEC-J2 cell line

    Species-specific and pathotype-specific binding of bacteria to zymogen granule membrane glycoprotein 2 (GP2)

    No full text
    With interest we read the paper by Juste et al 1 proposing the amount of zymogen-granule membrane glycoprotein 2 (GP2) on the surface of intestinal bacteria as a Crohn's disease (CD) marker. Indeed, a decreased GP2 level was found on microbes in patients with CD as compared to those of healthy controls. GP2 is a homologue to the urinary Tamm–Horsefall protein demonstrating an antimicrobial function by binding type 1-fimbriated uropathogenic Escherichia coli (UPEC). Likewise, GP2 seems to interact with intestinal bacteria as a specific receptor of bacterial type-1 fimbriae (FimH) on intestinal microfold cells that are partaking in immune responses against such microbes.2 GP2 is overexpressed in the inflamed intestine of patients with CD and has an immunomodulating role in innate and acquired immune responses.3 ,4Interestingly, GP2 was identified as autoantigen of pancreatic antibodies in CD.4 Altogether, these findings indicate two major GP2 sources (pancreatic/intestinal) and support a role for GP2 in the interaction between the immune system and intestinal microbiota.3 Thus, loss of tolerance to GP2 could play a role in CD's pathophysiology supposed to be exacerbated by preceding intestinal infections. In general, the findings by Juste et al 1 may be explained by a lower pancreatic GP2 secretion, an impaired GP2 binding to bacteria, or by a higher prevalence of bacteria with poor or no GP2 binding in patients with CD.This article is from Gut 64 (2015): 517–519, doi:10.1136/gutjnl-2014-307854. Posted with permission.</p
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