scholarly journals Comparison of Salmonellaenterica Serovar Typhimurium Colitis in Germfree Mice and Mice Pretreated with Streptomycin

2005 ◽  
Vol 73 (6) ◽  
pp. 3228-3241 ◽  
Author(s):  
Bärbel Stecher ◽  
Andrew J. Macpherson ◽  
Siegfried Hapfelmeier ◽  
Marcus Kremer ◽  
Thomas Stallmach ◽  
...  
Keyword(s):  
Type Iii Secretion ◽  
Intestinal Microflora ◽  
Specific Pathogen Free ◽  
Colonization Resistance ◽  
Pathogenetic Mechanisms ◽  
Colon Inflammation ◽  
Physiological Properties ◽  
Infection Models ◽  
Serovar Typhimurium ◽  
Specific Pathogen

ABSTRACT Salmonella enterica subspecies 1 serovar Typhimurium is a common cause of bacterial enterocolitis. Mice are generally protected from Salmonella serovar Typhimurium colonization and enterocolitis by their resident intestinal microflora. This phenomenon is called “colonization resistance” (CR). Two murine Salmonella serovar Typhimurium infection models are based on the neutralization of CR: (i) in specific-pathogen-free mice pretreated with streptomycin (StrSPF mice) antibiotics disrupt the intestinal microflora; and (ii) germfree (GF) mice are raised without any intestinal microflora, but their intestines show distinct physiologic and immunologic characteristics. It has been unclear whether the same pathogenetic mechanisms trigger Salmonella serovar Typhimurium colitis in GF and StrSPF mice. In this study, we compared the two colitis models. In both of the models Salmonella serovar Typhimurium efficiently colonized the large intestine and triggered cecum and colon inflammation starting 8 h postinfection. The type III secretion system encoded in Salmonella pathogenicity island 1 was essential in both disease models. Thus, Salmonella serovar Typhimurium colitis is triggered by similar pathogenetic mechanisms in StrSPF and GF mice. This is remarkable considering the distinct physiological properties of the GF mouse gut. One obvious difference was more pronounced damage and reduced regenerative response of the cecal epithelium in GF mice. Overall, StrSPF mice and GF mice provide similar but not identical models for Salmonella serovar Typhimurium colitis.

scholarly journals Characteristic Intestinal Microflora of Specific Pathogen-Free Mice Bred in Two Different Colonies and their Influence on Postnatal Murine Immunocyte Profiles

2005 ◽  
Vol 54 (2) ◽  
pp. 143-148 ◽  
Author(s):  
Taizo NAGURA ◽  
Satoshi HACHIMURA ◽  
Shuichi KAMINOGAWA ◽  
Tsutomu ARITSUKA ◽  
Kikuji ITOH
Keyword(s):  
Intestinal Microflora ◽  
Specific Pathogen Free ◽  
Specific Pathogen

scholarly journals Identification of Urinary Biomarkers of Colon Inflammation in IL10-/-Mice Using Short-Column LCMS Metabolomics

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Don Otter ◽  
Mingshu Cao ◽  
Hui-Ming Lin ◽  
Karl Fraser ◽  
Shelley Edmunds ◽  
...  
Keyword(s):  
Intestinal Microflora ◽  
Interleukin 10 ◽  
Xanthurenic Acid ◽  
Wild Type ◽  
Mass Spectral ◽  
Short Column ◽  
Colon Inflammation ◽  
Metabolite Concentrations ◽  
Specific Pathogen ◽  
Unidentified Metabolite

The interleukin-10-deficient (IL10-/-) mouse develops colon inflammation in response to normal intestinal microflora and has been used as a model of Crohn's disease. Short-Column LCMS metabolite profiling of urine from IL10-/-and wild-type (WT) mice was used, in two independent experiments, to identify mass spectral ions differing in intensity between these two genotypes. Three differential metabolites were identified as xanthurenic acid and as the glucuronides of xanthurenic acid and of α-CEHC (2,5,7,8-tetramethyl-2-(2′-carboxyethyl)-6-hydroxychroman). The significance of several differential metabolites as potential biomarkers of colon inflammation was evaluated in an experiment which compared metabolite concentrations in IL10-/-and WT mice housed, either under conventional conditions and dosed with intestinal microflora, or maintained under specific pathogen-free (SPF) conditions. Concentrations of xanthurenic acid, α-CEHC glucuronide, and an unidentified metabolitem/z495-/497+were associated with the degree of inflammation in IL10-/-mice and may prove useful as biomarkers of colon inflammation.

scholarly journals Development of the normal gastrointestinal microflora of specific pathogen-free chickens

1984 ◽  
Vol 92 (1) ◽  
pp. 79-87 ◽  
Author(s):  
P. J. Coloe ◽  
T. J. Bagust ◽  
L. Ireland
Keyword(s):  
Escherichia Coli ◽  
Small Intestine ◽  
Large Intestine ◽  
Intestinal Microflora ◽  
Strictly Anaerobic ◽  
Specific Pathogen Free ◽  
Specific Pathogen ◽  
Faecal Streptococci ◽  
Environmental Challenge ◽  
Limited Period

SUMMARYThe development of the normal intestinal microflora of the small intestine, caecum and large intestine of specific pathogen-free (SPF) chickens, was studied in the period from hatching to 84 days of age.No bacteria were detected in any of the sites at hatchery (day 1), but by day 3 significant levels of faecal streptococci and coliforms were isolated from all sites. The flora of the small intestine was limited to faecal streptococci and coliforms for the first 40 days and then lactobacilli became established and dominated the flora.A large variety of facultative and strictly anaerobic organisms colonized the caecum. Many of these species were transient and were only present for a limited period; after 40 days the flora stabilized to consist predominantly of faecal streptococci,Escherichia coli, Bacteroidesspp. andLactobacillussp.The flora of the large intestine was composed of organisms also present in the small intestine or the caecum.These findings differ from previously published studies on conventionally reared chickens in that the number of species isolated and the population levels of organisms are much lower. This probably reflects the absence of continuous environmental challenge to the chickens because of the housing and feeding facilities in which the chickens were maintained.

scholarly journals Natural Colonization of Laboratory Mice withStaphylococcus aureusPrimes a Systemic Immune Response

2017 ◽  
Author(s):  
Daniel Schulz ◽  
Dorothee Grumann ◽  
Patricia Trübe ◽  
Kathleen Pritchett-Corning ◽  
Sarah Johnson ◽  
...  
Keyword(s):  
Virulence Gene ◽  
Host Adaptation ◽  
Specific Pathogen Free ◽  
Laboratory Mice ◽  
Systemic Immune Response ◽  
Vaccine Candidates ◽  
Infection Models ◽  
Natural Hosts ◽  
Specific Pathogen ◽  
Infection Experiments

AbstractBackgroundWhether mice are an appropriate model forS.aureusinfection and vaccination studies is a matter of debate, because they are not considered as natural hosts ofS. aureus.Sparked by an outbreak of S.aureusinfections in laboratory mice, we investigated whether laboratory mice are commonly colonized with S.aureusand whether this might impact on infection experiments.MethodsWe characterized 99S. aureusisolates from laboratory mice (spatyping, virulence gene PCR), and quantified murine antibodies using FlexMap technology.ResultsSpecific-pathogen-free mice from various vendors were frequently colonized withS. aureus(0-21%).S. aureuswas readily transmitted from murine parents to offspring, which became persistently colonized. Most murine isolates belonged to the lineage CC88 (54%). Murine strains showed features of host adaptation, such as absence ofhlb-converting phages and superantigen genes, as well as enhanced coagulation of murine plasma. Importantly,S. aureuscolonization induced a systemic IgG response specific for numerousS. aureusproteins, including several vaccine candidates.ConclusionLaboratory mice are natural hosts ofS. aureusand, therefore, provide better infection models than previously assumed. Pre-exposure to S.aureusis a possible confounder inS. aureusinfection and vaccination studies.

Clostridium difficile-associated typhlitis in specific pathogen free guineapigs in the absence of antimicrobial treatment

1989 ◽  
Vol 23 (3) ◽  
pp. 203-207 ◽  
Author(s):  
R. Boot ◽  
A. F. Angulo ◽  
H. C. Walvoort
Keyword(s):  
Clostridium Difficile ◽  
Antimicrobial Treatment ◽  
Specific Pathogen Free ◽  
Colonization Resistance ◽  
Pathological Lesions ◽  
Specific Pathogen ◽  
Clostridium Difficile Toxin

Clostridium difficile (toxin) associated typhlitis was diagnosed in untreated barrier-maintained specific pathogen free guineapigs. It resembled the pathological lesions of antibiotic induced enterocolitis. The possible role of limited colonization resistance to C. difficile provided by mouse enteric microflora in the pathogenesis of the disease is discussed.

Laboratory Animal Research Centre (Larc) “A Specific Pathogen Free Rodent Facility” - Covid – 19 Pandemic Response Plan

2020 ◽  
Author(s):  
Muralitharan Shanmugakonar ◽  
Vijay Kanth Govindharajan ◽  
Kavitha Varadharajan ◽  
Hamda Al-Naemi
Keyword(s):  
Laboratory Animal ◽  
Animal Research ◽  
Research Centre ◽  
Functional Requirement ◽  
Specific Pathogen Free ◽  
Specific Pathogen ◽  
Response Plan ◽  
Pandemic Response ◽  
Operational Plan

Laboratory Animal Research Centre (LARC) has developed an early emergency operational plan for COVID-19 pandemic situation. Biosafety and biosecurity measures were planned and implemented ahead of time to check the functional requirement to prevent the infection. Identified necessary support for IT, transport, procurement, finance, admin and research to make the operations remotely and successfully.

scholarly journals Signal Pathway in Salt-Activated Expression of the Salmonella Pathogenicity Island 1 Type III Secretion System in Salmonella enterica Serovar Typhimurium

2008 ◽  
Vol 190 (13) ◽  
pp. 4624-4631 ◽  
Author(s):  
Hideaki Mizusaki ◽  
Akiko Takaya ◽  
Tomoko Yamamoto ◽  
Shin-Ichi Aizawa
Keyword(s):  
Electron Microscopy ◽  
Real Time ◽  
Protein Secretion ◽  
Real Time Pcr ◽  
Type Iii Secretion ◽  
Type Iii Secretion System ◽  
Secretion System ◽  
Sds Page ◽  
Two Component ◽  
Serovar Typhimurium

ABSTRACT Salmonella enterica serovar Typhimurium secretes virulence factors for invasion called Sip proteins or Sips into its hosts through a type III secretion system (T3SS). In the absence of a host, S. enterica induces Sip secretion in response to sucrose or simple salts, such as NaCl. We analyzed induction of host-independent Sip secretion by monitoring protein secretion by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), assembly of needle complexes by electron microscopy, and transcription of virulence regulatory genes by quantitative reverse transcriptase PCR (real-time PCR). SDS-PAGE showed that addition of sucrose or simple salts, such as NaCl, to the growth medium induced Sip secretion without altering flagellar protein secretion, which requires a distinct T3SS. Electron microscopy confirmed that the amount of secreted Sips increased as the number of assembled needle complexes increased. Real-time PCR revealed that added sucrose or NaCl enhanced transcription of hilA, hilC, and hilD, which encode known regulators of Salmonella virulence. However, epistasis analysis implicated HilD and HilA, but not HilC, in the direct pathway from the salt stimulus to the Sip secretion response. Further analyses showed that the BarA/SirA two-component signal transduction pathway, but not the two-component sensor kinase EnvZ, directly activated hilD and hilA transcription and thus Sip secretion in response to either sucrose or NaCl. Finally, real-time PCR showed that salt does not influence transcription of the BarA/SirA-dependent csrB and csrC genes. A model is proposed for the major pathway in which sucrose or salt signals to enhance virulence gene expression.

scholarly journals Curcumin reduces enteric isoprostane 8-iso-PGF2α and prostaglandin GF2α in specific pathogen-free Leghorn chickens challenged with Eimeria maxima

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Victor M. Petrone-Garcia ◽  
Raquel Lopez-Arellano ◽  
Gabriela Rodríguez Patiño ◽  
Miriam Aide Castillo Rodríguez ◽  
Daniel Hernandez-Patlan ◽  
...  
Keyword(s):  
Pilot Study ◽  
Broiler Chickens ◽  
Solid Phase ◽  
Oxidation Products ◽  
Specific Pathogen Free ◽  
Post Challenge ◽  
Eimeria Maxima ◽  
Lipid Oxidation Products ◽  
Challenge Control ◽  
Specific Pathogen

AbstractThe purpose of this pilot study was to evaluate and determine the concentration of prostaglandin GF2α (PGF2α) and isoprostane 8‐iso‐PGF2α in plasma and intestine of specific pathogen-free (SPF) Leghorn chickens challenged with Eimeria maxima, with or without dietary supplementation of curcumin using solid‐phase microextraction and ultra‐performance liquid chromatography/tandem mass spectrometry. Eighty 1-day-old male SPF chickens were randomly allocated to one of four groups with four replicates (n = 5 chickens/replicate). Groups consisted of: (1) Control (no challenge), (2) Curcumin (no challenge), (3) Eimeria maxima (challenge), and (4) Eimeria maxima (challenge) + curcumin. At day 28 of age, all chickens in the challenge groups were orally gavaged with 40,000 sporulated E. maxima oocysts. No significant differences (P > 0.05) were observed in the groups regardless of the treatment or challenge with E. maxima. Enteric levels of both isoprostane 8‐iso‐PGF2α and PGF2α at 7 days and 9 days post-challenge were significantly increased (P < 0.01) compared to the non-challenge control chickens. Interestingly, the enteric levels of both isoprostane 8‐iso‐PGF2α and PGF2α at 7 days post-challenge were significantly reduced in chickens fed curcumin, compared to control chickens challenge with E. maxima. At 9 days post-challenge, only levels of isoprostane 8‐iso‐PGF2α in the enteric samples were significantly reduced in chickens challenged with E. maxima supplemented with curcumin, compared with E. maxima challenge chickens. No differences of isoprostane 8‐iso‐PGF2α or PGF2α were observed in plasma at both days of evaluation. Similarly, no significant differences were observed between the challenge control or chickens challenge with E. maxima and supplemented with curcumin at both times of evaluation. The results of this pilot study suggests that the antioxidant anti-inflammatory properties of curcumin reduced the oxidative damage and subsequent intestinal mucosal over-production of lipid oxidation products. Further studies to confirm and extend these results in broiler chickens are required.

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