scholarly journals Vibrio vulnificus detected in the spleen leads to fatal outcome in a mouse oral infection model

2015 ◽  
Vol 362 (7) ◽  
Author(s):  
Takashige Kashimoto ◽  
Chiemi Iwasaki ◽  
Masanori Gojo ◽  
Hiroyuki Sugiyama ◽  
Kazuki Yoshioka ◽  
...  
Keyword(s):  
Vibrio Vulnificus ◽  
Fatal Outcome ◽  
Oral Infection ◽  
Infection Model

scholarly journals Listeria Monocytogenes: A Model Pathogen Continues to Refine Our Knowledge of the CD8 T Cell Response

Pathogens ◽  
2018 ◽  
Vol 7 (2) ◽  
pp. 55 ◽  
Author(s):  
Zhijuan Qiu ◽  
Camille Khairallah ◽  
Brian Sheridan
Keyword(s):  
Listeria Monocytogenes ◽  
T Cell ◽  
Cell Response ◽  
Protective Immunity ◽  
T Cell Responses ◽  
Cd8 T Cell ◽  
Oral Infection ◽  
T Cell Response ◽  
Infection Model ◽  
Cell Responses

Listeria monocytogenes (Lm) infection induces robust CD8 T cell responses, which play a critical role in resolving Lm during primary infection and provide protective immunity to re-infections. Comprehensive studies have been conducted to delineate the CD8 T cell response after Lm infection. In this review, the generation of the CD8 T cell response to Lm infection will be discussed. The role of dendritic cell subsets in acquiring and presenting Lm antigens to CD8 T cells and the events that occur during T cell priming and activation will be addressed. CD8 T cell expansion, differentiation and contraction as well as the signals that regulate these processes during Lm infection will be explored. Finally, the formation of memory CD8 T cell subsets in the circulation and in the intestine will be analyzed. Recently, the study of CD8 T cell responses to Lm infection has begun to shift focus from the intravenous infection model to a natural oral infection model as the humanized mouse and murinized Lm have become readily available. Recent findings in the generation of CD8 T cell responses to oral infection using murinized Lm will be explored throughout the review. Finally, CD8 T cell-mediated protective immunity against Lm infection and the use of Lm as a vaccine vector for cancer immunotherapy will be highlighted. Overall, this review will provide detailed knowledge on the biology of CD8 T cell responses after Lm infection that may shed light on improving rational vaccine design.

scholarly journals A silkworm infection model to investigate Vibrio vulnificus virulence genes

2016 ◽  
Vol 14 (5) ◽  
pp. 4243-4247 ◽  
Author(s):  
Mai Yamamoto ◽  
Takashige Kashimoto ◽  
Yukihiro Yoshimura ◽  
Nao Tachibana ◽  
Shiho Kuroda ◽  
...  
Keyword(s):  
Virulence Genes ◽  
Vibrio Vulnificus ◽  
Infection Model

scholarly journals Establishment of a Poliovirus Oral Infection System in Human Poliovirus Receptor-Expressing Transgenic Mice That Are Deficient in Alpha/Beta Interferon Receptor

2007 ◽  
Vol 81 (15) ◽  
pp. 7902-7912 ◽  
Author(s):  
Seii Ohka ◽  
Hiroko Igarashi ◽  
Noriyo Nagata ◽  
Mai Sakai ◽  
Satoshi Koike ◽  
...  
Keyword(s):  
Small Intestine ◽  
Transgenic Mice ◽  
Alimentary Tract ◽  
Oral Route ◽  
Oral Infection ◽  
Infection Model ◽  
Oral Infections ◽  
Beta Interferon ◽  
Interferon Receptor ◽  
Alpha Beta

ABSTRACT Poliovirus (PV) is easily transferred to humans orally; however, no rodent model for oral infections has been developed because of the alimentary tract's low sensitivity to the virus. Here we showed that PV is inactivated by the low pH of the gastric contents in mice. The addition of 3% NaHCO3 to the viral inoculum increased the titer of virus reaching the small intestine through the stomach after intragastric inoculation of PV. Transgenic mice (Tg) carrying the human PV receptor (hPVR/CD155) gene and lacking the alpha/beta interferon receptor (IFNAR) gene (hPVR-Tg/IfnarKO) were sensitive to the oral administration of PV with 3% NaHCO3, whereas hPVR-Tg expressing IFNAR were much less sensitive. The virus was detected in the epithelia of the small intestine and proliferated in the alimentary tract of hPVR-Tg/IfnarKO. By the ninth day after the administration of a virulent PV, the mice had died. These results suggest that IFNAR plays an important role in determining permissivity in the alimentary tract as well as the generation of virus-specific immune responses to PV via the oral route. Thus, hPVR-Tg/IfnarKO are considered to be the first oral infection model for PV, although levels of anti-PV antibodies were not elevated dramatically in serum and intestinal secretions of surviving mice when hPVR-Tg/IfnarKO were administered an attenuated PV.

scholarly journals Genetic Requirements for Klebsiella pneumoniae-Induced Liver Abscess in an Oral Infection Model

2009 ◽  
Vol 77 (7) ◽  
pp. 2657-2671 ◽  
Author(s):  
Ya-Chun Tu ◽  
Min-Chi Lu ◽  
Ming-Ko Chiang ◽  
Shu-Ping Huang ◽  
Hwei-Ling Peng ◽  
...  
Keyword(s):  
Klebsiella Pneumoniae ◽  
Liver Abscess ◽  
Regulatory Networks ◽  
Oral Infection ◽  
Genetic Regulatory Networks ◽  
Class I ◽  
Infection Model ◽  
Wild Type ◽  
Virulence Attenuation ◽  
Mutant Strains

ABSTRACT Klebsiella pneumoniae is the predominant pathogen of primary liver abscess. However, our knowledge regarding the molecular basis of how K. pneumoniae causes primary infection in the liver is limited. We established an oral infection model that recapitulated the characteristics of liver abscess and conducted a genetic screen to identify the K. pneumoniae genes required for the development of liver abscess in mice. Twenty-eight mutants with attenuated growth in liver or spleen samples out of 2,880 signature-tagged mutants that produced the wild-type capsule were identified, and genetic loci which were disrupted in these mutants were identified to encode products with roles in cellular metabolism, adhesion, transportation, gene regulation, and unknown functions. We further evaluated the virulence attenuation of these mutants in independent infection experiments and categorized them accordingly into three classes. In particular, the class I and II mutant strains exhibited significantly reduced virulence in mice, and most of these strains were not detected in extraintestinal tissues at 48 h after oral inoculation. Interestingly, the mutated loci of about one-third of the class I and II mutant strains encode proteins with regulatory functions, and the transcript abundances of many other genes identified in the same screen were markedly changed in these regulatory mutant strains, suggesting a requirement for genetic regulatory networks for translocation of K. pneumoniae across the intestinal barrier. Furthermore, our finding that preimmunization with certain class I mutant strains protected mice against challenge with the wild-type strain implied a potential application for these strains in prophylaxis against K. pneumoniae infections.

scholarly journals Immune Response and Alveolar Bone Resorption in a Mouse Model of Treponema denticola Infection

2008 ◽  
Vol 77 (2) ◽  
pp. 694-698 ◽  
Author(s):  
Song F. Lee ◽  
Elisoa Andrian ◽  
Elden Rowland ◽  
Ignacio Christian Marquez
Keyword(s):  
Immune Response ◽  
Bone Resorption ◽  
Alveolar Bone ◽  
Interleukin 10 ◽  
Oral Infection ◽  
Infection Model ◽  
Treponema Denticola ◽  
Outer Sheath ◽  
Oral Inoculation ◽  
Animal Infection

ABSTRACT Treponema denticola is considered to be an agent strongly associated with periodontal disease. The lack of an animal infection model has hampered the understanding of T. denticola pathogenesis and the host's immune response to infection. In this study, we have established an oral infection model in mice, demonstrating that infection by oral inoculation is feasible. The presence of T. denticola in the oral cavities of the animals was confirmed by PCR. Mice given T. denticola developed a specific immune response to the bacterium. The antibodies generated from the infection were mainly of the immunoglobulin G1 subclass, indicating a Th2-tilted response. The antibodies recognized 11 T. denticola proteins, of which a 62-kDa and a 53-kDa protein were deemed immunodominant. The two proteins were identified, respectively, as dentilisin and the major outer sheath protein by mass spectrometry. Splenocytes cultured from the infected mice no longer produced interleukin-10 and produced markedly reduced levels of gamma interferon relative to those produced by naïve splenocytes upon stimulation with T. denticola. Mandibles of infected mice showed significantly greater bone resorption (P < 0.01) than those of mock-infected controls.

scholarly journals Morphine Withdrawal Lowers Host Defense to Enteric Bacteria: Spontaneous Sepsis and Increased Sensitivity to Oral Salmonella enterica Serovar Typhimurium Infection

2006 ◽  
Vol 74 (9) ◽  
pp. 5221-5226 ◽  
Author(s):  
Pu Feng ◽  
Allan L. Truant ◽  
Joseph J. Meissler ◽  
John P. Gaughan ◽  
Martin W. Adler ◽  
...  
Keyword(s):  
Host Defense ◽  
Salmonella Enterica ◽  
Bacterial Colonization ◽  
Bacterial Species ◽  
Enteric Bacteria ◽  
Oral Infection ◽  
Morphine Withdrawal ◽  
Infection Model ◽  
Abrupt Withdrawal ◽  
Serovar Typhimurium

ABSTRACT Understanding the consequences of drug withdrawal on immune function and host defense to infection is important. We, and others, previously demonstrated that morphine withdrawal results in immunosuppression and sensitizes to lipopolysaccharide-induced septic shock. In the present study, the effect of morphine withdrawal on spontaneous sepsis and on oral infection with Salmonella enterica serovar Typhimurium was examined. Mice were chronically exposed to morphine for 96 h by implantation of a slow-release morphine pellet. Abrupt withdrawal was induced by removal of the pellet. In the sepsis model, bacterial colonization was examined and bacterial species were identified by necropsy of various tissues. It was found that at 48 h postwithdrawal, morphine-treated mice had enteric bacteria that were detected in the Peyer's patches (4/5), mesenteric lymph nodes (4/5), spleens (4/10), livers (6/10), and peritoneal cavities (8/10). In placebo pellet-withdrawn mice, only 2/40 cultures were positive. The most frequently detected organisms in tissues of morphine-withdrawn mice were Enterococcus faecium followed by Klebsiella pneumoniae. Both organisms are part of the normal gastrointestinal flora. In the infection model, mice were orally inoculated with S. enterica 24 h post-initiation of abrupt withdrawal from morphine. Withdrawal significantly decreased the mean survival time and significantly increased the Salmonella burden in various tissues of infected mice compared to placebo-withdrawn animals. Elevated levels of the proinflammatory cytokines were observed in spleens of morphine-withdrawn mice, compared to placebo-withdrawn mice. These findings demonstrate that morphine withdrawal sensitizes to oral infection with a bacterial pathogen and predisposes mice to bacterial sepsis.

scholarly journals MukB Is a Gene Necessary for Rapid Proliferation of Vibrio vulnificus in the Systemic Circulation but Not at the Local Infection Site in the Mouse Wound Infection Model

2021 ◽  
Vol 9 (5) ◽  
pp. 934
Author(s):  
Takashige Kashimoto ◽  
Kohei Yamazaki ◽  
Takehiro Kado ◽  
Kaho Matsuda ◽  
Shunji Ueno
Keyword(s):  
Wound Infection ◽  
Vibrio Vulnificus ◽  
Systemic Circulation ◽  
The Other ◽  
Infection Model ◽  
Infection Site ◽  
Bacterial Burden ◽  
Inoculation Site ◽  
Aggressive Debridement ◽  
Novel Therapeutic

Vibrio vulnificus causes rapid septicemia in susceptible individuals who have ingested contaminated foods or have open wounds exposed to seawater contaminated with the bacteria. Despite antibiotic therapy and aggressive debridement, mortality from septicemia is high. In this study, we showed that MukB mutation (mukB::Tn) affected the proliferation of V. vulnificus in the systemic circulation but not at the inoculation site in the wound infection model. A comparison of mukB::Tn with WT and a mukB complement strain (mukB::Tn/pmukB) on the bacterial burden in the muscle at the infection site showed that spreading and proliferation of the mukB::Tn strain was similar to those of the other strains. However, the bacterial burden of mukB::Tn in the spleen was reduced compared to that of the WT strain in the wound infection model. In a competition experiment, we found a lower bacterial burden of mukB::Tn in the spleen than that of the WT strain infecting the systemic circulation. Here, we report on a gene required for the rapid proliferation of V. vulnificus only in the systemic circulation and potentially required for its survival. Our finding may provide a novel therapeutic target for V. vulnificus septicemia.

scholarly journals Mucosal Bacteria Modulate Candida albicans Virulence in Oropharyngeal Candidiasis

mBio ◽  
2021 ◽  
Author(s):  
M. Bertolini ◽  
R. Vazquez Munoz ◽  
L. Archambault ◽  
S. Shah ◽  
J. G. S. Souza ◽  
...  
Keyword(s):  
Candida Albicans ◽  
Carbon Source ◽  
Oral Infection ◽  
Infection Model ◽  
Oropharyngeal Candidiasis ◽  
Fungal Virulence ◽  
Bacterial Composition ◽  
Content Type ◽  
Host Environment ◽  
Bacterial Microbiome

By comparing Candida albicans virulence and the mucosal bacterial composition in a mouse oral infection model, we were able to dissect the effects of the host environment (immunosuppression), infection with C. albicans , and local modulating factors (availability of sucrose as a carbon source) on the mucosal bacterial microbiome and its role on fungal virulence. We showed that changes in endogenous microbial communities in response to sucrose can lead to attenuation of fungal disease.

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