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Academic literature on the topic 'Peritonitis model in mice'

Author: Grafiati

Published: 5 June 2025

Last updated: 16 July 2025

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Journal articles on the topic "Peritonitis model in mice"

1

Goswami, Manish, Deepak Sharma, Nazir M. Khan, Rahul Checker, Santosh Kumar Sandur, and Narendra Jawali. "Antioxidant supplementation enhances bacterial peritonitis in mice by inhibiting phagocytosis." Journal of Medical Microbiology 63, no. 3 (2014): 355–66. http://dx.doi.org/10.1099/jmm.0.067173-0.

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Antioxidants are known to exhibit numerous health benefits including anti-ageing, anti-apoptotic and immuno-stimulatory effects. However, we present the data showing counterproductive effects of therapeutically relevant antioxidants on bacterial clearance by the immune system in a murine peritonitic model. The antioxidants ascorbic acid, glutathione and N-acetylcysteine augmented morbidity and mortality in mice carrying Eshcerichia coli-induced acute bacterial peritonitis. Treatment of peritonitic mice with antioxidants significantly increased their bacterial load in the range of 0.3–2 logs. Antioxidant administration to peritonitic mice resulted in decreased numbers of macrophages, B-cells and dendritic cells at the primary site of infection and increased neutrophil infiltration. Serum TNF-α levels were also decreased in antioxidant-treated peritonitic mice. In vitro experiments showed that antioxidants reduced the phagocytic efficacy of peritoneal macrophages by ~60–75 % and also decreased E. coli-induced oxidative burst in macrophages cells. Taken together, our data indicate that the antioxidants increased the severity of peritonitis by decreasing the phagocytic efficiency, oxidative burst, and TNF-α production, and increasing neutrophil infiltration. Based on these results, we propose that antioxidant supplementation during the course of bacterial infection is not recommended as it could be detrimental for the host. In addition, the present study underlines the importance of timing and context of antioxidant administration rather than indiscriminate usage to gain the best possible therapeutic advantage of these redox compounds.

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Ishii, Yasuo, Tokihiko Sawada, Akira Shimizu, et al. "An experimental sclerosing encapsulating peritonitis model in mice." Nephrology Dialysis Transplantation 16, no. 6 (2001): 1262–66. http://dx.doi.org/10.1093/ndt/16.6.1262.

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Clark, Jessica A., Heng Gan, Alexandr J. Samocha, Amy C. Fox, Timothy G. Buchman, and Craig M. Coopersmith. "Enterocyte-specific epidermal growth factor prevents barrier dysfunction and improves mortality in murine peritonitis." American Journal of Physiology-Gastrointestinal and Liver Physiology 297, no. 3 (2009): G471—G479. http://dx.doi.org/10.1152/ajpgi.00012.2009.

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Systemic administration of epidermal growth factor (EGF) decreases mortality in a murine model of septic peritonitis. Although EGF can have direct healing effects on the intestinal mucosa, it is unknown whether the benefits of systemic EGF in peritonitis are mediated through the intestine. Here, we demonstrate that enterocyte-specific overexpression of EGF is sufficient to prevent intestinal barrier dysfunction and improve survival in peritonitis. Transgenic FVB/N mice that overexpress EGF exclusively in enterocytes ( IFABP-EGF) and wild-type (WT) mice were subjected to either sham laparotomy or cecal ligation and puncture (CLP). Intestinal permeability, expression of the tight junction proteins claudins-1, -2, -3, -4, -5, -7, and -8, occludin, and zonula occludens-1; villus length; intestinal epithelial proliferation; and epithelial apoptosis were evaluated. A separate cohort of mice was followed for survival. Peritonitis induced a threefold increase in intestinal permeability in WT mice. This was associated with increased claudin-2 expression and a change in subcellular localization. Permeability decreased to basal levels in IFABP-EGF septic mice, and claudin-2 expression and localization were similar to those of sham animals. Claudin-4 expression was decreased following CLP but was not different between WT septic mice and IFABP-EGF septic mice. Peritonitis-induced decreases in villus length and proliferation and increases in apoptosis seen in WT septic mice did not occur in IFABP-EGF septic mice. IFABP-EGF mice had improved 7-day mortality compared with WT septic mice (6% vs. 64%). Since enterocyte-specific overexpression of EGF is sufficient to prevent peritonitis-induced intestinal barrier dysfunction and confers a survival advantage, the protective effects of systemic EGF in septic peritonitis appear to be mediated in an intestine-specific fashion.

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Ni, Jie, Yvette Cnops, Rachel M. McLoughlin, Nicholas Topley, and Olivier Devuyst. "Inhibition of Nitric Oxide Synthase Reverses Permeability Changes in a Mouse Model of Acute Peritonitis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 25, no. 3_suppl (2005): 11–14. http://dx.doi.org/10.1177/089686080502503s03.

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Acute peritonitis is the most frequent complication of peritoneal dialysis. Previous studies have suggested a major role for nitric oxide (NO) in the permeability changes and loss of ultrafiltration induced by acute peritonitis. In this study, we further investigated the potential role of NO in a mouse model of peritonitis induced by Escherichia coli lipopolysaccharide (LPS). A 2-hour peritoneal equilibration test was performed in control and LPS-treated mice using 7% glucose dialysate supplemented or not with the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME). The levels of NO metabolites in the dialysate were maximal 18 hours after LPS injection. At that time, acute peritonitis induced by LPS was reflected by an increased recruitment of leukocytes, an increased intraperitoneal release of interleukin-6, a significant increase in the peritoneal permeability for small solutes, a loss of sodium sieving, and a loss of ultrafiltration in comparison with controls. Addition of L-NAME in LPS-treated mice significantly reversed permeability modifications and prevented the release of NO metabolites into the dialysate. These results confirm that increased NO mediates permeability modifications during acute peritonitis, and illustrate the potential of mouse models to investigate the molecular mechanisms regulating peritoneal permeability.

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Liu, Shaoguang, Shaotong Zhang, Yulong Sun, and Wence Zhou. "Transcriptomics Changes in the Peritoneum of Mice with Lipopolysaccharide-Induced Peritonitis." International Journal of Molecular Sciences 22, no. 23 (2021): 13008. http://dx.doi.org/10.3390/ijms222313008.

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Peritonitis caused by LPS is a severe clinical challenge, which causes organ damage and death. However, the mechanism of LPS-induced peritonitis has not been fully revealed yet. Here, we investigated the transcriptome profile of the peritoneal tissue of LPS-induced peritonitis in mice. A model of LPS-induced peritonitis in mice was established (LPS 10 mg/kg, i.p.), and the influence of TAK 242 (TLR4 inhibitor) on the level of inflammatory cytokines in mouse peritoneal lavage fluid was investigated by using an ELISA test. Next, the peritoneal tissues of the three groups of mice (Control, LPS, and LPS+TAK 242) (n = 6) were isolated and subjected to RNA-seq, followed by a series of bioinformatics analyses, including differentially expressed genes (DEGs), enrichment pathway, protein-protein interaction, and transcription factor pathway. Then, qPCR verified-hub genes that may interact with TAK 242 were obtained. Subsequently, the three-dimensional structure of hub proteins was obtained by using homology modeling and molecular dynamics optimization (300 ns). Finally, the virtual docking between TAK 242 and hub proteins was analyzed. Our results showed that TAK 242 significantly inhibited the production of inflammatory cytokines in the peritoneal lavage fluid of mice with peritonitis, including IL-6, IFN-γ, IL-1β, NO, and TNF-α. Compared with the Control group, LPS treatment induced 4201 DEGs (2442 down-regulated DEGs and 1759 up-regulated DEGs). Compared with the LPS group, 30 DEGs were affected by TAK 242 (8 down-regulated DEGs and 22 up-regulated DEGs). A total of 10 TAK 242-triggered hub genes were obtained, and the possible docking modes between TAK 242 and hub proteins were acquired. Overall, our data demonstrated that a large number of DEGs were affected in LPS-triggered peritonitis mice. Moreover, the TLR4 inhibitor TAK 242 is capable of suppressing the inflammatory response of LPS-induced peritonitis. Our work provides clues for understanding the pathogenesis of LPS-induced peritonitis in mice.

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Steinhauser, Matthew L., Cory M. Hogaboam, Nickolas W. Lukacs, Robert M. Strieter, and Steven L. Kunkel. "Multiple Roles for IL-12 in a Model of Acute Septic Peritonitis." Journal of Immunology 162, no. 9 (1999): 5437–43. http://dx.doi.org/10.4049/jimmunol.162.9.5437.

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Abstract The present study addressed the role of IL-12 in a murine model of septic peritonitis, induced by cecal ligation and puncture (CLP). Although CLP surgery induced IL-12 production at 6 and 24 h after surgery, IL-12 immunoneutralization was clearly deleterious in this model: 54% of CLP mice receiving preimmune serum survived, whereas mice administered IL-12 antisera prior to CLP experienced a 25% survival rate. IL-12 immunoneutralization not only led to increased mortality, but also appeared to promote a shift away from IL-12 and IFN-γ, in favor of IL-10. This cytokine shift corresponded to changes in bacterial load, as CLP mice receiving IL-12 antiserum yielded more CFUs from the peritoneal cavity at 24 h after CLP. To address the role of bacterial infection in IL-12 antiserum-induced mortality following CLP, antibiotics were administered for 4 days after surgery. Despite regular antibiotic administration, IL-12 immunoneutralization still reduced survival in CLP mice. Furthermore, histology of the ceca revealed that mice administered IL-12 antisera failed to show typical organization of the damaged cecum wall. Accordingly, Gram staining revealed bacteria within peritoneal fluids from these mice, while peritoneal fluids from CLP mice that received preimmune serum and antibiotics were free of bacteria. Altogether, these data suggested multiple important roles for IL-12 in the evolution of murine septic peritonitis.

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Lan, Jing, Hong Zhang, Hui Zhao, et al. "Cord Blood Natural Killer Cells Inhibit Sepsis Caused by Feces-Induced Acute Peritonitis via Increasing Endothelium Integrity." Cell Transplantation 31 (January 2022): 096368972210902. http://dx.doi.org/10.1177/09636897221090257.

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Sepsis is associated with acute peritonitis, which can be induced by lipopolysaccharide exposure and feces. Generally, lipopolysaccharide induces mono-microbial peritonitis, whereas feces cause poly-microbial peritonitis; the latter is a more complicated and closer to the clinical diseases. Although several reports have discussed the mechanism of immune response in peritonitis-induced sepsis, however, the role of natural killer (NK) cells in sepsis, especially the relationship between NK cells and stabilization of the vascular endothelial barrier, is still unclear. Accordingly, in this study, we assessed the roles of NK cells in an acute sepsis model in mice. NK cells were injected via the tail vein into mice with acute sepsis, and nitric oxide (NO), anti-inflammatory cytokine, and angiogenic factors were tested to explore the effects of NK cells on sepsis. The survival rate of septic model mice infused with NK cells was significantly improved compared with the control group. Interestingly, the levels of NO, interleukin-10, and vascular endothelial growth factor (VEGF) decreased in NK cells therapy group. After the injection of NK cells, CD31 positive endothelial cells significantly increased in the kidneys and liver, although the expression of VEGF, ANGPT-1, and ET-1 was downregulated. Consistent with our hypothesis, the transfusion of NK cells into mice with sepsis blocked inflammation and increased endothelium integrity. Overall, these findings suggest that NK cells may block sepsis by modulating the VEGF pathway.

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Kang, Xu-Qi, Yue Qiao, Xiao-Yang Lu, et al. "Tocopherol polyethylene glycol succinate-modified hollow silver nanoparticles for combating bacteria-resistance." Biomaterials Science 7, no. 6 (2019): 2520–32. http://dx.doi.org/10.1039/c9bm00343f.

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Diedrich, Stephan, Julia van der Linde, Michael Nielson, et al. "The MRI Sepsis Score: An Innovative Tool for the Evaluation of Septic Peritonitis in Mice Using 7-Tesla Small Animal MRI." European Surgical Research 59, no. 3-4 (2018): 126–42. http://dx.doi.org/10.1159/000490663.

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Background: Magnetic resonance imaging (MRI) techniques are rarely used in the context of abdominal sepsis and in sepsis research. This study investigates the impact of MRI for monitoring septic peritonitis in an animal model (colon ascendens stent-induced peritonitis, CASP). The CASP model closely mimics that of human disease and is highly standardized. The most frequently employed readout parameter in mouse CASP studies is prolonged or decreased rate of survival. Monitoring the progression of peritonitis via MRI could provide a helpful tool in the evaluation of severity. The use of alternative readout systems could very well reduce the number of research animals. Perspectively, clinical improvement after certain treatment could be classified. Methods: This study describes for the first time MRI findings following the induction of septic peritonitis in mice using the CASP model. Two sublethal groups of mice with septic peritonitis were investigated. Each had received one of two differing stent diameters in order to control the leakage of feces into the abdominal cavity. Each mouse served as its own control. Imaging and analyses were performed blinded. Gut diameters, stomach volume, abdominal organ wall diameters, and volume of the adrenal glands were measured. Serum corticosterone levels were detected using ELISA. Serum IL-6, TNF-α, IL-1β, and IL-10 levels were screened by cytometric bead array. Statistical analysis was performed using the Mann-Whitney U test for nonparametric probes and the Kruskal-Wallis and t tests. Results: Using a 7-tesla MRI scanner 24 and 48 h after induction of septic peritonitis, interenteric fluid, organ swelling of spleen and adrenal glands, as well as dilatation of the stomach were compared to nonseptic conditions. Swelling of adrenal glands resulted in an increased serum corticosterone level. In addition, the wall of the intestine bowel was thickened. Based upon these findings, an MRI score (MRI sepsis score, MSS) for abdominal sepsis in mice was established. Reduced stent sizes led to reduced severity of the abdominal sepsis, which could be reproduced in the MSS, which is described here for the first time. Conclusions: Intraabdominal variations during septic peritonitis are detectable by MRI techniques. MRI methods should become a more important tool for the evaluation of abdominal peritonitis. MSS could provide an interesting tool for the evaluation of therapeutic strategies.

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Zantl, N., C.-D. Heidecke, B. Holzmann, and K. Pfeffer. "COLON ASCENDENS STENT PERITONITIS: A NOVEL SURGICAL MODEL FOR THE INDUCTION OF BACTERIAL PERITONITIS/SEPSIS IN MICE." Shock 7, Supplement (1997): 137. http://dx.doi.org/10.1097/00024382-199703001-00556.

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Dissertations / Theses on the topic "Peritonitis model in mice"

1

Diedrich, Stephan, der Linde Julia van, Michael Nielson, et al. "The MRI Sepsis Score: An Innovative Tool for the Evaluation of Septic Peritonitis in Mice Using 7-Tesla Small Animal MRI." Karger, 2018. https://tud.qucosa.de/id/qucosa%3A38909.

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Background: Magnetic resonance imaging (MRI) techniques are rarely used in the context of abdominal sepsis and in sepsis research. This study investigates the impact of MRI for monitoring septic peritonitis in an animal model (colon ascendens stent-induced peritonitis, CASP). The CASP model closely mimics that of human disease and is highly standardized. The most frequently employed readout parameter in mouse CASP studies is prolonged or decreased rate of survival. Monitoring the progression of peritonitis via MRI could provide a helpful tool in the evaluation of severity. The use of alternative readout systems could very well reduce the number of research animals. Perspectively, clinical improvement after certain treatment could be classified. Methods: This study describes for the first time MRI findings following the induction of septic peritonitis in mice using the CASP model. Two sublethal groups of mice with septic peritonitis were investigated. Each had received one of two differing stent diameters in order to control the leakage of feces into the abdominal cavity. Each mouse served as its own control. Imaging and analyses were performed blinded. Gut diameters, stomach volume, abdominal organ wall diameters, and volume of the adrenal glands were measured. Serum corticosterone levels were detected using ELISA. Serum IL-6, TNF-α, IL-1β, and IL-10 levels were screened by cytometric bead array. Statistical analysis was performed using the Mann-Whitney U test for nonparametric probes and the Kruskal-Wallis and t tests. Results: Using a 7-tesla MRI scanner 24 and 48 h after induction of septic peritonitis, interenteric fluid, organ swelling of spleen and adrenal glands, as well as dilatation of the stomach were compared to nonseptic conditions. Swelling of adrenal glands resulted in an increased serum corticosterone level. In addition, the wall of the intestine bowel was thickened. Based upon these findings, an MRI score (MRI sepsis score, MSS) for abdominal sepsis in mice was established. Reduced stent sizes led to reduced severity of the abdominal sepsis, which could be reproduced in the MSS, which is described here for the first time. Conclusions: Intraabdominal variations during septic peritonitis are detectable by MRI techniques. MRI methods should become a more important tool for the evaluation of abdominal peritonitis. MSS could provide an interesting tool for the evaluation of therapeutic strategies.

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2

Gallimore, Barbara. "Characterization of experimental Staphylococcus epidermidis peritonitis in chronically uremic mice." Thesis, McGill University, 1987. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75686.

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A mouse model of surgically induced renal failure was utilized to investigate the pathogenesis of Staphylococcus epidermidis peritonitis which is a frequent and serious complication of continuous ambulatory peritoneal dialysis (CAPD). Compared to sham-operated controls, chronically uremic mice were more susceptible to intraperitoneal S. epidermidis inoculation, presenting decreased survival time and survival (10$ sp9$ cfu, 10$ sp8$ cfu), delayed bacterial clearance and attenuated peritoneal inflammatory response (10$ sp6$ cfu). In mice bearing a peritoneal catheter implant, the catheter was a preferred site for peritoneal bacterial persistence up to one month after intracatheter inoculation. Despite in vitro cytotoxicity of commercial peritoneal dialysis solutions toward peritoneal leucocytes, repeated peritoneal instillation of dialysis solutions did not influence S. epidermidis recoveries following inoculation. Although the mouse preparation did not undergo peritoneal dialysis, these studies nevertheless demonstrate that chronic uremia and the peritoneal catheter may be important etiological factors in the development and persistence of CAPD peritonitis.

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Su, FUHONG. "Adjunctive therapies in an ovine model of septic shock due to fecal peritonitis." Doctoral thesis, Universite Libre de Bruxelles, 2007. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/210580.

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Sepsis remains a severe issue in critically ill patients. Adjunctive therapies might play important role to decrease morbidity and mortality. The aim of this thesis is to investigate new adjunctive therapies role in the treatment of sepsis and septic shock.<br>Doctorat en Sciences biomédicales et pharmaceutiques<br>info:eu-repo/semantics/nonPublished

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Brant, Jamet Ann. "Devleopment of an in vitro model of peritonitis complicating continuous ambulatory peritoneal dialysis." Thesis, University of Brighton, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337400.

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Wang, YueYi. "Ca2+ handling in a mice model of CPVT." Thesis, Université Paris-Saclay (ComUE), 2016. http://www.theses.fr/2016SACLS156/document.

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Le canal calcique de libération du Ca2+, appelé récepteur à la ryanodine (RyR) est localisé dans la membrane du réticulum sarcoplasmique des cardiomyocytes, en incluant ceux du pacemaker, et a un rôle important dans le couplage excitation contraction et la génération du rythme cardiaque. Des mutations dans leur gène sont responsables de la tachycardie catécholergique (CPVT), qui est une maladie létale, manifestée par des syncopes ou mort subite lors de stress émotionnel ou physique. Au repos, ces patients ont un électrocardiogramme normal, mais une tendance plus importante à la bradycardie.Nos collaborateurs ont identifié la mutation RyR2R420Q dans une famille espagnole atteinte de CPVT. Nous avons construit une souris portant cette mutation et étudié l’activité du nœud sinoatrial (NSA, pacemaker principale) afin d’élucider les mécanismes.Nous avons trouvé que les cellules du NSA présentent une activité spontanée plus lente que les souris sauvages (WT). Dans la cellule in situ, on peut étudier l’activité des RyRs par l’analyse des « sparks » Ca2+, qui sont des évenements élémentaires produits par l’activation d’un cluster des RyRs. Nos analyses en microscopie confocale sur des NSA disséquées on montré que la fréquence des sparks Ca2+ était légèrement augmentée. Par contre, la longueur de ces sparks est fortement prolongée dans les cellules KI. Ceci produit une libération plus importante de Ca2+ pendant la diastole dans les cellules KI qui réduit l’automatisme, en réduisant la charge en Ca2+ du réticulum sarcoplasmique et en inactivant le courant calcique type L. Donc les thérapies en étude qi favoriseraient la stabilisation du RyR2 en état fermé pourraient ne pas Être efficaces, et il faudra plutôt essayer des thérapies qui faciliteraient la fermeture du canal, une fois il est ouvert<br>The cardiac type-2 ryanodine receptor (RyR2) encodes a Ca2+ release channel on sarcoplasmic reticulum (SR) membrane in cardiomyocytes, including sinoatrial node (SAN) myocytes, and releases Ca2+ required for contraction and SAN spontaneous rhythm. Its genetic defects are related to catecholaminergic polymorphic ventricular tachycardia (CPVT), which is a lethal heritable disease characterized by exercise/stress-induced syncope and/or sudden cardiac death. Interestingly, CPVT patients frequently present SAN dysfunction as bradycardia at rest.In a previous study, a novel CPVT-related RyR2 mutation (RyR2R420Q) in a Spanish family, associated with SAN dysfunction was reported. R420 is located at the N-terminal portion of the channel and seems to be an important site for maintaining a stable A/B/C domain of N-terminus in RyR2. As N-terminal mutation resultant RyR2 behaviour and SAN function are never analyzed before, we created the KI mice model bearing mutation R420Q to understand the underlying mechanism.In this thesis, we found increased Ca2+ release during diastole, indicating a gain-of-function effect of RyR2 N-terminal mutation R420Q. Interestingly, this defect may not be only an enhanced activity, as the Ca2+ sparks frequency was only slightly increased in KI, but also the closing mechanism, producing longer Ca2+ sparks. That is, the number of Ca2+ sparks is increased by the RyR2R420Q mutation, and meanwhile the amount of Ca2+ released in each Ca2+ spark is also dramatically enhanced. This increased Ca2+ release retards SR Ca2+ replenishment, disrupting the Ca2+ clock and the coupled clock, resulting in the slower SAN function. Thus favouring RyR stabilization in the closing state might not be an adequate therapy but accelerating its closure

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Luiza, Batista Camilla. "Humanized mice as model for Plasmodium vivax infection." Electronic Thesis or Diss., Sorbonne université, 2021. http://www.theses.fr/2021SORUS232.

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Le paludisme est une maladie transmise par les moustiques causée par des espèces de Plasmodium, parmi lesquelles P. falciparum et P. vivax représentent problème de santé majeur avec plus de 400 000 victimes et 250 millions de cas cliniques signalés chaque année. P. vivax est reconnu comme une maladie débilitante et terrible. La mauvaise compréhension de la biologie des parasites est due au manque de culture à long terme et de modèles murins fidèles, ce qui reste difficile en raison de son tropisme pour les globules rouges (GR) immatures CD71+. Le nouveau modèle chimérique appelé HERYHIS pour Human ERYthrocytes Human Immune System héberge des cellules cibles CD71+ lors d'une greffe avec des progéniteurs hématopoïétiques humains et prendre en charge une infection de novo par P. vivax après injection de GR infectés d'isolats de patients, y compris l'infection d'érythrocytes en développement nucléés dans la moëlle osseuse (MO) chimérique. P. vivax a été maintenu après le transfert de cellules MO de souris infectées dans des chimères secondaires. Des parasites sexués ont également été détectés et transmis à Anopheles lors d'un repas directe, suivie de la production de sporozoïtes des glandes salivaires. Enfin, il pourrait s’avérer être une plateforme idéale pour tester l’efficacité de nouvelles approches thérapeutiques et vaccinales, constituant un modèle préclinique de choix<br>Malaria is mosquito-borne disease caused by Plasmodium species, among which P. falciparum and P. vivax are a major health burden with more than 400.000 victims and 250 million clinical cases reported annually. P. vivax is now recognized as a debilitating and dreadful disease. The poor understanding of parasite biology is mainly due to the lack of long-term culture and reliable rodent models which remains challenging due to its tropism for CD71+ immature RBCs, a subset that is rare in circulating blood. Devising a new chimeric model able to support efficient human erythropoiesis upon engraftment with human hematopoietic progenitors overcame this problem. This chimeric model called HERYHIS for Human ERYthrocytes Human Immune System can support de novo productive infection by P. vivax upon injection of P. vivax infected RBCs from patients’ isolates including the infection of nucleated developing erythrocytes within the chimeric bone marrow (BM). P. vivax was maintained after BM cells transfer from infected mice into secondary chimeras. Sexual stages parasites were also detected and transmitted to Anopheles upon direct feeding, followed by of salivary gland sporozoites production. Together, these results show that HERYHIS mice should constitute ideal platform for the screening of drug library and the pre-clinical test of new drug and vaccine efficacy

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Swartz, Daniel E. "Alterations of polymorphonuclear neutrophi, PMN, recruitment in a murine model of peritonitis and a secondary injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0021/MQ55091.pdf.

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Swartz, Daniel E. "Alterations of Polymorphonuclear neutrophil (PMN) recruitment in a murine model of peritonitis and a secondary injury." Thesis, McGill University, 1999. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=29924.

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Secondary peritonitis is a significant cause of morbidity and mortality in the ICU and ICU patients as a group have the highest rate of nosocomial infections. Once recruited to the site of injury, the PMN interacts with endothelial cells (ECs) via rolling adhesion, firm adhesion, and transendothelial migration. Using a murine cecal ligation and puncture peritonitis model and either skin or cremaster injury as the secondary site in a two-front injury model, we examined the role of injury severity on the triage of PMNs to competing sites of injury. We demonstrated that a finite pool of PMNs was recruited to tissues in numbers correlating to the severity major injury. With intravital microscopy we demonstrated that numbers of PMNs involved in rolling adhesion, rolling velocity and stationary adhesion in the presence of one or more sites of injury were predictable, consistent and likely mediated by changes in surface adhesion molecule expression.

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So, Chi-leung. "Transgenic mouse model of human chondrodysplasia /." Hong Kong : University of Hong Kong, 1997. http://sunzi.lib.hku.hk/hkuto/record.jsp?B19161347.

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Bishop, Katherine Mary. "A threshold model for development of the corpus callosum in normal and acallosal mice." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/nq22952.pdf.

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Books on the topic "Peritonitis model in mice"

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Martin, Hrabé de Angelis, Chambon Pierre, and Brown Stephen D. M, eds. Standards of mouse model phenotyping. Wiley-VCH, 2006.

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Lamoreux, M. Lynn. The colors of mice: A model genetic network. Wiley-Blackwell, 2010.

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Lynn, Lamoreux M., ed. The colors of mice: A model genetic network. Wiley-Blackwell, 2010.

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A, Goffinet, ed. The reeler mouse as a model of brain development. Springer, 1998.

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Ferrick, David A. Transgenic mice as a in vivo model for self reactivity. R.G. Landes Co., 1994.

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1947-, McQueen Charlene A., ed. In vitro toxicology: Model systems and methods. Telford Press, 1989.

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1931-, Takeda Toshio, ed. The SAM model of senescence: Proceedings of the first International Conference on Senescence, the SAM model, Kyoto, 17-18 March 1994. Excerpta Medica, 1994.

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Brakebusch, Cord. Mouse as a Model Organism: From Animals to Cells. Springer Science+Business Media B.V., 2011.

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International Conference on Senescence (2nd 2003 Sapporo-shi, Japan). The senescence-accelerated mouse (SAM): An animal model of senescence : proceedings of the 2nd International Conference on Senescence, the SAM model, held in Sapporo, Japan between 21 and 23 July 2003. Edited by Nomura Yasuyuki Ph D, Takeda Toshio 1931-, and Okuma Yasunobu Ph D. Elsevier, 2004.

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Stilton, Gerónimo. Top model per un giorno. Piemme, 2011.

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Book chapters on the topic "Peritonitis model in mice"

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Giraud, Antoine. "Axenic Mice Model." In Innate Immunity. Humana Press, 2008. http://dx.doi.org/10.1007/978-1-59745-570-1_19.

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Kyuwa, S., Y. Tagawa, K. Machii, et al. "MHV-Induced Fatal Peritonitis in Mice Lacking IFN-γ." In Advances in Experimental Medicine and Biology. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_56.

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Sasaki, Takeshi, Kae Nakamura, and Masafumi Kuzuya. "Plaque Rupture Model in Mice." In Methods in Molecular Medicine™. Humana Press, 2007. http://dx.doi.org/10.1007/978-1-59745-571-8_3.

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Heljasvaara, Ritva, and Taina Pihlajaniemi. "Experimental Tumour Models in Mice." In Mouse as a Model Organism. Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-0750-4_5.

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Ray Banerjee, Ena. "Aseptic Peritonitis Model for Drug Discovery (As Therapy)." In Perspectives in Translational Research in Life Sciences and Biomedicine. Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0989-1_3.

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Ray Banerjee, Ena. "Aseptic Peritonitis Model for Drug Discovery (for Prophylaxis)." In Perspectives in Translational Research in Life Sciences and Biomedicine. Springer Singapore, 2016. http://dx.doi.org/10.1007/978-981-10-0989-1_4.

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Quan, D., Z. Zhang, A. Jevnikar, R. Zhong, and D. Grant. "Intestinal Transplantation in the Murine Model." In Organtransplantation in Rats and Mice. Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_66.

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Vennema, Harry, Raoul J. de Groot, David A. Harbour, et al. "Immunogenicity of Recombinant Feline Infectious Peritonitis Virus Spike Protein in Mice and Kittens." In Advances in Experimental Medicine and Biology. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5823-7_30.

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Grimm, H., P. Mages, and G. Lindemann. "Technique of Plasmapheresis in the Xenogeneic Rat Model." In Organtransplantation in Rats and Mice. Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-72140-3_59.

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Cesano, Alessandra, and Daniela Santoli. "SCID Mice as a Model for Human Leukemias." In Human Hematopoiesis in SCID Mice. Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-662-22008-5_9.

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Conference papers on the topic "Peritonitis model in mice"

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Lee, Yu-Hsuan, Yi-Ke Lin, Ta-Ching Chen, and Lih-Chu Chiou. "Novel glaucoma therapy rescuing excitotoxicity in an ischemia-reperfusion mice model." In Mechanisms of Photobiomodulation Therapy XIX, edited by James D. Carroll, Ann Liebert, and Jeri-Anne Lyons. SPIE, 2025. https://doi.org/10.1117/12.3054809.

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Subramani, Nishant, Jason Eisner, Justin Svegliato, Benjamin Van Durme, Yu Su, and Sam Thomson. "MICE for CATs: Model-Internal Confidence Estimation for Calibrating Agents with Tools." In Proceedings of the 2025 Conference of the Nations of the Americas Chapter of the Association for Computational Linguistics: Human Language Technologies (Volume 1: Long Papers). Association for Computational Linguistics, 2025. https://doi.org/10.18653/v1/2025.naacl-long.615.

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Obanina, Natalia, and Nataliya Bgatova. "Effect of Lithium and Chloroquine on Neuronal Ultrastructure in a Melanoma Mice Model." In 2024 IEEE International Multi-Conference on Engineering, Computer and Information Sciences (SIBIRCON). IEEE, 2024. http://dx.doi.org/10.1109/sibircon63777.2024.10758443.

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Seeley, Eric J., Sophia S. Kim, Michael A. Matthay, and Paul J. Wolters. "Endogenous Catecholamines Impair Innate Immune Responses And Worsen Survival During Septic Peritonitis In Mice." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a3852.

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Du, Liping, Hongyan Niu, Xuekuang Zhang, and Dongguang Xiao. "Preparation of Glucan Sulfates with Different Degree of Substitution and Their Immunoprophylaxis Potentials in Escherichia coli Induced Mice Peritonitis." In 2010 4th International Conference on Bioinformatics and Biomedical Engineering (iCBBE). IEEE, 2010. http://dx.doi.org/10.1109/icbbe.2010.5516040.

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Stergar, Jost, Katja Lakota, Martina Perseˇ, Matija Tomsic, and Matija Milanic. "Vasculature-based biomarkers and segmentation from hyperspectral images of murine peritonitis model." In Translational Biophotonics: Diagnostics and Therapeutics, edited by Lothar D. Lilge and Zhiwei Huang. SPIE, 2021. http://dx.doi.org/10.1117/12.2614589.

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Wahyudin, Nanang, Sandy Pratama, and Echo Perdana Kusumah. "MICE Model: Artificial Tourism Potential." In Proceedings of the International Conference on Maritime and Archipelago (ICoMA 2018). Atlantis Press, 2019. http://dx.doi.org/10.2991/icoma-18.2019.56.

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Tackett, S., R. Zamora, C. Clifford, et al. "Respiratory and Neuro-Inflammatory Control Networks in a Rat Model of E. Coli Peritonitis." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a7610.

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Ueda-Arima, Tomomi, Koichi Fukunaga, Jun Miyata, Hiroshi Seki, Junzo Takeda, and Koichiro Asano. "The Effect Of Anti-Inflammatory Lipid Mediator, Lipoxin A4, In A Murine Peritonitis Model." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4678.

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Plotkin, Dmitry, Tatiana Vinogradova, Mikhail Reshetnikov, Mikhail Sinitsyn, and Sergey Okovityi. "IDDF2021-ABS-0013 The method for obtaining a reproducible model of tuberculous peritonitis in rabbits." In Abstracts of the International Digestive Disease Forum (IDDF), Hong Kong, 4–5 September 2021. BMJ Publishing Group Ltd and British Society of Gastroenterology, 2021. http://dx.doi.org/10.1136/gutjnl-2021-iddf.21.

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Reports on the topic "Peritonitis model in mice"

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ศิริวิชยกุล, สุณี, เอกชัย พรหมเพชร, ภัทรวัจน์ ตันติวรสิทธิ์, นิธิรา อนัคกุล та เกียรติ รักษ์รุ่งธรรม. โครงการ การแยกเซลล์ต้นกำเนิดจากสายสะดือเพื่อสร้าง humanized mice เพื่อใช้ในการทดสอบวัคซีนเอดส์ในระดับก่อนการทดสอบในมนุษย์ : รายงานการวิจัยฉบับสมบูรณ์. คณะแพทยศาสตร์ จุฬาลงกรณ์มหาวิทยาลัย, 2016. https://doi.org/10.58837/chula.res.2016.24.

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ในความพยายามที่จะหาสัตว์ทดลองที่จะใช้ทดสอบวัคซีนเพื่อให้ได้ผลการตอบสนองทางภูมิคุ้มกันที่ใกล้เคียงกับคนที่สุดนั้น humanized mice model เป็นทางเลือกที่สามารถให้การตอบสนองทางภูมิคุ้มกันที่ใกล้เคียงกับการตอบสนองในคนมากที่สุด กล่าวคือ humanized mice เป็นหนูทดลองที่ได้รับการปลูกถ่ายเซลล์ต้นกำเนิดของคน (C034+ human hematopoietic stem cells) ที่แยกได้จากเลือดที่เจาะจากสายสะดือทารกแรกคลอด เพื่อให้เซลล์ต้นกำเนิดของคนไปเจริญเติบโตเป็นเซลล์ที่รับผิดชอบต่อการตอบสนองทางภูมิคุ้มกัน เช่น lymphocytes และ macrophages ในหนู โดยถือว่าการปลูกถ่ายเซลล์ต้นกำเนิดประสบความสำเร็จ ต่อเมื่อสามารถตรวจพบเซลล์ที่เกี่ยวกับระบบภูมิคุ้มกันของคนได้มากกว่า 20% เมื่อเจาะเลือดหนูมาตรวจ จากการปลูกถ่ายเซลล์ต้นกำเนิด 200,000 เซลล์แก่ลูกหนูแรกคลอดอายุระหว่าง 3-5 วัน จำนวน 57 ตัว พบว่ามีลูกหนูเพียง 13/57 (22.8%) ที่มีเซลล์ภูมิคุ้มกันของคนอยู่มากกว่า 20% แต่มีเพียง 8 ตัวที่รอดชีวิตอยู่จนสามารถนำมาทดสอบวัคซีนได้ โดยมีค่าเฉลี่ยเซลล์ภูมิคุ้มกันของคนอยู่ที่ 56.7% (24.5), range 22.9-89.2% ก่อนที่จะมีการฉีดวัคซีน หนู 6 ตัวได้รับ Asian mosaic HIV DNA vaccine โดยการฉีดเข้ากล้ามและตามด้วยการกระตุ้นด้วยไฟฟ้า (electroporator) ในปริมาณ 100 ไมโครกรัม 3 ครั้ง แต่ละครั้งห่างกัน 2 สัปดาห์ และทำการประเมินการตอบสนองทางภูมิคุ้มกันหลังจากฉีดเข็มที่ 3 ครบ 1 สัปดาห์ ในขณะที่หนูอีก 2 ตัวเป็น negative control ซึ่งถูกฉีดด้วย plasmid vector (pCMVKan) การศึกษานี้ตรวจการตอบสนองทางด้านแอนติบอดีด้วยวิธี western blot เพื่อดูว่าหนูมีการสร้าง anti-gp41, anti-gp120 หรือ anti-gp160 หรือไม่ ซึ่งผลของการทดลอง พบว่าหนูไม่มีการสร้างแอนติบอดีดังกล่าวเลย คณะผู้วิจัยตรวจการตอบสนองทางด้านเซลล์ด้วยวิธี ELISpot โดยกระตุ้นเซลล์ด้วย pooled peptides ของ HIV-1 CRF01_AE และ HIV-1 B พบว่ามีหนู 1 ตัว ที่มีการตอบสนองต่อการกระตุ้นด้วย HIV-1 CRF01 AE ที่ 90.7 SPC (spot forming cells)/10⁶ splenocytes และตอบสนองต่อการกระตุ้นด้วย HIV-1 B pooled peptides ที่ 153.3 SPC/10⁶ splenocytes และหนู 1 ตัว มีเพียงการตอบสนองต่อการกระตุ้นด้วย HIV-1 B pooled peptides ที่ 85.3 SPC/10⁶ splenocytes โดยที่ไม่มีการตอบสนองต่อการกระตุ้นด้วย HIV-l CRF01 AE pooled peptides ผลการศึกษาแสดงว่า humanized mice model นี้สามารถนำมาใช้ทดสอบการตอบสนองทางภูมิคุ้มกันต่อวัคซีนในระดับ pre-clinical ได้ แต่ขบวนการผลิต humanized mice จะต้องได้รับการพัฒนาให้มีประสิทธิภาพมากกว่านี้

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Robins, Diane M. Humanized Androgen Receptor Mice: A Genetic Model for Differential Response to Prostate Cancer Therapy. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada582175.

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Robins, Diane. Humanized Androgen Receptor Mice: A Genetic Model for Differential Response to Prostate Cancer Therapy. Defense Technical Information Center, 2011. http://dx.doi.org/10.21236/ada547343.

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Pilitkul, Trairak, Prapaporn Pisitkun, Asada Leelahavanichkul, and Poorichaya Somparn. Systems-investigation of aberrant signaling in immune cells of SLE mouse model. Faculty of Medicine, Chulalongkorn University, 2020. https://doi.org/10.58837/chula.res.2020.21.

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Autoimmune diseases occur when the immune cells react against self antigens and subsequently lead to inflammation in the tissues. The interactions between genetics and environmental triggers regulate the phenotypes and outcome of the diseases. Type I interferon has been shown as one of the most crucial cytokines involving in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SLE is a chronic systemic autoimmune disease which can result in autoantibody production and fatal glomerulonephritis. Activation via nucleic acid sensors can induce the production of type I interferon from dendritic cells and promote SLE severity. Stimulator of interferon genes (Sting) is a cytoplasmic DNA sensor that signals downstream to enhance type I interferon production after its activation. Recently, it was shown that a gain mutation in the STING gene resulting in over activity of the IFN pathway can cause familial inflammatory syndrome with lupus like manifestations in humans. However, the functional studies of Sting in different autoimmune mouse models suggest the conflicting roles of Sting in the pathogenesis of autoimmune diseases. In order to determine if Sting participates in lupus pathogenesis, the Fcgr2b deficienct mice (lupus mouse model) were bred with Sting deficient mice to create the double deficient mice. In the absence of Sting, the Fcgr2b deficient mice do not develop fatal glomerulonephritis and autoantibodies. The original knowledge from this study is a proof of concept for targeting Sting as a future promising treatment in autoimmune diseases.

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Pilitkul, Trairak, Prapaporn Pisitkun, and Asada Leelahavanichkul. Systems-investigation of aberrant signaling in immune cells of SLE mouse model. Faculty of Medicine, Chulalongkorn University, 2015. https://doi.org/10.58837/chula.res.2015.22.

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Autoimmune diseases occur when the immune cells react against self-antigens and subsequently lead to inflammation in the tissues. The interactions between genetics and environmental triggers regulate the phenotypes and outcome of the diseases. Type I interferon has been shown as one of the most crucial cytokines involving in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). SLE is a chronic systemic autoimmune disease which can result in autoantibody production and fatal glomerulonephritis. Activation via nucleic acid sensors can induce the production of type I interferon from dendritic cells and promote SLE severity. Stimulator of interferon genes (Sting) is a cytoplasmic DNA sensor that signals downstream to enhance type I interferon production after its activation. Recently, it was shown that a gain mutation in the STING gene resulting in over-activity of the IFN pathway can cause familial inflammatory syndrome with lupus-like manifestations in humans. However, the functional studies of Sting in different autoimmune mouse models suggest the conflicting roles of Sting in the pathogenesis ofautoimmune diseases. In order to determine if Sting participates in lupus pathogenesis, the Fcgr2b-deficienct mice (lupus mouse model) were bred with Sting-deficient mice to create the double-deficient mice. In the absence of Sting, the Fcgr2b-deficient mice do not develop fatal glomerulonephritis and autoantibodies. The original knowledge from this study is a proof of concept for targeting Sting as a future promising treatment in autoimmune diseases.

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Matory, Yvedt L. Evaluation of a Mouse Model for Prophylactic Mastectomy in Mice Genetically Predisposed to Breast Cancer. Defense Technical Information Center, 2001. http://dx.doi.org/10.21236/ada400613.

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Deng, Yingjun, ShengJing Liu, Ming Zhao, Feng Zhao, Jun Guo, and Bin Yan. Diet-induced male infertility in mice models: a systematic review and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, 2022. http://dx.doi.org/10.37766/inplasy2022.5.0116.

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Review question / Objective: In order to compare the different high energy diet such as high-fat diet and high sugar diet how to damage the male mice model in metabolize and fertility,and explore a reliable mice model method in the study of obesity with male infertility. P：obesity mice model with male infertility. I: High energy diet such as High-fat or High-sugar diet. C:High-fat diet,High-sugar diet, compared with normal diet in mice model. O:High energy diet induce male mice obesity model and damage their fertility. S: Use network meta-analysis. Condition being studied: The relationship between obesity and male infertility attacth more and more attention at present.So many animal expriments are carried out on this problem,there are enough exprimental article to support this meta analysis.

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Li, Xiao-Nan. Harnessing Autopsied DIPG Tumor Tissues for Orthotopic Xenograft Model Development in the Brain Stems of SCID Mice. Defense Technical Information Center, 2012. http://dx.doi.org/10.21236/ada568355.

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Alves-Borba, Laryssa, Verónica Espinosa-Fernández, Ania Canseco Rodriguez, and Ana María Sánchez-Pérez. ABA Supplementation Rescues IRS2 and BDNF mRNA Expression in a Triple-Transgenic Mice Model of Alzheimer’s Disease. Universitat Jaume I, 2023. http://dx.doi.org/10.6035/uji_b201801.

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Tumwasorn, Somying, and Asada Leelahavanichkul. Effect of Lactobacillus and Bifidobacterium on the inhibition of Clostridium difficile in mouse infection model. Chulalongkorn University, 2018. https://doi.org/10.58837/chula.res.2018.25.

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Clostridium difficile is a major cause antibiotic-associated diarrhea and colitis in patients with broad-spectrum antibiotic therapy. A disruption of the gut microbiota by using antibiotics results in colonization with C. difficile and release of toxins that cause leaky gut and the production inflammatory cytokines. We identified six specific strains of Lactobacillus or Bifidobacterium are able to reduce leaky gut and inflammation caused by C. difficile in vitro. In this study, we aim to investigate the effect of these strains either alone or in combination on the inhibition of C. difficile infection in a C57BL/6 mouse model. The administration of L. rhamnosus L34 (1x10⁶ cells) for 4 days at the day of clindamycin injection to the day before sacrifice (D-1 to D2) reduced mortality, body weight change, diarrhea, gut leakage and pathology of mice and also suppressed the production of tissue and systemic inflammatory cytokines including MIP-2, KC, IL-1β and TNF-α. The administration of 1x10⁸ cells of L. casei L39, L. casei B13, L. casei B106, B. bifidum NB42 or B. pseudocatenulatum NB48 alone reduced mortality, body weight change and diarrhea in mice. L. casei L39, L. casei B13 and L. casei 106 administration also reduced the production of some tissue and systemic inflammatory cytokines. The effect of Bifidobacterium spp. on cytokine production was not determined yet. Only Lacto cocktail (L. rhamnosus L34 and L. casei L39) attenuated the disease severity whereas Bifido cocktail (B. bifidum NB42 or B. pseudocatenulatum NB48) or Lacto-Bifido cocktail (L. rhamnosus L34, L. casei L39, B. bifidum NB42, B. pseudocatenulatum NB48) did not. These strains are promising probiotics for C. difficile infection.

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