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 Modulation of the Local Neutrophil Response by a Novel Hyaluronic Acid-Binding Peptide Reduces Bacterial Burden during Staphylococcal Wound Infection

2010 ◽  
Vol 78 (10) ◽  
pp. 4176-4186 ◽  
Author(s):  
Jerry C. Lee ◽  
Jennifer L. Greenwich ◽  
George G. Zhanel ◽  
Xiaobing Han ◽  
Andrew Cumming ◽  
...  
Keyword(s):  
Wound Infection ◽  
Surgical Wound Infection ◽  
Infection Site ◽  
Bacterial Burden ◽  
Surgical Wound ◽  
Antibiotic Resistant ◽  
Binding Peptide ◽  
Cxc Chemokine ◽  
Neutrophil Response ◽  
Hyaluronic Acid Binding

ABSTRACT Novel approaches targeting the host's immune response to treat Staphylococcus aureus infections have significant potential to improve clinical outcomes, in particular during infection with antibiotic-resistant strains. The hyaluronic acid-binding peptide (HABP) PEP35 was assessed for its ability to treat S. aureus infections using a clinically relevant murine model of surgical wound infection. PEP35 demonstrated no direct antimicrobial activity against a range of antibiotic-susceptible and antibiotic-resistant clinical isolates of Staphylococcus aureus. However, when this peptide was administered at the onset of infection and up to 4 h postchallenge with a methicillin-susceptible (MSSA) or a methicillin-resistant (MRSA) strain of S. aureus, it significantly reduced the bacterial burden at the wound infection site. PEP35 reduced the tissue bacterial burden by exclusively modulating the local neutrophil response. PEP35 administration resulted in a significant early increase in local CXCL1 and CXCL2 production, which resulted in a more rapid influx of neutrophils to the infection site. Importantly, neutrophil influx was not sustained after treatment with PEP35, and administration of PEP35 alone did not induce a local inflammatory response. The immunomodulatory effects of PEP35 on CXC chemokine production were TLR2 and NF-κB dependent. We propose a novel role for a HABP as an innate immunomodulator in the treatment of MSSA and MRSA surgical wound infection through enhancement of the local CXC chemokine-driven neutrophil response.

scholarly journals Immunogenicity and protective efficacy of Vibrio vulnificus flagellin protein FlaB in a wound infection model

2018 ◽  
Vol 80 (1) ◽  
pp. 55-58 ◽  
Author(s):  
Kohei YAMAZAKI ◽  
Takashige KASHIMOTO ◽  
Yuki HASHIMOTO ◽  
Takehiro KADO ◽  
Shunji UENO
Keyword(s):  
Wound Infection ◽  
Vibrio Vulnificus ◽  
Protective Efficacy ◽  
Infection Model

scholarly journals Expansion of Necrosis Depending on Hybrid Motor-Driven Motility of Aeromonas hydrophila in a Murine Wound Infection Model

2020 ◽  
Vol 9 (1) ◽  
pp. 10
Author(s):  
Kohei Yamazaki ◽  
Takashige Kashimoto ◽  
Ayuha Niwano ◽  
Moeko Yamasaki ◽  
Mayu Nomura ◽  
...  
Keyword(s):  
Wound Infection ◽  
Aeromonas Hydrophila ◽  
Systemic Circulation ◽  
Rapid Expansion ◽  
Infection Model ◽  
Survival Times ◽  
Genes Encoding ◽  
Vitro Analysis

The gram-negative bacterium Aeromonas hydrophila is a cause of fulminant and lethal necrotizing soft tissue infections (NSTIs). Suppressing the rapid proliferation of the pathogen and expansion of the necrosis caused in the host is an important issue in clinical practice, but the pathogenic mechanism for the rapid aggravation has not been clarified. In this study, we characterized the function of two types of motor stators in A. hydrophila and explored the role of motility during wound infection. In vitro analysis showed that the motility was reliably maintained while being complemented by the stators. We created a non-motile strain that lacked genes encoding two types of motor stators and analyzed the role of motility in a murine wound infection model. Examination of the bacterial burden in the local infection site and systemic circulation revealed that motility was not essential for the proliferation of A. hydrophila in the host. However, the extent of necrosis at the lesions was lower, and survival times were prolonged in mice infected with the non-motile strain compared with mice infected with the parent strain. These results provide evidence that the rapid expansion of necrosis and the progression to death within a short time period is dependent on the motility of A. hydrophila.

scholarly journals Antimicrobial efficacy and toxicity of novel CAMPs against P. aeruginosa infection in a murine skin wound infection model

2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Ming Yang ◽  
Chunye Zhang ◽  
Sarah A. Hansen ◽  
William J. Mitchell ◽  
Michael Z. Zhang ◽  
...  
Keyword(s):  
Antimicrobial Peptides ◽  
Wound Infection ◽  
Topical Application ◽  
Bacterial Load ◽  
Systemic Infection ◽  
Chemotherapeutic Agents ◽  
Infection Model ◽  
Bacterial Burden ◽  
Dose Equivalent ◽  
Promising Alternative

Abstract Background Treatment of P. aeruginosa wound infection is challenging due to its inherent and acquired resistance to many conventional antibiotics. Cationic antimicrobial peptides (CAMPs) with distinct modes of antimicrobial action have been considered as the next-generation therapeutic agents. In the present study, a murine skin surgical wound infection model was used to evaluate the in vivo toxicity and efficacy of two newly designed antimicrobial peptides (CAMP-A and CAMP-B), as chemotherapeutic agents to combat P. aeruginosa infection. Results In the first trial, topical application of CAMPs on the wounds at a dose equivalent to 4 × MIC for 7 consecutive days did not cause any significant changes in the physical activities, hematologic and plasma biochemical parameters, or histology of systemic organs of the treated mice. Daily treatment of infected wounds with CAMP-A and CAMP-B for 5 days at a dose equivalent to 2× MIC resulted in a significant reduction in wound bacterial burden (CAMP-A: 4.3 log10CFU/g of tissue and CAMP-B: 5.8 log10CFU/g of tissue), compared to that of the mock-treated group (8.1 log10CFU/g of tissue). Treatment with CAMPs significantly promoted wound closure and induced epidermal cell proliferation. Topical application of CAMP-A on wounds completely prevented systemic dissemination of P. aeruginosa while CAMP-B blocked systemic infection in 67% of mice and delayed the onset of systemic infection by at least 2 days in the rest of the mice (33%). In a second trial, daily application of CAMP-A at higher doses (5× MIC and 50× MIC) didn’t show any significant toxic effect on mice and the treatments with CAMP-A further reduced wound bacterial burden (5× MIC: 4.5 log10CFU/g of tissue and 50× MIC: 3.8 log10CFU/g of tissue). Conclusions The data collectively indicated that CAMPs significantly reduced wound bacterial load, promoted wound healing, and prevented hepatic dissemination. CAMP-A is a promising alternative to commonly used antibiotics to treat P. aeruginosa skin infection.

scholarly journals Impact of Frequent Administration of Bacteriophage on Therapeutic Efficacy in an A. baumannii Mouse Wound Infection Model

2020 ◽  
Vol 11 ◽  
Author(s):  
Michael D. Rouse ◽  
Joshua Stanbro ◽  
Jessica A. Roman ◽  
Michelle A. Lipinski ◽  
Anna Jacobs ◽  
...  
Keyword(s):  
Wound Infection ◽  
Therapeutic Efficacy ◽  
Infection Model ◽  
Frequent Administration

Das Komplementsystem

2012 ◽  
Vol 32 (04) ◽  
pp. 276-285 ◽  
Author(s):  
V. Frauenknecht ◽  
V. Schroeder
Keyword(s):  
Coronary Artery Disease ◽  
Complement System ◽  
Innate Immune System ◽  
Innate Immune ◽  
The Other ◽  
Atherosclerotic Plaques ◽  
Inflammatory Processes ◽  
Artery Disease ◽  
The Complement System ◽  
Novel Therapeutic

SummaryAtherosclerotic diseases such as coronary artery disease and ischaemic stroke are caused by chronic inflammation in arterial vessel walls. The complement system is part of the innate immune system. It is involved in many processes contributing to onset and development of atherosclerotic plaques up to the final stage of acute thrombotic events. This is due to its prominent role in inflammatory processes. In addition, there is increasing evidence that interactions between complement and coagulation provide a link between inflammation and thrombosis. On the other hand, the complement system also has an atheroprotective function through the clearance of apoptotic material.The knowledge of these complex mechanisms will become increasingly important, also for clinicians, since it may lead to novel therapeutic and diagnostic options. Therapies targeting the complement system have the potential to reduce tissue damage caused by acute ischaemic events. Whether early anti-inflammatory and anti-complement therapy may be able to prevent atherosclerosis, remains a hot topic for research.

scholarly journals Antibacterial Efficacy of Silver-Impregnated Polyelectrolyte Multilayers Immobilized on a Biological Dressing in a Murine Wound Infection Model

2012 ◽  
Vol 256 (2) ◽  
pp. 371-377 ◽  
Author(s):  
Kathleen M. Guthrie ◽  
Ankit Agarwal ◽  
Dana S. Tackes ◽  
Kevin W. Johnson ◽  
Nicholas L. Abbott ◽  
...  
Keyword(s):  
Wound Infection ◽  
Polyelectrolyte Multilayers ◽  
Infection Model ◽  
Antibacterial Efficacy ◽  
Biological Dressing

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 IL-17C and IL-17RE Promote Wound Closure in a Staphylococcus aureus-Based Murine Wound Infection Model

2021 ◽  
Vol 9 (9) ◽  
pp. 1821
Author(s):  
Linda Pätzold ◽  
Alexandra Stark ◽  
Felix Ritzmann ◽  
Carola Meier ◽  
Thomas Tschernig ◽  
...  
Keyword(s):  
Staphylococcus Aureus ◽  
Wound Infection ◽  
Wound Closure ◽  
Skin Diseases ◽  
Infection Model ◽  
Interleukin 17 ◽  
Immune Mediated ◽  
Significant Difference ◽  
Infected Skin

The epithelial cytokine interleukin-17C (IL-17C) mediates inflammation through the interleukin 17 receptor E (IL-17RE). Prior studies showed a detrimental role of IL-17C in the pathogenesis of immune-mediated skin diseases (e.g., psoriasis). Here, we examined the role of IL-17C/IL-17RE in wound closure in a Staphylococcus aureus wound infection model. We demonstrate that wound closure is significantly delayed in IL-17RE (Il-17re−/−)- and 17C (Il-17c−/−)-deficient mice. There was no significant difference between WT, Il-17re−/−, and Il-17c−/− mice in the absence of infection. Deficiency for IL-17RE and IL-17C did not significantly affect the elimination of bacteria. IL-17C expression was increased in the epidermis of human S. aureus-infected skin. Our results indicate that the IL-17C/IL-17RE axis contributes to the closure of infected wounds but does not contribute to the elimination of S. aureus.

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
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