Role of Polymorphonuclear Neutrophils in the Clearance of Enterococcus faecalis Derived from Saliva and Infected Root Canals

Ma, Zeyun; Wang, Yixiang; Zhu, Xiaofei; Zhang, Chengfei; Li, Shenglin; Li, Jin; Shen, Ya; Haapasalo, Markus

doi:10.1016/j.joen.2010.11.033

Cited by 9 publications

(8 citation statements)

References 31 publications

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“…faecalis colonization is also significantly increased in the bladders of neutropenic mice following urinary implantation, corroborating previous reports that neutrophils are important mediators of the antienterococcal host response in humans and other animal models of infections (66)(67)(68)(69). Previous studies demonstrated that E. faecalis and E. faecium isolated from saliva and root canals are efficiently killed by neutrophils recruited to the site of infection (70) and that TLR-2 is involved in the immune response against E. faecium (71). However, the immune defense during E. faecalis infections of the urinary tract at 24 hpi occurs in a TLR-2-and IL-6-independent manner, as infection of implanted animals deficient in these immune modulators did not alter the outcome of infection (see Fig.…”

Section: Discussionsupporting

confidence: 87%

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

et al. 2013

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Urinary catheterization elicits major histological and immunological changes that render the bladder susceptible to microbial invasion, colonization, and dissemination. However, it is not understood how catheters induce these changes, how these changes act to promote infection, or whether they may have any protective benefit. In the present study, we examined how catheter-associated inflammation impacts infection by Enterococcus faecalis, a leading cause of catheter-associated urinary tract infection (CAUTI), a source of significant societal and clinical challenges. Using a recently optimized murine model of foreign body-associated UTI, we found that the implanted catheter itself was the primary inducer of inflammation. In the absence of the silicone tubing implant, E. faecalis induced only minimal inflammation and was rapidly cleared from the bladder. The catheter-induced inflammation was only minimally altered by subsequent enterococcal infection and was not suppressed by inhibitors of the neurogenic pathway and only partially by dexamethasone. Despite the robust inflammatory response induced by urinary implantation, E. faecalis produced biofilm and high bladder titers in these animals. Induction of inflammation in the absence of an implanted catheter failed to promote infection, suggesting that the presence of the catheter itself is essential for E. faecalis persistence in the bladder. Immunosuppression prior to urinary catheterization enhanced E. faecalis colonization, suggesting that implant-mediated inflammation contributes to the control of enterococcal infection. Thus, this study underscores the need for novel strategies against CAUTIs that seek to reduce the deleterious effects of implant-mediated inflammation on bladder homeostasis while maintaining an active immune response that effectively limits bacterial invaders. U rinary catheterization is directly associated with 80% of hospital-acquired urinary tract infections (UTIs) (1). The insertion and presence of indwelling urinary catheters disrupt the normal mechanical and host defenses of the urinary tract, allow extracellular microbes access to the sterile environment of the bladder by ascending through the catheter lumen or from the urethral meatus along the catheter, and provide an additional surface for biofilm formation and the establishment of antibioticrecalcitrant chronic or recurrent infections (2-9). Even in the absence of microbial colonization, urinary catheterization was shown to be associated with histological and immunological alterations in the bladder, including urothelial damage and exfoliation, bladder wall edema, inflammatory cytokine production, immune cell infiltration, and mucosal lesions of the bladders and kidneys (7, 10-13) which can lead to bladder cancers (14, 15). However, there remains a need to uncover molecular details and the functional role of the catheter-induced host responses during bacterial colonization and catheter-associated UTIs (CAUTIs).We recently optimized a murine model of foreign body-associated UTI to inv...

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Section: Discussionsupporting

confidence: 87%

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

et al. 2013

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“…E. faecalis can recruit PMNs at the site of infection, leading to inflammation by upregulating IL‐1α, TNFα, MMP‐8 and COX‐2 (Ma et al . , Somma et al . ).…”

Section: Discussionmentioning

confidence: 93%

“…The difference between E. faecalis and P. gingivalis on jaw bone destruction may be due to differences in virulence factors, cytokines and pathways of activation. E. faecalis can recruit PMNs at the site of infection, leading to inflammation by upregulating IL-1a, TNFa, MMP-8 and COX-2 (Ma et al 2011, Somma et al 2011). In addition, E. faecalis in vitro can induce osteoclastic differentiation in the osteoblast/osteoclast co-culture system through the ephrinB2-EphB4 bidirectional signalling pathway .…”

Section: Discussionmentioning

confidence: 99%

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

et al. 2019

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Aim To conduct three‐dimensional micro‐CT analysis of bone destruction, periapical sclerotic changes and inflammatory root resorption (IRR) to compare the differences between Enterococcus faecalis (Ef)‐ and Porphyromonas gingivalis (Pg)‐induced chronic apical periodontitis (CAP). Methodology Mono‐species bacteria‐induced CAP was established in the first and second molars of the right maxilla and mandible of male Sprague–Dawley rats. Fifteen animals were divided into three groups with five rats in each group: control group, Ef‐CAP group and Pg‐CAP group. The maxilla and mandible were harvested and then scanned by micro‐CT. Alveolar bone destruction was evaluated by measuring the volume of alveolar bone resorption, bone volume fraction (BV/TV), trabecular thickness (Tb. Th), trabecular number (Tb. N) and trabecular spacing (Tb. Sp). The results were analysed using one‐way analysis of variance and Fisher's least significant difference methods (LSD). The sclerotic changes in the periapical bone were graded and the IRR indexes were scored. The data were analysed using the chi‐square test. Results The alveolar bone resorption volume of the Pg‐CAP group was significantly larger than that of the Ef‐CAP group (P < 0.01). In the maxilla, both Pg‐CAP and Ef‐CAP groups had a significant decrease in BV/TV and increase in Tb. Sp (P < 0.01) with the more significant changes of trabecular bone in the Pg‐CAP group. A significant reduction of Tb. N was only found in the Pg‐CAP group (P < 0.05). There was no significant change in Tb. Th in either group (P > 0.05). In the mandible, except for an increase in Tb. Sp in the Pg‐CAP group (P < 0.05), there was no significant change in BV/TV, Tb. Th or Tb. N (P > 0.05). No obvious sclerotic change was observed. IRR was detected in significantly more root surfaces in the Pg‐CAP group (240 surfaces, 60%) than those in the Ef‐CAP group (178 surfaces, 44.5%) (P < 0.001). The IRR extension was also significantly more advanced in the Pg‐CAP group (P < 0.05). Conclusions Pg‐CAP caused more substantial alveolar bone destruction and IRR than Ef‐CAP. The maxilla was more susceptible to CAP in terms of microstructural changes of trabecular bone than the mandible. Tb. Sp was the most sensitive index for evaluating the residual alveolar bone of CAP.

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“…4). Additionally, other studies have reported the regulation of gene expression in PMNs stimulated with pathogens (Fradin et al, 2007;Ma et al, 2011). The discrepancy between ELISA and qRT-PCR results concerning TNFα detection could be related to either the short half-life of PMNs in culture or most probably, the few RNA they contain due to their high content of dense chromatin (Dockrell et al, 2007).…”

Section: Discussionmentioning

confidence: 97%

Feline polymorphonuclear neutrophils produce pro-inflammatory cytokines following exposure to Microsporum canis

Cambier

Mathy

Baldo

et al. 2013

Veterinary Microbiology

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The mechanisms involved in the establishment of the specific immune response against dermatophytes remain unknown. Polymorphonuclear neutrophils (PMNs) are recruited early during the infection process and participate in the elimination of dermatophytes. They could therefore be involved in the induction of the immune response during dermatophytoses by producing specific cytokines. The aim of this work was to assess the in vitro cytokine production by feline PMNs exposed to living arthroconidia from the dermatophyte species Microsporum canis or stimulated with either a secreted or a structural component of M. canis, the latter consisting of heat-killed arthroconidia. The levels of specific cytokines produced by PMNs was determined by capture ELISA and/or quantitative RT-PCR. Results showed that PMNs secrete TNFα, IL-1β and IL-8 following exposure to M. canis living arthroconidia and stimulation with both a secreted component and heat-killed arthroconidia. The level of IL-8 mRNA was also increased in PMNs stimulated with M. canis living arthroconidia. In conclusion, infective M. canis arthroconidia induce the production of pro-inflammatory cytokines by feline PMNs that can be activated either by secreted or structural fungal components. Our results suggest that these granulocytes are involved in the initiation of the immune response against M. canis. We would like to thank you for your consideration of our work as well as for your comments and the opportunity you gave us to submit an amended version of our manuscript. We would like also to thank the reviewers for their critical remarks.Our specific answers to comments are as follow:Editor's comments: As an Editor it is not only my duty to assure the scientific quality of manuscripts, but also to make sure that the limited printing space available is used as efficient as possible. In this respect I have to ask you to reduce the length of your Introduction to one page. I have asked this from numerous authors and do not wish to make an exception for your manuscript.The length of the introduction was reduced as requested. Reviewer 1:My main concerns relates to:-some minor typo-errors occurring in the manuscript (i.e., line 258 "Trichomonas vaginalis") that should be corrected during revision.Line 254: "Trichomona vaginalis" was replaced by "Trichomonas vaginalis".-the discussion section, which would benefit from some modification. The content of lines 214-215 is over repeated in this part, so I would ask to the Authors to adjust it throughout the text. The concepts of lines 215-219 should be for other parts of the work.The content of the lines 214-219 was deleted to avoid repetition in the work. Reviewer 2:Revision Note However, a fungal culture was performed and was negative for dermatophytes in all cases.Concerning haematological analyses, a blood smear confirmed that feline PMNs had no morphological abnormalities and represented 40-75% of total white blood cells. Cats were negative after testing for infection with Feline Leukemia Virus and Feline Immunodef...

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Role of Polymorphonuclear Neutrophils in the Clearance of Enterococcus faecalis Derived from Saliva and Infected Root Canals

Cited by 9 publications

References 31 publications

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Enterococcus faecalis Overcomes Foreign Body-Mediated Inflammation To Establish Urinary Tract Infections

Micro‐CT analysis of chronic apical periodontitis induced by several specific pathogens

Feline polymorphonuclear neutrophils produce pro-inflammatory cytokines following exposure to Microsporum canis

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