scholarly journals Local inflammatory response to suture material in surgical practice: experimental data

2020 ◽  
Vol 22 (2) ◽  
pp. 151-157
Author(s):  
T. N. Akentyeva ◽  
D. K. Shishkova ◽  
A. Yu. Burago ◽  
Yu. A. Kudryavtseva
Keyword(s):  
Inflammatory Response ◽  
Surgical Outcomes ◽  
Titanium Nickelide ◽  
Suture Material ◽  
Adhesion Formation ◽  
In Vivo Studies ◽  
Suture Materials ◽  
Local Inflammatory Response ◽  
Polypropylene Sutures

Objective: to study the effect of various types of suture materials, potentially suitable for cardiovascular surgery, on experimental surgical outcomes. Materials and methods. Polypropylene sutures (Prolene 6/0), titanium nickelide (TiNi) sutures (6/0) and absorbable polydioxanone sutures (Monoplus 6/0) were used in the study. Male Wistar rats were used for in vivo studies. The effect of suture materials on abdominal adhesions was studied. In vivo calcification process was examined, and response of blood components in contact with suture materials was also assessed in vitro. Results. There is a negative inflammatory response to suture materials. The severity of this response depended on the type of material used. Polypropylene sutures demonstrated the most severe inflammatory response provoking massive adhesion formation. In addition, large calcium deposits were found both in the suture area and in the thickness of the biomaterial, stitched with prolene and implanted subcutaneously in the rats. Titanium nickelide sutures showed high hemocompatibility and biocompatibility. The Monoplus sutures caused minimal inflammatory response and provoked calcification of the biomaterial to a lesser degree. Conclusion. The suture material could have significant effects on surgical outcomes and could cause postoperative complications.

Stanniocalcin-1, an inhibitor of macrophage chemotaxis and chemokinesis

2004 ◽  
Vol 286 (2) ◽  
pp. F356-F362 ◽  
Author(s):  
John Kanellis ◽  
Roger Bick ◽  
Gabriela Garcia ◽  
Luan Truong ◽  
Chun Chui Tsao ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Intracellular Calcium ◽  
In Vivo Studies ◽  
Cellular Processes ◽  
Multiple Organs ◽  
Chemotactic Protein ◽  
Stromal Cell Derived Factor ◽  
Mammalian Counterpart

In macrophages, changes in intracellular calcium have been associated with activation of cellular processes that regulate cell adhesion and motility and are important for the response of macrophages to antigenic stimuli. The mammalian counterpart of the fish calcium-regulating hormone stanniocalcin-1 (STC1) is expressed in multiple organs including the thymus and spleen, and hence, we hypothesized that it may have a role in modulating the immune/inflammatory response. Using murine macrophage-like (RAW264.7) and human monoblast-like (U937) cells to study chemotaxis in vitro, we found that STC1 attenuated chemokinesis and diminished the chemotactic response to monocyte chemotactic protein-1 (MCP-1) and stromal cell-derived factor-1α. Consistent with these findings, STC1 blunted the rise in intracellular calcium following MCP-1 stimulation in RAW264.7 cells. In vivo studies suggested differential expression of STC1 in obstructed kidney and localization to macrophages. MCP-1 and STC1 transcripts were both upregulated following ureteric obstruction, suggesting a functional association between the two genes. Our data suggest a role for mammalian STC1 in modulating the immune/inflammatory response.

scholarly journals Mycolactone toxin induces an inflammatory response by targeting the IL-1β pathway: Mechanistic insight into Buruli ulcer pathophysiology

2020 ◽  
Vol 16 (12) ◽  
pp. e1009107
Author(s):  
M. Foulon ◽  
M. Robbe-Saule ◽  
J. Manry ◽  
L. Esnault ◽  
Y. Boucaud ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Buruli Ulcer ◽  
Mycobacterium Ulcerans ◽  
Inflammatory Factors ◽  
Dependent Manner ◽  
Local Inflammatory Response ◽  
Mechanistic Insight ◽  
Insight Into

Mycolactone, a lipid-like toxin, is the major virulence factor of Mycobacterium ulcerans, the etiological agent of Buruli ulcer. Its involvement in lesion development has been widely described in early stages of the disease, through its cytotoxic and immunosuppressive activities, but less is known about later stages. Here, we revisit the role of mycolactone in disease outcome and provide the first demonstration of the pro-inflammatory potential of this toxin. We found that the mycolactone-containing mycobacterial extracellular vesicles produced by M. ulcerans induced the production of IL-1β, a potent pro-inflammatory cytokine, in a TLR2-dependent manner, targeting NLRP3/1 inflammasomes. We show our data to be relevant in a physiological context. The in vivo injection of these mycolactone-containing vesicles induced a strong local inflammatory response and tissue damage, which were prevented by corticosteroids. Finally, several soluble pro-inflammatory factors, including IL-1β, were detected in infected tissues from mice and Buruli ulcer patients. Our results revisit Buruli ulcer pathophysiology by providing new insight, thus paving the way for the development of new therapeutic strategies taking the pro-inflammatory potential of mycolactone into account.

Control of local blood flow in pulmonary inflammation: role for neutrophils, PAF, and thromboxane

1991 ◽  
Vol 70 (3) ◽  
pp. 1184-1193 ◽  
Author(s):  
P. G. Hellewell ◽  
P. M. Henson ◽  
G. P. Downey ◽  
G. S. Worthen
Keyword(s):  
Blood Flow ◽  
Inflammatory Response ◽  
Lung Inflammation ◽  
Pulmonary Inflammation ◽  
Local Blood Flow ◽  
Synthesis Inhibitor ◽  
Rabbit Lung ◽  
Local Inflammatory Response ◽  
Paf Antagonists

The intrapulmonary instillation of C5a results in a local inflammatory response that, in this site, is accompanied by a decrease in local blood flow. Reversal of this decrease by vasodilators or the thromboxane synthesis inhibitor dazmegral has been shown to result in enhanced lung inflammation. In the present study the mechanisms underlying the decrease in flow in pulmonary inflammation were investigated in the rabbit in vivo and in the isolated blood-perfused rabbit lung. In vivo, the decrease in local blood flow was shown to be dependent on circulating neutrophils. In the isolated blood-perfused lung, inflammation induced by airway instillation of C5a was similar histologically to that seen in vivo and was also accompanied by a decrease in local blood flow. The decrease in blood flow appeared to require circulating neutrophils and was prevented by dazmegral and the platelet-activating factor (PAF) antagonists WEB 2086 and L-659,989. Furthermore, no decrease occurred in aspirin-treated lungs perfused with normal blood, suggesting that the source of thromboxane was lung rather than circulating cells. The decrease in blood flow in inflammation did not appear to be a consequence of hypoxic vasoconstriction. Inflammation in the guinea pig lung was also accompanied by a decrease in local blood flow and was also prevented by dazmegral and PAF antagonists. We conclude that local inflammation in the lung is accompanied by a decrease in blood flow that involves neutrophils and the lipid mediators PAF and thromboxane. We suggest that this form of negative feedback by the neutrophil serves to control the inflammatory response.

scholarly journals Short- and long-term results of chordal reconstruction using artificial suture material (polytetrafluoroethylene and polypropylene) in the dog

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Isamu Kanemoto ◽  
Tomonari Masumoto ◽  
Kiminari Ohara ◽  
Yusuke Kimura ◽  
Noboru Machida
Keyword(s):  
Suture Material ◽  
Long Term Results ◽  
Short Term ◽  
Suture Materials ◽  
Mitral Valve Plasty ◽  
Polypropylene Suture ◽  
Group 12 ◽  
Short And Long Term ◽  
Polypropylene Sutures

No previous reports have compared the suitability of expanded polytetrafluoroethylene (ePTFE) and polypropylene as artificial suture materials for chordal reconstruction in mitral valve plasty (MVP) in the dog. Twelve normal dogs were subjected to MVP using surfaceinduced deep hypothermia. In the short-term group (1.5-4 months after surgery), all ePTFE sutures were covered by a tissue sheath including the paired suture arms, which gave the appearance of native chordae from 2 months after surgery. In contrast, all polypropylene sutures were not covered by tissue, and appeared the same as the paired polypropylene suture arms at the operation. In the long-term group (12 months after surgery), all ePTFE sutures were covered by a tissue sheath, which appeared the same as that in the short-term group, and had flexibility without increased thickness with time. In contrast, although the polypropylene suture was covered completely by a tissue sheath in 1 dog, all the other polypropylene sutures were exposed except for both ends of the suture. ePTFE may be superior to polypropylene as an artificial suture material for chordal reconstruction in MVP.

In Vivo Comparison of the Inflammatory Response Induced by Different Vascular Biomaterials

Vascular ◽  
2005 ◽  
Vol 13 (4) ◽  
pp. 230-235 ◽  
Author(s):  
Steven J. Busuttil ◽  
Carla Drumm ◽  
Edward F. Plow
Keyword(s):  
Stainless Steel ◽  
Inflammatory Response ◽  
Inflammatory Responses ◽  
Disk Surface ◽  
The Other ◽  
Vascular Prostheses ◽  
Local Inflammatory Response ◽  
Macrophage Recruitment ◽  
Significant Difference

Biomaterial implants induce a local inflammatory response. A comparison of the inflammatory cell response was made between several biomaterials commonly used as vascular prostheses. Disks of polyethylene terephthalate (PET), polytetrafluoroethylene (PTFE), aluminum, titanium, copper, and stainless steel were surgically placed into the peritoneum of mice. Recruited macrophage and neutrophil populations were measured after recovery from the disk surface and peritoneal lavage. Following peritoneal biomaterial implants, there was no difference in total neutrophil or macrophage recruitment between mice implanted with PET, PTFE, aluminum, or titanium disks. However, there was significant attenuation of total neutrophil and macrophage recruitment to stainless steel compared with the other implants. Similarly, there was no significant difference in the percentage of leukocytes adherent to the PET, aluminum, or titanium disks. Macrophage adherence to the stainless steel disks was attenuated by 19.1%, and the number of neutrophils was attenuated by 69.1% when compared with PET implant mice. Mice implanted with copper disks universally expired. Leukocyte recruitment did not differ between PET, PTFE, aluminum, or titanium disks, suggesting that these materials stimulate similar inflammatory responses. Stainless steel disks recruited both fewer neutrophils and fewer macrophages and support lower adherence of these cells than the other biomaterials. Copper incited an overwhelming and fatal response.

scholarly journals Clinical and histologic tissue responses of skin incisions closed with glycomer 631 and lactomer 9-1 using subcuticular technique in pigs

2019 ◽  
Author(s):  
Tanja Plavec ◽  
Tanja Švara ◽  
Irena Zdovc ◽  
Mitja Gombač ◽  
Marija Damjanovska ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Suture Material ◽  
Giant Cells ◽  
Tissue Reaction ◽  
Absorbable Suture ◽  
Suture Materials ◽  
Tissue Samples ◽  
Trueperella Pyogenes ◽  
Cumulative Score ◽  
Tissue Reactions

Abstract Background: Glycomer 631 and lactomer 9-1 are absorbable suture materials indicated for soft tissue approximation in non-infected wounds. Pigs are often used as surgical models in translational research, however, the reports of tissue reactions to both suture materials in pigs are lacking. The aim of this study was to assess clinical and histologic responses of skin incisions closed with subcuticular technique using glycomer 631 and lactomer 9-1 in pigs. Results: Skin incisions of 17 pigs were closed with glycomer 631 and lactomer 9-1 and clinical reactive score (CRS) including erythema, swelling, discharge, and dehiscence was calculated on postoperative days 7 and 14. Subcuticular tissue reaction was assessed histologically on postoperative day 14 (the presence of extravascular neutrophils, macrophages, multinucleated giant cells, lymphocytes, fibroblasts, bacterial colonies, overall severity of inflammatory response to suture material), and the cumulative score of variables calculated as aggregate tissue irritation score (ATIS). Tissue samples were examined for suture extrusion and evaluated microbiologically. Clinical reactive score did not differ between the suture materials. Only one variable of ATIS, overall severity of inflammatory response, was lower ( p = 0.029) when glycomer 631 was used. Suture extrusion was found in 10/17 of incisions closed by glycomer 631 and in 7/13 of incisions closed by lactomer 9-1. Trueperella pyogenes was isolated from the skin and from the area of tissue reaction in six pigs. Conclusions: No difference in CRS between the suture materials was observed. Glycomer 631 induced less tissue reaction only in terms of overall severity of inflammatory response. Suture extrusion was observed in more than 50% of incisions regardless of the suture material. Trueperella pyogenes was the only pathogen isolated from the tissue surrounding the suture material.

IN SILICO AND IN VIVO STUDIES MODELING THE AGED ACUTE INFLAMMATORY RESPONSE

Shock ◽  
2006 ◽  
Vol 25 (Supplement 1) ◽  
pp. 39-40 ◽  
Author(s):  
Y. Vodovotz ◽  
R. Hoffman ◽  
A. Barratt ◽  
J. Wei ◽  
C. Lagoa ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
In Silico ◽  
In Vivo Studies ◽  
Acute Inflammatory Response

scholarly journals Intra-Amniotic Infection with Ureaplasma parvum Causes Preterm Birth and Neonatal Mortality That Are Prevented by Treatment with Clarithromycin

mBio ◽  
2020 ◽  
Vol 11 (3) ◽  
Author(s):  
Kenichiro Motomura ◽  
Roberto Romero ◽  
Yi Xu ◽  
Kevin R. Theis ◽  
Jose Galaz ◽  
...  
Keyword(s):  
Preterm Birth ◽  
Inflammatory Response ◽  
Neonatal Outcomes ◽  
Amniotic Cavity ◽  
Local Inflammatory Response ◽  
Content Type ◽  
Ureaplasma Parvum ◽  
Adverse Pregnancy

ABSTRACT Intra-amniotic infection is strongly associated with adverse pregnancy and neonatal outcomes. Most intra-amniotic infections are due to Ureaplasma species; however, the pathogenic potency of these genital mycoplasmas to induce preterm birth is still controversial. Here, we first laid out a taxonomic characterization of Ureaplasma isolates from women with intra-amniotic infection, which revealed that Ureaplasma parvum is the most common bacterium found in this clinical condition. Next, using animal models, we provided a causal link between intra-amniotic inoculation with Ureaplasma species and preterm birth. Importantly, the intra-amniotic inoculation of Ureaplasma species induced high rates of mortality in both preterm and term neonates. The in vivo potency of U. parvum to induce preterm birth was not associated with known virulence factors. However, term-derived and preterm-derived U. parvum isolates were capable of inducing an intra-amniotic inflammatory response. Both U. parvum isolates invaded several fetal tissues, primarily the fetal lung, and caused fetal inflammatory response syndrome. This bacterium was also detected in the placenta, reproductive tissues, and most severely in the fetal membranes, inducing a local inflammatory response that was replicated in an in vitro model. Importantly, treatment with clarithromycin, a recently recommended yet not widely utilized antibiotic, prevented the adverse pregnancy and neonatal outcomes induced by U. parvum. These findings shed light on the maternal-fetal immunobiology of intra-amniotic infection. IMPORTANCE Preterm birth is the leading cause of neonatal morbidity and mortality worldwide. Multiple etiologies are associated with preterm birth; however, 25% of preterm infants are born to a mother with intra-amniotic infection, most commonly due to invasion of the amniotic cavity by Ureaplasma species. Much research has focused on establishing a link between Ureaplasma species and adverse pregnancy/neonatal outcomes; however, little is known about the taxonomy of and host response against Ureaplasma species. Here, we applied a multifaceted approach, including human samples, in vivo models, and in vitro manipulations, to study the maternal-fetal immunobiology of Ureaplasma infection during pregnancy. Furthermore, we investigated the use of clarithromycin as a treatment for this infection. Our research provides translational knowledge that bolsters scientific understanding of Ureaplasma species as a cause of adverse pregnancy/neonatal outcomes and gives strong evidence for the use of clarithromycin as the recommended treatment for women intra-amniotically infected with Ureaplasma species.

scholarly journals Pulsed Electromagnetic Field Stimulation in Osteogenesis and Chondrogenesis: Signaling Pathways and Therapeutic Implications

2021 ◽  
Vol 22 (2) ◽  
pp. 809
Author(s):  
Katia Varani ◽  
Fabrizio Vincenzi ◽  
Silvia Pasquini ◽  
Irene Blo ◽  
Simona Salati ◽  
...  
Keyword(s):  
Inflammatory Response ◽  
Signaling Pathways ◽  
Tissue Repair ◽  
Chondrogenic Differentiation ◽  
Cartilage Defects ◽  
Invasive Treatment ◽  
Local Inflammatory Response ◽  
Pulsed Electromagnetic

Mesenchymal stem cells (MSCs) are the main cell players in tissue repair and thanks to their self-renewal and multi-lineage differentiation capabilities, they gained significant attention as cell source for tissue engineering (TE) approaches aimed at restoring bone and cartilage defects. Despite significant progress, their therapeutic application remains debated: the TE construct often fails to completely restore the biomechanical properties of the native tissue, leading to poor clinical outcomes in the long term. Pulsed electromagnetic fields (PEMFs) are currently used as a safe and non-invasive treatment to enhance bone healing and to provide joint protection. PEMFs enhance both osteogenic and chondrogenic differentiation of MSCs. Here, we provide extensive review of the signaling pathways modulated by PEMFs during MSCs osteogenic and chondrogenic differentiation. Particular attention has been given to the PEMF-mediated activation of the adenosine signaling and their regulation of the inflammatory response as key player in TE approaches. Overall, the application of PEMFs in tissue repair is foreseen: (1) in vitro: to improve the functional and mechanical properties of the engineered construct; (2) in vivo: (i) to favor graft integration, (ii) to control the local inflammatory response, and (iii) to foster tissue repair from both implanted and resident MSCs cells.

scholarly journals Expression and role of ABIN1 in sepsis: In vitro and in vivo studies

Open Medicine ◽  
2020 ◽  
Vol 16 (1) ◽  
pp. 033-040
Author(s):  
Haolan Li ◽  
Aichen Sun ◽  
Taocheng Meng ◽  
Yan Zhu
Keyword(s):  
Inflammatory Response ◽  
Molecular Mechanisms ◽  
Organ Injury ◽  
In Vivo Studies ◽  
Inflammatory Factors ◽  
Septic Mouse ◽  
Raw264.7 Macrophages ◽  
Tnf Α

AbstractIn this research, we attempted to explain the effect and the related molecular mechanisms of ABIN1 in lipopolysaccharide (LPS)-induced septic mice or RAW264.7 macrophages. LPS was adopted to treat RAW264.7 macrophages for 4 h, and the levels of inflammatory factors were assessed by ELISA. Besides, ABIN1 expression was measured by quantitative reverse transcription polymerase chain reaction. Apparently, LPS enhanced immunoreaction, suggested by increased expression of IL-1β, tumor necrosis factor (TNF)-α, and IL-6. ABIN1 levels were obviously reduced compared to the control. Furthermore, we evaluated the roles of ABIN1-plasmid in immunoreaction and nuclear factor-κB (NF-κB) pathway. We found that ABIN1-plasmid significantly reduced the expression of IL-1β, TNF-α, and IL-6 in LPS-treated cells and inhibited NF-κB pathway activation. Meanwhile, a septic mouse mode was conducted to validate the role of ABIN1 in inflammatory response and organ damage in vivo. These data suggested that ABIN1-plasmid significantly inhibited the secretion of inflammatory cytokines and Cr, BUN, AST, and ALT levels in the serum of LPS-stimulated mice compared to LPS + control-plasmid group, reflecting the relieved inflammation and organ injury. In summary, the present findings indicated that ABIN1 alleviated sepsis by repressing inflammatory response through NF-κB signaling pathway, emphasizing the potential value of ABIN1 as therapeutic strategy for sepsis.

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