Intestinal barrier dysfunction in severe burn injury

He, Wen; Wang, Yu; Wang, Pei; Wang, Fengjun

doi:10.1186/s41038-019-0162-3

Cited by 62 publications

(54 citation statements)

References 109 publications

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“…The intestinal epithelium functions as a natural barrier against the invasion of intestinal bacteria, toxins and other harmful substances, and serves and important role in the occurrence and development of multiple organ dysfunction syndrome (MODS) (1). Intestinal injury is the most common organ damage during the early stages of severe burn injuries (2). Severe burns can directly or indirectly result in the overgrowth of pathogenic bacteria in the intestines and the disruption of intestinal mechanical barriers, which in turn can trigger the translocation of intestinal bacteria or toxins, leading to systemic inflammatory response syndrome, sepsis and MODS (3,4).…”

Section: Introductionmentioning

confidence: 99%

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

et al. 2020

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Severe burns may lead to intestinal inflammation and oxidative stress, resulting in intestinal barrier damage and gut dysfunction. Loganin, an iridoid glycoside compound, has been isolated from Cornus officinalis Sieb. et Zucc; however, its role in the treatment of burn injury is yet to be fully elucidated. Therefore, the present study examined the effect of loganin administration on burn-induced intestinal inflammation and oxidative stress after severe burns in male Sprague-Dawley rats. Histological injury was assessed by hematoxylin and eosin staining. Furthermore, cytokine expression in intestinal tissues was measured by ELISA and reverse transcription-quantitative PCR. Antioxidative activities were assessed by determining the levels of reactive oxygen species (ROS), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA). Apoptosis was detected by flow cytometry. Apoptosis-related proteins, toll-like receptor 4 (TLR4) protein and NF-κB translocation were examined by western blotting. Immunohistochemical staining was used to observe TLR4 and NF-κB p65 expression in intestinal tissues. The present study suggested that loganin administration significantly reduced burn injury-induced intestinal histological changes, tumor necrosis factor-α, interleukin (IL)-6 and IL-1β production and oxidative stress, evidenced by decreased ROS levels and MDA content (P<0.05). Furthermore, loganin increased SOD, CAT and GSH-Px levels and intestinal epithelial cell apoptosis. Loganin treatment also significantly inhibited activation of the TLR4/NF-κB signaling pathway in the intestine of severely burned rats (P<0.05). In conclusion, loganin reduced burns-induced intestinal inflammation and oxidative stress, potentially by regulating the TLR4/NF-κB signaling pathway.

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Section: Introductionmentioning

confidence: 99%

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

et al. 2020

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“…To confirm this hypothesis, cell culture studies were performed (Caco-2 cell monolayer), which were treated for 24 h with the LPS. The LPS caused a considerable increase in Caco-2 cells of NLRP3, ASC, caspase-1, IL-1β, pro-IL-1β and pro-IL-18 (65).…”

Section: The Involvement Of Inflammasomes In Burn and Host Immune Resmentioning

confidence: 95%

Immunological approaches and therapy in burns (Review)

Boldeanu

Bogdan

et al. 2020

Exp Ther Med

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Burns have become an important public health problem in the last two decades, with just over a quarter of a million deaths annually. Major burns are accompanied by a strong inflammatory response, which will most often lead to systemic response inflammatory syndrome, followed by sepsis and finally induce multiple organ failure. The main mechanism involved in wound healing after burns is the inflammatory process, characterized by the recruitment of myeloid and T cells and by the involvement of numerous cytokines, chemokines, complement fractions, as well as various growth factors. Inflammasomes, protein-based cytosolic complexes, activated during metabolic stress or infection, play a role in modulating and improving the defense capacity of the innate immune system. Nucleotide-binding domain and leucine-rich repeat protein 3 (NLRP3) inflammasome has been studied predominantly and several hypotheses have been issued. Restoring the balance between the pro-inflammatory response and the anti-inflammatory activity is the key element to effective therapy in burns. Severe burns require nutritional support and pharmacotherapy not only for burn area but for different pathological complications of burn injury. In-depth research is required to find new ways to modulate the defense capacity, to prevent the complications of abnormal immune response and to treat burn injuries efficiently. Contents 1. Introduction 2. Burns and host immune response 3. The involvement of inflammasomes in burn and host immune response 4. Burns and the therapy 5. Conclusions

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“…Disruption of the intestinal barrier that leads to increased intestinal permeability and translocation of bacteria [ 21 22 ] or endotoxins are the frequent adverse events affecting gut colonocytes after a severe burn injury [ 23 ]. The loss of the structural integrity in the intestinal epithelial barrier may cause sepsis and subsequent multiple organ dysfunction syndromes, leading to a higher risk of mortality in burn victims [ 24–26 ]. Nonetheless, most of the supposed underlying mechanisms behind gut disruption were derived from other better investigated, critically ill populations [ 27 , 28 ].…”

Section: Reviewmentioning

confidence: 99%

Microbiome in the setting of burn patients: implications for infections and clinical outcomes

2020

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Burn damage can lead to a state of immune dysregulation that facilitates the development of infections in patients. The most deleterious impact of this dysfunction is the loss of the skin’s natural protective barrier. Furthermore, the risk of infection is exacerbated by protracted hospitalization, urinary catheters, endotracheal intubation, inhalation injury, arterial lines and central venous access, among other mainstays of burn care. Currently, infections comprise the leading cause of mortality after major burn injuries, which highlights the improvements observed over the last 50 years in the care provided to burn victims. The need to implement the empirical selection of antibiotic therapy to treat multidrug-resistant bacteria may concomitantly lead to an overall pervasiveness of difficult-to-treat pathogens in burn centres, as well as the propagation of antimicrobial resistance and the ultimate dysregulation of a healthy microbiome. While preliminary studies are examining the variability and evolution of human and mice microbiota, both during the early and late phase burn injury, one must consider that abnormal microbiome conditions could influence the systemic inflammatory response. A better understanding of the changes in the post-burn microbiome might be useful to interpret the provenance and subsequent development of infections, as well as to come up with inferences on the prognosis of burn patients. This review aims to summarise the current findings describing the microbiological changes in different organs and systems of burn patients and how these alterations affect the risks of infections, complications, and, ultimately, healing.

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Intestinal barrier dysfunction in severe burn injury

Cited by 62 publications

References 109 publications

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

Loganin attenuates intestinal injury in severely burned rats by regulating the toll‑like receptor 4/NF‑κB signaling pathway

Immunological approaches and therapy in burns (Review)

Microbiome in the setting of burn patients: implications for infections and clinical outcomes

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