Special Issue "Histological Effects of Endotoxins"

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Bacterial Toxins".

Deadline for manuscript submissions: closed (30 September 2021).

Special Issue Editors

Prof. Dr. Manuel Garrosa
E-Mail Website
Guest Editor
Department of Cell Biology, Histology and Pharmacology, University of Valladolid, 47005 Valladolid, Spain
Interests: nerve regeneration; ribosome-inactivating lectins; endotoxins
Special Issues and Collections in MDPI journals
Prof. Dr. Maria Angeles Rojo
E-Mail Website
Guest Editor
Department of Experimental Sciences, University of Europea Miguel de Cervantes, 47012 Valladolid, Spain
Interests: environmental sciences;ribosome-inactivating lectins; endotoxins; biofilms and microbiology
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Endotoxins are the lipopolysaccharide present in the cell wall of Gram-negative bacteria responsible for pathogenicity. The lipopolysaccharide, also called lipoglycan, is composed of the lipid A, covalently bound to a core of oligosaccharides, and to a side chain made of a polysaccharide. The lipid A shows toxic effects, while the glycan part confers the immunogenicity, the core being known as antigen R and the polysaccharide the antigen O, which displays a wide variety specific for each species or even for different strains.

Macrophages and endothelial cells secrete pro-inflammatory cytokines and nitric oxide in response to endotoxins, leading to the production of prostaglandins and leukotrienes mediating inflammation, and also elicit the activation of the complement alternative pathway and the coagulation cascade. Consequently, inflammation and/or degenerations occurs, along with fever and behavioral effects secondary to endotoxemia and, if high amounts of lipopolysaccharide enter the blood stream, it may lead to sepsis, multiple organ failure, and eventually death.

Due to fever triggering, endotoxins comprise a main type of pyrogen, which is of particular interest in the pharmaceutical industry, especially regarding parenteral administration. On the other hand, lipopolysaccharides may also bring beneficial effects, such as low-level immune activation induced by the gut microbiota, and are also used as biomarkers. Therefore, endotoxins have an outstanding clinical, pharmaceutical, and laboratory impact, and for this reason the study of endotoxins has gained considerable attention in the literature recently, with an increasing number of both descriptive and experimental papers on the matter. Nonetheless, further investigation is required, mainly on their organic toxicity. Accordingly, we encourage researchers to devote work to this field and to conduct research on their histological effects.

In this regard, we put forward a very good opportunity in the form of a Toxins Special Issue focused on the “Histological Effects of Endotoxins”, and we are very pleased to kindly invite you to participate by sending an article on the topic, including the methodology in the field, to be published in this prestigious journal.

Sincerely,

Prof. Dr. Manuel Garrosa
Prof. Dr. Maria Angeles Rojo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2400 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • endotoxins
  • lipopolysaccharide
  • lipoglycan
  • organ toxicity
  • pyrogen
  • histology
  • endotoxemia
  • Gram-negative bacteria

Published Papers (4 papers)

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Research

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Article
Sodium Butyrate More Effectively Mitigates the Negative Effects of High-Concentrate Diet in Dairy Cows than Sodium β-Hydroxybutyrate via Reducing Free Bacterial Cell Wall Components in Rumen Fluid and Plasma
Toxins 2021, 13(5), 352; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13050352 - 14 May 2021
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Abstract
The present study was aimed at investigating the effects of sodium butyrate and sodium β-hydroxybutyrate on lactation and health of dairy cows fed a high-concentrate (HC) diet. Eighty mid-lactation dairy cows with an average milk yield of 33.75 ± 5.22 kg/d were [...] Read more.
The present study was aimed at investigating the effects of sodium butyrate and sodium β-hydroxybutyrate on lactation and health of dairy cows fed a high-concentrate (HC) diet. Eighty mid-lactation dairy cows with an average milk yield of 33.75 ± 5.22 kg/d were randomly allocated to four groups (n = 20 per group) and were fed either a low-concentrate (LC) diet, a HC diet, the HC diet with 1% sodium butyrate (HCSB), or the HC diet with 1% sodium β-hydroxybutyrate (HCHB). The feeding trial lasted for 7 weeks, with a 2-week adaptation period and a 5-week measurement period, and the trial started from 96 ± 13 d in milk. Sodium butyrate supplementation delayed the decline in milk production and improved milk synthesis efficiency and milk fat content. Additionally, it decreased the proinflammatory cytokines and acute phase proteins (APPs) in plasma, the leucocytes in blood, the somatic cell count (SCC) in milk, and the gene expression of pattern recognition receptors (PRRs) and proinflammatory cytokines in the mammary gland, due to decreasing the contents of bacterial cell wall components (lipopolysaccharide, LPS; peptidoglycan, PGN; and lipoteichoic acid, LTA) in the rumen and plasma, compared with the HC diet. Sodium β-hydroxybutyrate supplementation also improved milk yield, milk synthesis efficiency and milk fat content and partially reduced the adverse effects caused by the HC diet, but it had no effect on decreasing bacterial cell wall components in the rumen and plasma, compared with the HC diet. Collectively, both sodium butyrate and sodium β-hydroxybutyrate mitigated the negative effects of HC diet on lactation and health of dairy cows, with sodium butyrate being more effective than sodium β-hydroxybutyrate. Full article
(This article belongs to the Special Issue Histological Effects of Endotoxins)
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Article
Curcumin Alleviates LPS-Induced Oxidative Stress, Inflammation and Apoptosis in Bovine Mammary Epithelial Cells via the NFE2L2 Signaling Pathway
Toxins 2021, 13(3), 208; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13030208 - 12 Mar 2021
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Abstract
Lipopolysaccharide (LPS) is an endotoxin, which may cause immune response and inflammation of bovine mammary glands. Mastitis impairs animal health and results in economic loss. Curcumin (CUR) is a naturally occurring diketone compound, which has attracted widespread attention as a potential anti-inflammatory antioxidant. [...] Read more.
Lipopolysaccharide (LPS) is an endotoxin, which may cause immune response and inflammation of bovine mammary glands. Mastitis impairs animal health and results in economic loss. Curcumin (CUR) is a naturally occurring diketone compound, which has attracted widespread attention as a potential anti-inflammatory antioxidant. The purpose of this study is to investigate whether CUR can reduce the damage of bovine mammary epithelial cells (MAC-T) induced by LPS and its underlying molecular mechanism. The MAC-T cell line was treated with different concentrations of LPS and CUR for 24 h. The results showed that CUR rescued the decrease of MAC-T cell viability and cell damage induced by LPS. At the same time, 10 µM CUR and 100 µg/mL LPS were used to treat the cells in the follow-up study. The results showed CUR treatment reduced the accumulation of reactive oxygen species (ROS), the expression of inflammatory cytokines (tumor necrosis factor-a (TNF-α), interleukin-8 (IL-8), IL-6 and IL-1β) and the rate of apoptosis induced by LPS. These effects were associated with the activation of the nuclear factor E2-related factor 2 (NFE2L2)-antioxidant response element (ARE) pathway coupled with inactivation of the nuclear factor-κB (NF-κB) inflammatory and caspase/Bcl2 apoptotic pathways. Full article
(This article belongs to the Special Issue Histological Effects of Endotoxins)
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Review

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Review
Pathological and Therapeutic Approach to Endotoxin-Secreting Bacteria Involved in Periodontal Disease
Toxins 2021, 13(8), 533; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13080533 - 29 Jul 2021
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Abstract
It is widely recognized that periodontal disease is an inflammatory entity of infectious origin, in which the immune activation of the host leads to the destruction of the supporting tissues of the tooth. Periodontal pathogenic bacteria like Porphyromonas gingivalis, that belongs to [...] Read more.
It is widely recognized that periodontal disease is an inflammatory entity of infectious origin, in which the immune activation of the host leads to the destruction of the supporting tissues of the tooth. Periodontal pathogenic bacteria like Porphyromonas gingivalis, that belongs to the complex net of oral microflora, exhibits a toxicogenic potential by releasing endotoxins, which are the lipopolysaccharide component (LPS) available in the outer cell wall of Gram-negative bacteria. Endotoxins are released into the tissues causing damage after the cell is lysed. There are three well-defined regions in the LPS: one of them, the lipid A, has a lipidic nature, and the other two, the Core and the O-antigen, have a glycosidic nature, all of them with independent and synergistic functions. Lipid A is the “bioactive center” of LPS, responsible for its toxicity, and shows great variability along bacteria. In general, endotoxins have specific receptors at the cells, causing a wide immunoinflammatory response by inducing the release of pro-inflammatory cytokines and the production of matrix metalloproteinases. This response is not coordinated, favoring the dissemination of LPS through blood vessels, as well as binding mainly to Toll-like receptor 4 (TLR4) expressed in the host cells, leading to the destruction of the tissues and the detrimental effect in some systemic pathologies. Lipid A can also act as a TLRs antagonist eliciting immune deregulation. Although bacterial endotoxins have been extensively studied clinically and in a laboratory, their effects on the oral cavity and particularly on periodontium deserve special attention since they affect the connective tissue that supports the tooth, and can be linked to advanced medical conditions. This review addresses the distribution of endotoxins associated with periodontal pathogenic bacteria and its relationship with systemic diseases, as well as the effect of some therapeutic alternatives. Full article
(This article belongs to the Special Issue Histological Effects of Endotoxins)
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Review
Effect of Food Endotoxin on Infant Health
Toxins 2021, 13(5), 298; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13050298 - 22 Apr 2021
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Abstract
Endotoxin is a complex molecule derived from the outer membrane of Gram-negative bacteria, and it has strong thermal stability. The processing of infant food can kill pathogenic bacteria but cannot remove endotoxin. Because the intestinal structure of infants is not fully developed, residual [...] Read more.
Endotoxin is a complex molecule derived from the outer membrane of Gram-negative bacteria, and it has strong thermal stability. The processing of infant food can kill pathogenic bacteria but cannot remove endotoxin. Because the intestinal structure of infants is not fully developed, residual endotoxin poses a threat to their health by damaging the intestinal flora and inducing intestinal inflammation, obesity, and sepsis, among others. This paper discusses the sources and contents of endotoxin in infant food and methods for preventing endotoxin from harming infants. However, there is no clear evidence that endotoxin levels in infant food cause significant immune symptoms or even diseases in infants. However, in order to improve the safety level of infant food and reduce the endotoxin content, this issue should not be ignored. The purpose of this review is to provide a theoretical basis for manufacturers and consumers to understand the possible harm of endotoxin content in infant formula milk powder and to explore how to reduce its level in infant formula milk powder. Generally, producers should focus on cleaning the milk source, securing the cold chain, avoiding long-distance transportation, and shortening the storage time of raw milk to reduce the level of bacteria and endotoxin. After production and processing, the endotoxin content should be measured as an important index to test the quality of infant formula milk powder so as to provide high-quality infant products for the healthy growth of newborns. Full article
(This article belongs to the Special Issue Histological Effects of Endotoxins)
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