ijms-logo

Journal Browser

Journal Browser

Molecular Response to Endotoxin

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Toxicology".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 14147

Special Issue Editors


E-Mail Website
Guest Editor
Departamento de Fisiología, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain
Interests: endotoxin; muscle wasting; IGF-I; growth hormone; glucocorticoids; inflammatory diseases

E-Mail Website
Guest Editor
Departamento de Fisiología, Facultad de Medicina, Universidad Complutense de Madrid, Madrid, Spain
Interests: muscular atrophy; IGF-1 system; inflammation; stress
Special Issues, Collections and Topics in MDPI journals

E-Mail Website
Guest Editor
Department of Physiology, Faculty of Nursing, Physiotherapy and Podiatry, Complutense University of Madrid, 28040 Madrid, Spain
Interests: muscular atrophy; IGF-1 system; inflammation; stress; metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear colleagues,

The response to inflammation after endotoxin exposure is a broad response that includes fever, anorexia, and a number of hormonal and metabolic changes which are necessary to adapt the body to this new situation. This complex response leads to an increase in catabolism and a decrease in anabolism. The global effect is an increased release of energy substrates stored in the liver, adipose tissue, and skeletal muscle in order to provide energy to the activated immune cells. In this response, glucocorticoids play an important role, but cytokines also exert important effects.   

Endotoxin is a well-known modulator of hypothalamic and anterior pituitary hormones. The acute phase of inflammation induces a decreased activity of the thyroid and gonadal axes, with an increased activity of the adrenal axis. Inflammation also affects the hypothalamic neurons that regulate feeding behavior and basal metabolism. Several data suggest that sepsis or high-grade hypothalamic inflammation is associated with anorexia, decreased fat mass, skeletal muscle wasting, and weakness. By contrast, low-grade hypothalamic inflammation has been associated to obesity and insulin resistance. Both conditions increase morbidity and mortality in several diseases. Therefore, it is important to understand the molecular mechanisms by which inflammation modifies the hypothalamic regulation of energy homeostasis.

In addition to the effects on the metabolic and neuroendocrine system, endotoxin produces severe dysfunction in major organ systems such as brain, liver, heart and kidney. Molecular mechanisms involved in the pathophysiology include glucocorticoids and pro-inflammatory mediators, epigenetic changes, gut dysbiosis and the expression and secretion (in exosomes) of microRNAs.

We invite investigators to contribute with original research articles, as well as meta-analyses and review articles that will stimulate the comprehension of the molecular mechanisms underlying the relevance of neuroendocrine and metabolic responses to endotoxin and the pathophysiology related to the major organs dysfunction.

Potential topics include but are not limited to:            
- Molecular mechanisms involve in the pathophysiology of sepsis;
- Metabolic endotoxemia;
- Inflammation-induced epigenetic changes;
- Adipose tissue: a site of inflammation, adipocyte dysfunction, and the pathogenesis of obesity;
- Inflammation, intestinal microbiota, and insulin resistance;
- Hypothalamic inflammation and energy balance disruption;
- Inflammation-induced body weight loss, muscle wasting, and cachexia;
- Role of microRNAs in the response to inflammation induced by endotoxin.

Keywords

  • Endotoxin
  • Inflammation 
  • Anorexia 
  • Adipokines 
  • Cachexia 
  • Epigenetic 
  • Microbiota 
  • mirRNA

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (3 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

17 pages, 3337 KiB  
Article
Effect of Acute and Prolonged Inflammation on the Gene Expression of Proinflammatory Cytokines and Their Receptors in the Anterior Pituitary Gland of Ewes
by Karolina Wojtulewicz, Agata Krawczyńska, Dorota Tomaszewska-Zaremba, Maciej Wójcik and Andrzej P. Herman
Int. J. Mol. Sci. 2020, 21(18), 6939; https://doi.org/10.3390/ijms21186939 - 21 Sep 2020
Cited by 13 | Viewed by 2631
Abstract
An acute and prolonged inflammation inhibits the reproduction process by the disruption of the neurohormonal activity of the hypothalamic-pituitary-gonadal axis. It is thought that these changes may be caused by proinflammatory cytokines, i.e., interleukin (IL) -1β, IL-6 and tumor necrosis factor (TNF) α. [...] Read more.
An acute and prolonged inflammation inhibits the reproduction process by the disruption of the neurohormonal activity of the hypothalamic-pituitary-gonadal axis. It is thought that these changes may be caused by proinflammatory cytokines, i.e., interleukin (IL) -1β, IL-6 and tumor necrosis factor (TNF) α. The aim of this study was to determine the effect of an acute and prolonged inflammation on the expression of genes encoding cytokine and their receptors, gonadotropin releasing hormone receptor (GnRHR), beta subunits of luteinizing hormone (LHβ) and follicle-stimulating (FSHβ) in the anterior pituitary (AP). Moreover, the circulating concentration of LH and FSH was also assayed. Two experiments were carried out on adult ewes which were divided into two control groups and treated with lipopolysaccharide (LPS; 400 ng / kg). Acute inflammation was caused by a single injection of LPS into the external jugular vein, while the chronic inflammation was induced by seven times LPS injection (one a day). In both experiments, animals were euthanized 3h after the last LPS / NaCl injection and the blood samples collected 15 min before euthanasia. An acute inflammation stimulates the expression of the IL-1β, IL-6 and TNFα genes and their receptors in the AP of sheep. Prolonged inflammation increased TNFα gene expression and both types of TNFα and IL-6 receptors. Both an acute and prolonged inflammation inhibited LHβ gene expression in the AP and reduced LH level in blood. A sevenfold LPS injection raises FSH concentration. The gene expression of GnRHR was reduced in the ovine AP only after a single injection of endotoxin. Our results suggest that there are important differences in the way how an acute and prolonged inflammation influence proinflammatory cytokines and their receptors gene expression in the AP of anestrous ewes, which could be reflected by differences in the AP secretory activity during these states. Full article
(This article belongs to the Special Issue Molecular Response to Endotoxin)
Show Figures

Figure 1

Review

Jump to: Research

16 pages, 1607 KiB  
Review
Opioids and Sepsis: Elucidating the Role of the Microbiome and microRNA-146
by Yaa Abu, Nicolas Vitari, Yan Yan and Sabita Roy
Int. J. Mol. Sci. 2022, 23(3), 1097; https://doi.org/10.3390/ijms23031097 - 20 Jan 2022
Cited by 10 | Viewed by 3899
Abstract
Sepsis has recently been defined as life-threatening organ dysfunction caused by the dysregulated host response to an ongoing or suspected infection. To date, sepsis continues to be a leading cause of morbidity and mortality amongst hospitalized patients. Many risk factors contribute to development [...] Read more.
Sepsis has recently been defined as life-threatening organ dysfunction caused by the dysregulated host response to an ongoing or suspected infection. To date, sepsis continues to be a leading cause of morbidity and mortality amongst hospitalized patients. Many risk factors contribute to development of sepsis, including pain-relieving drugs like opioids, which are frequently prescribed post-operatively. In light of the opioid crisis, understanding the interactions between opioid use and the development of sepsis has become extremely relevant, as opioid use is associated with increased risk of infection. Given that the intestinal tract is a major site of origin of sepsis-causing microbes, there has been an increasing focus on how alterations in the gut microbiome may predispose towards sepsis and mediate immune dysregulation. MicroRNAs, in particular, have emerged as key modulators of the inflammatory response during sepsis by tempering the immune response, thereby mediating the interaction between host and microbiome. In this review, we elucidate contributing roles of microRNA 146 in modulating sepsis pathogenesis and end with a discussion of therapeutic targeting of the gut microbiome in controlling immune dysregulation in sepsis. Full article
(This article belongs to the Special Issue Molecular Response to Endotoxin)
Show Figures

Figure 1

11 pages, 956 KiB  
Review
IGF-1 and IGFBP-3 in Inflammatory Cachexia
by Ana Isabel Martín, Teresa Priego, Álvaro Moreno-Ruperez, Daniel González-Hedström, Miriam Granado and Asunción López-Calderón
Int. J. Mol. Sci. 2021, 22(17), 9469; https://doi.org/10.3390/ijms22179469 - 31 Aug 2021
Cited by 35 | Viewed by 6803
Abstract
Inflammation induces a wide response of the neuroendocrine system, which leads to modifications in all the endocrine axes. The hypothalamic–growth hormone (GH)–insulin-like growth factor-1 (IGF-1) axis is deeply affected by inflammation, its response being characterized by GH resistance and a decrease in circulating [...] Read more.
Inflammation induces a wide response of the neuroendocrine system, which leads to modifications in all the endocrine axes. The hypothalamic–growth hormone (GH)–insulin-like growth factor-1 (IGF-1) axis is deeply affected by inflammation, its response being characterized by GH resistance and a decrease in circulating levels of IGF-1. The endocrine and metabolic responses to inflammation allow the organism to survive. However, in chronic inflammatory conditions, the inhibition of the hypothalamic–GH–IGF-1 axis contributes to the catabolic process, with skeletal muscle atrophy and cachexia. Here, we review the changes in pituitary GH secretion, IGF-1, and IGF-1 binding protein-3 (IGFBP-3), as well as the mechanism that mediated those responses. The contribution of GH and IGF-1 to muscle wasting during inflammation has also been analyzed. Full article
(This article belongs to the Special Issue Molecular Response to Endotoxin)
Show Figures

Figure 1

Back to TopTop