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Life
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Current Research in Inflammatory Response to Injury and Diseases
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Current Research in Inflammatory Response to Injury and Diseases

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Medical Research".

Deadline for manuscript submissions: closed (15 July 2022) | Viewed by 14709

Special Issue Editors

Prof. Dr. Huang-Ping Yu

E-Mail Website
Guest Editor
1. Department of Anesthesiology, Chang Gung Memorial Hospital, 5 Fuxing Street, Kweishan, Taoyuan 333, Taiwan
2. School of Medicine, College of Medicine, Chang Gung University, Kweishan, Taoyuan 333, Taiwan
Interests: anesthesiology; critical care medicine; emergency medicine; inflammation; surgery; transplantation; sepsis; hemorrhagic shock; molecular biology
Dr. Fu-Chao Liu

E-Mail Website
Guest Editor
Division of General Surgery, Department of Anesthesiology, Chang Gung Memorial Hospital, 5 Fuxing Street, Kweishan, Taoyuan 333, Taiwan
Interests: inflammation; anesthesiology; critical care medicine; toxicology ; shock; transplantation; platelets function

Special Issue Information

Dear Colleagues,

Inflammation is a major problem of the host response against external pathogen invasion or internal pathologic progression. Immune responses are complex and essential, affecting the organ function and survival of an individual. Therefore, we invite researchers and clinicians to submit original articles, as well as review articles, associated with inflammation. We are particularly interested in articles describing new insights and findings on the effectiveness or mechanisms of inflammatory responses to injury or disease. The work could be based on animal studies, human studies or clinical trials and may include anti-inflammatory prevention and the treatment of inflammatory diseases. Potential topics of interest include, but are not limited to, the following:

  • Clinical and animal research on inflammation;
  • Effect and mechanism of inflammatory response to injury and disease;
  • Immune responses and inflammatory processes;
  • Current research and development with inflammatory aspects;
  • New aspects of therapeutic strategies of anti-inflammatory prevention and treatment.

Prof. Dr. Huang-Ping Yu
Dr. Fu-Chao Liu
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 submissions that pass pre-check are 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 single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Life 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 2600 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

  • inflammation
  • injury
  • reactive oxygen species
  • superoxide anion
  • immune response

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

Published Papers (4 papers)

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Research

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13 pages, 5273 KiB  
Article
Neutrophils in Extravascular Body Fluids: Cytological-Energy Analysis Enables Rapid, Reliable and Inexpensive Detection of Purulent Inflammation and Tissue Damage
by Petr Kelbich, Petr Vachata, Vilem Maly, Tomas Novotny, Jan Spicka, Inka Matuchova, Tomas Radovnicky, Ivan Stanek, Jan Kubalik, Ondrej Karpjuk, Frantisek Smisko, Eva Hanuljakova and Jan Krejsek
Life 2022, 12(2), 160; https://doi.org/10.3390/life12020160 - 21 Jan 2022
Cited by 4 | Viewed by 4802
Abstract
The simultaneous cytological and metabolic investigation of various extravascular body fluids (EBFs) provides clinically relevant information about the type and intensity of the immune response in particular organ systems. The oxidative burst of professional phagocytes with the concomitant production of reactive oxygen species [...] Read more.
The simultaneous cytological and metabolic investigation of various extravascular body fluids (EBFs) provides clinically relevant information about the type and intensity of the immune response in particular organ systems. The oxidative burst of professional phagocytes with the concomitant production of reactive oxygen species consumes a large amount of oxygen and is the cause of switch to the development of anaerobic metabolism. We assessed the relationships between percentages of neutrophils, aerobic and anaerobic metabolism, and tissue damage via the determination of aspartate aminotransferase catalytic activities (AST) in cerebrospinal fluid (CSF), pleural effusions (PE), abdominal effusions (AE), and synovial fluids (SF). EBFs with 0.0–20.0% neutrophils: 83.0% aerobic and 1.3% strongly anaerobic cases with median of AST = 13.8 IU/L in CSF; 68.0% aerobic and 9.0% strongly anaerobic cases with median of AST = 20.4 IU/L in PE; 77.5% aerobic and 10.5% strongly anaerobic cases with median of AST = 18.0 IU/L in AE; 64.1% aerobic and 7.7% strongly anaerobic cases with median of AST = 13.8 IU/L in SF. EBFs with 80.0–100.0% neutrophils: 4.2% aerobic and 73.7% strongly anaerobic cases with median of AST = 19.2 IU/L in CSF; 7.4% aerobic and 77.3% strongly anaerobic cases with median of AST = 145.2 IU/L in PE; 11.8% aerobic and 73.7% strongly anaerobic cases with median of AST = 61.8 IU/L in AE; 25.5% aerobic and 38.2% strongly anaerobic cases with median of AST = 37.2 IU/L in SF. The significant presence of neutrophils, concomitant strong anaerobic metabolism, and elevated AST in various EBFs are reliable signs of damaging purulent inflammation. Full article
(This article belongs to the Special Issue Current Research in Inflammatory Response to Injury and Diseases)
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16 pages, 7893 KiB  
Article
The Timing and Effects of Low-Dose Ethanol Treatment on Acetaminophen-Induced Liver Injury
by Fu-Chao Liu, Huang-Ping Yu, Chia-Chih Liao, An-Hsun Chou and Hung-Chen Lee
Life 2021, 11(10), 1094; https://doi.org/10.3390/life11101094 - 15 Oct 2021
Cited by 5 | Viewed by 2601
Abstract
Acetaminophen (APAP) overdose is the major cause of drug-induced liver injury and acute liver failure. Approximately 10% of APAP is metabolized by cytochrome P450 (CYP2E1) into toxic N-acetyl-p-benzoquinone imine (NAPQI). CYP2E1 also contributes to ethanol metabolism, especially during conditions of high blood [...] Read more.
Acetaminophen (APAP) overdose is the major cause of drug-induced liver injury and acute liver failure. Approximately 10% of APAP is metabolized by cytochrome P450 (CYP2E1) into toxic N-acetyl-p-benzoquinone imine (NAPQI). CYP2E1 also contributes to ethanol metabolism, especially during conditions of high blood ethanol concentration. Acute and chronic ethanol consumption appears to have opposite effects on APAP-induced liver injury. We determined the effects of different doses, pre- and post-treatment, and various schedules of ethanol exposure in APAP-induced liver injury. Treatment with ethanol (0.5 g/kg) after 1 h of APAP (300 mg/kg) administration decreased serum ALT levels, histopathological features, and inflammatory cell infiltration. Moreover, ethanol treatment 1 h after APAP treatment reduced APAP-induced liver injury compared with later administration. Interestingly, ethanol pretreatment did not provide any protective effect. Furthermore, ethanol treatment was associated with a significant decrease in ERK and AKT phosphorylation during the acute injury phase. Ethanol exposure also increased CYP2E1 expression and decreased PCNA expression during the liver regeneration phase. Full article
(This article belongs to the Special Issue Current Research in Inflammatory Response to Injury and Diseases)
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18 pages, 6825 KiB  
Article
Transcriptomic Analysis of Long Noncoding RNA and mRNA Expression Profiles in the Amygdala of Rats with Bone Cancer Pain-Depression Comorbidity
by Shuyan Wu, Xiaohui Chen, Fengyi Huang, Mingxue Lin, Pinzhong Chen, Haiyang Wan, Fei Gao, Ting Zheng and Xiaochun Zheng
Life 2021, 11(8), 834; https://doi.org/10.3390/life11080834 - 14 Aug 2021
Cited by 5 | Viewed by 2649
Abstract
Bone cancer pain (BCP)–depression comorbidity has become a complex clinical problem during cancer treatment; however, its underlying molecular mechanisms have not been clarified. Several long noncoding RNAs (lncRNAs) have been demonstrated to be promising therapeutic targets in depression, but research on the role [...] Read more.
Bone cancer pain (BCP)–depression comorbidity has become a complex clinical problem during cancer treatment; however, its underlying molecular mechanisms have not been clarified. Several long noncoding RNAs (lncRNAs) have been demonstrated to be promising therapeutic targets in depression, but research on the role of lncRNAs in BCP–depression comorbidity has been limited. Therefore, high-throughput RNA sequencing was performed to detect differentially expressed profiles in the amygdala of a BCP–depression rat model in this study. We detected 330 differentially expressed mRNAs (DEmRNAs) and 78 differentially expressed lncRNAs (DElncRNAs) in the BCP–depression comorbidity model and then verified the expression of six DEmRNAs and six DElncRNAs with the greatest degrees of difference by RT-qPCR. Furthermore, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that differentially expressed genes were strongly enriched in inflammatory and immunologic systemic responses. Then the nuclear factor kappa B (NF-κB) signaling pathway and the Th17 differentiation pathway showed significant differences, as determined by Western blot analysis. Finally, we constructed a protein–protein interaction (PPI) network to explore the potential regulatory mechanism of DEmRNAs. In conclusion, our study reveals a new resource for the understanding of dysregulated lncRNAs and mRNAs in BCP–depression comorbidity and provides novel potential therapeutic targets for further approaches. Full article
(This article belongs to the Special Issue Current Research in Inflammatory Response to Injury and Diseases)
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Review

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16 pages, 1078 KiB  
Review
Credibility of the Neutrophil-to-Lymphocyte Count Ratio in Severe Traumatic Brain Injury
by Dorota Siwicka-Gieroba and Wojciech Dabrowski
Life 2021, 11(12), 1352; https://doi.org/10.3390/life11121352 - 7 Dec 2021
Cited by 4 | Viewed by 3721
Abstract
Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality worldwide. The consequences of a TBI generate the activation and accumulation of inflammatory cells. The peak number of neutrophils entering into an injured brain is observed after 24 h; [...] Read more.
Traumatic brain injury (TBI) is one of the leading causes of morbidity and mortality worldwide. The consequences of a TBI generate the activation and accumulation of inflammatory cells. The peak number of neutrophils entering into an injured brain is observed after 24 h; however, cells infiltrate within 5 min of closed brain injury. Neutrophils release toxic molecules including free radicals, proinflammatory cytokines, and proteases that advance secondary damage. Regulatory T cells impair T cell infiltration into the central nervous system and elevate reactive astrogliosis and interferon-γ gene expression, probably inducing the process of healing. Therefore, the neutrophil-to-lymphocyte ratio (NLR) may be a low-cost, objective, and available predictor of inflammation as well as a marker of secondary injury associated with neutrophil activation. Recent studies have documented that an NLR value on admission might be effective for predicting outcome and mortality in severe brain injury patients. Full article
(This article belongs to the Special Issue Current Research in Inflammatory Response to Injury and Diseases)
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