COVID-19 Fatalities Influenced by Cytokine and Cytokine Storm | Chapter 3 | Current Advances in Plant Science, Molecular Biology and Health Sector

 

Since December 2019, COVID-19 disease caused by SARS-CoV-2 virus has spread worldwide pandemic resulting in a large number of infected persons and a lot of deaths of COVID-19 patients. There is currently no definite medicine for the treatment of the disease, as well any preventive measures. Cytokines have been a central topic in research on inflammatory diseases for more than fifty years since interferon (IFN) was discovered. Recently, this has gained great importance among immunologists, doctors and even common people in the pandemic situation of COVID-19.

 

Primarily, cytokines act as lymphocyte growth factors, as well as function as pro-inflammatory and anti-inflammatory molecules and also promote immune response to an antigen. With the progress of multiplication of viruses in humans, activation and amplification of host immune response take place, causing massive release of varieties of cytokines like interleukin (IL)-1, IL-6, IL-17, etc., and different types of interferons (IFNs), tumour necrosis factor (TNF) to form cytokine storm. From studies of COVID-19 patients in hospitals, it has also been noted that uncontrolled inflammation due to elevated levels of cytokines (cytokine storm) is responsible for causing the severity of the disease.

 

This study explores the properties and types of cytokines, their signalling mechanisms in immunity, and their critical role in the pathogenesis of COVID-19. Low infection of the virus persists in the upper airway that causing symptoms similar to seasonal respiratory illness, but with severe infections virus remains in the lower respiratory tract, leading to lung injury, acute respiratory distress syndrome (ARDS) and sometimes death. The role of cytokine storm in causing the severity of the disease was discussed. Ongoing research aims to identify biomarkers that can predict patients at risk of developing a cytokine storm, which may guide timely therapeutic interventions and improve outcomes.

 

Author(s) Details

Professor Satyesh Chandra Roy
Department of Botany, Centre of Advanced Study for Cell and Chromosome Research, University of Calcutta, India.

 

Please see the book here: https://doi.org/10.9734/bpi/mono/978-81-989371-7-9/CH3

Distinct Inflammatory Profiles Distinguish COVID-19 from Influenza with Limited Contributions from Cytokine Storm | Chapter 3 | Diagnostic and Treatment Advances in COVID-19 and SARS-CoV-2

 We pursued a study of immune responses in coronavirus disease 2019 (COVID-19) and influenza patients. Compared to patients with influenza, patients with COVID-19 exhibited largely equivalent lymphocyte counts, fewer monocytes, and lower surface human leukocyte antigen (HLA)–class II expression on selected monocyte populations. Furthermore, decreased HLA-DR on intermediate monocytes predicted severe COVID-19 disease. In contrast to prevailing assumptions, very few (7 of 168) patients with COVID-19 exhibited cytokine profiles indicative of cytokine storm syndrome. After controlling for multiple factors including age and sample time point, patients with COVID-19 exhibited lower cytokine levels than patients with influenza. Up-regulation of IL-6, G-CSF, IL-1RA, and MCP1 predicted death in patients with COVID-19 but were not statistically higher than patients with influenza. Single-cell transcriptional profiling revealed profound suppression of interferon signaling among patients with COVID-19. When considered across the spectrum of peripheral immune profiles, patients with COVID-19 are less inflamed than patients with influenza.

Author(s) Details:

Philip A. Mudd,
Department of Emergency Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

Jeremy Chase Crawford,
Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN, USA.

Jackson S. Turner,
Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO, USA.

Aisha Souquette,
Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN, USA.

Daniel Reynolds,
Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

Diane Bender,
Bursky Center for Human Immunology and Immunotherapy Program, Washington University School of Medicine, Saint Louis, MO, USA.

James P. Bosanquet,
Department of Critical Care, Missouri Baptist Medical Center, Saint Louis, MO, USA.

Nitin J. Anand,
Department of Critical Care, Missouri Baptist Medical Center, Saint Louis, MO, USA.

David A. Striker,
Department of Critical Care, Missouri Baptist Medical Center, Saint Louis, MO, USA.

R. Scott Martin,
Department of Critical Care, Missouri Baptist Medical Center, Saint Louis, MO, USA.

Adrianus C. M. Boon,
Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN, USA.

Stacey L. House,
Department of Emergency Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

Kenneth E. Remy,
Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA, Department of Pediatrics, Washington University School of Medicine, Saint Louis, MO, USA and Department of Anesthesiology, Washington University School of Medicine, Saint Louis, MO, USA.

Richard S. Hotchkiss,
Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA, Department of Anesthesiology, Washington University School of Medicine, Saint Louis, MO, USA and Department of Surgery, Washington University School of Medicine, Saint Louis, MO, USA.

Rachel M. Presti,
Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

Jane A. O’Halloran,
Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

William G. Powderly,
Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA.

Paul G. Thomas,
Department of Immunology, St. Jude Children’s Research Hospital, Memphis, TN, USA.

Ali H. Ellebedy,
Department of Pathology and Immunology, Washington University School of Medicine, Saint Louis, MO, USA, Department of Internal Medicine, Washington University School of Medicine, Saint Louis, MO, USA and Bursky Center for Human Immunology and Immunotherapy Program, Washington University School of Medicine, Saint Louis, MO, USA.

Please see the link here: https://stm.bookpi.org/DTACSC/article/view/9553

Role of Gene Polymorphisms Might Contribute to Endometriosis Susceptibility | Chapter 9 | Current Innovations in Medicine and Medical Science Vol. 5

 Endometriosis is a condition in which the tissue that normally lines the uterus grows outside the uterus. Endometriosis is characterized by the presence of tissue attached to the ovaries, fallopian tubes, or intestines. Several recent studies have examined genetic polymorphisms as possible factors in the development of endometriosis. The purpose of this study is to review case-control studies of recent data on genes with nucleotide polymorphisms associated with endometriosis. A PubMed search of endometriosis, polymorphisms, and interleukins found 50 publications between 2001 and 2020. These were classified according to the type of polymorphism tested and whether the results supported or did not support an association with endometriosis. We have found a whole range of conflicting results. About half of the studies surveyed found an association between various polymorphisms and endometriosis. Based on this review, it can be concluded that there are strong gene-environment interactions that could certainly influence approaches to identify genetic variants associated with endometriosis.

Author(s) Details:

Nandhini Balunathan,
Department of Human Genetics, Faculty of Biomedical sciences and technology, Sri Ramachandra Institute of Higher Education and Research (Deemed to be University), Chennai-116, India.

S. Nandhini,
Department of Human Genetics, Faculty of Biomedical sciences and technology, Sri Ramachandra Institute of Higher Education and Research (Deemed to be University), Chennai-116, India.

J. Akshaya,
Department of Human Genetics, Faculty of Biomedical sciences and technology, Sri Ramachandra Institute of Higher Education and Research (Deemed to be University), Chennai-116, India.

Please see the link here: https://stm.bookpi.org/CIMMS-V5/article/view/8467

Study on the Role of Cell Signaling Molecules in the Pathogenesis of Glomerulonephritis in Children | Chapter 09 | New Frontiers in Medicine and Medical Research Vol. 17

 Background: Cytokines are a functional group of small proteins and glycoproteins that serve as soluble mediators in an autocrine or paracrine way. Cytokines are produced by a range of cell types, the majority of which are leukocytes, and they have immune and non-immune cells as their targets.

The goal of the study was to determine the concentration of cellular signalling molecules in the urine of children with glomerulonephritis at various clinical-evolutionary stages.

Materials and Procedures: 75 children with glomerulonephritis (GN) ranging in age from 2 to 17 were included in this study. Steroid-sensitive nephrotic syndrome (SSNS), steroid-resistant nephrotic syndrome (SRNS), chronic glomerulonephritis (GN) nephrotic form, and chronic GN mixed type were found in 20 children. This study looked at patients who had relapsed from disease or were in clinical remission. The control group consisted of 20 healthy children.

Increased levels of cell signalling molecules (IL-8, TNF-, MCP-1, MIP-1) in the urine during clinical symptoms were discovered in this study, which is a notable result considering their role in the immunopathogenic mechanism of proteinuria in nephrotic syndrome (NS).

Conclusions: Using urinary concentrations of cellular signalling molecules as a non-invasive predictive method for estimating disease activity, monitoring disease progression, distinguishing steroid-sensitive nephrotic syndrome from steroid-resistant nephrotic syndrome, and assessing treatment effectiveness in children with glomerulonephritis could be beneficial.

Author(S) Details

Angela Ciuntu
Department of Pediatrics, Nicolae Testemitanu State University of Medicine and Pharmacy, Chisinau, the Republic of Moldova. and Institute of Mother and Child, Chisinau, the Republic of Moldova.

View Book:- https://stm.bookpi.org/NFMMR-V17/article/view/4205

Oral Epithelial Cytokines: A Review | Chapter 8 | Issues and Development in Health Research Vol. 4

 Oral mucosal epithelia, like other forms of mucosal epithelia, has a reputation for being protective. Oral epithelia was introduced as a non-lymphoid, non-myeloid tissue with immunological potentials in the current chapter. The plural form of the singular epithelium is epithelia. They are specialised layers that cover the outside of the organs that make up the human body. Oral epithelial cells, according to popular belief, contain a TLR system and can recognise microbial invaders. Microbial invaders, in turn, cause epithelia to release pro-inflammatory TH1,TH2 cytokines and chemokines. Chemokines. Species and strain-specific induction procedures are reported. A number of in-vitro models have confirmed natural epithelial cytokine production. Oral epithelial cytokine has multiple immunological activities, including regulating local immune responses, mediating autoimmune illness, and inducing tissue damage when release is elevated. They show multi-factorial influences on the mucosal immune compartment, are an important component of local innate immune responses, and may have implications for vaccine immunity in the future.

Author(s) Details

Prof. Ibrahim Mohamed Saeed Shnawa
College of Biotechnology University of Qasim, Qasim, Babylon, Iraq. Hilla University College, Babylon, Iraq.

View Book :- https://stm.bookpi.org/IDHR-V4/article/view/3376

Calcite Type Fired Shell Powder of Bivalve Corbicula japonica Improved Mal-Functions of Liver in Animal and in Calcite-Ingested Clients | Chapter 13 | Challenges in Disease and Health Research Vol.1

It has been inherited for a long preriod in a small village that the fired shell powder of bivalve Corbicula japonica has been working against liver disorder without any scientific evidences. Experiment was initiated by the village office requirement to ascertain an anti-hepatitis activity of the fired shell powder of the Corbicula japonica. Shell of the Corbicula japonica was fired to analyze a crystal structure by the X-ray diffraction apparatus, followed by animal tests by hepatitis model Long Evans Cinnamon (LEC) rat. In C57BL/6 mouse model additional biofunctions like immune activation, lipid controlling, anti-alcoholic damage activity and liver cells proliferation tests were evaluated. The fired shell powder of the Corbicula japonica (calcite type) fired at 500°C for 2 hrs demonstrated the liver function improving activity in LEC rat model via orally administerationt. The calcite type shell powder fed-LEC rats elongated survival times by the improving acute hepatitis symptoms, however, the Corbicula japonica aragonite and Ruditapes philippinarum calcite did not work effectively. Further Corbicula japonica calcite lowered AST(glutamic oxaloacetic transaminase) ALT (glutamic pyruvic transaminase), TBiI (total bilirubin) and IAP (immunosuppressive acidic protein) value in serum, and enforced cellular immune by increasing NK (natural killer) cells activity. Cytokines generation as TNFα (tumor necrosis factor), IL-2 (interleukin) and IFN-γ (interferon) in spleen cells cultivation assay was not clearly admitted. In the alcohol-fed mouse test, the Corbicula japonica calcite reduced alcoholic caused damages in liver and lowered lipid level in serum. 

Author(s) Details

Sasaki Jin-Ichi,
Hirosaki University of Health and Welfare, Junior College, 2  He was born in Iwate, Japan,

Minegishi Yoshinori 
Fuji Clean-Tec Co. Ltd. 2-19-21, Tomita Aomori 038-0004, Japan

Someya Tetsunei
Neo Circle Co. Ltd. 8-8-4, Akasaka Minato-Ku Tokyo 107-0052, Japan.

View Book :- http://bp.bookpi.org/index.php/bpi/catalog/book/203

Immuno-inflammatory Aspects of Interleukin-21 in Periodontal Sequelae: Current Development | Chapter 16 | Research Trends and Challenges in Medical Science Vol.2

Interleukin-21 (IL-21) has a dual anti-inflammatory and pro-inflammatory role in chronic inflammation. It causes breakdown of other surrounding hard and soft tissues by coupling with other destructive mediators, along with increasing several other proinflammatory cytokines. This chapter describes concepts in relation to effects of IL-21 on critical immune cells of both innate and adaptive immune systems, and how the cytokine evades its deactivation through a positive feedback loop. The chapter also reports results of an original study regarding quantification of IL-21 among types of periodontitis and comparing its levels to healthy subjects. Previous literature and our current study results suggest that IL-21 has a definite role in chronic and acute kind of inflammatory progression. Although, further longitudinal studies will strengthen its evidence to be characterized as a true diagnostic periodontal marker.  

Author (s) Details

Dr. Archana Mootha
Hiroshima University, Hiroshima, Japan.

View Book :- http://bp.bookpi.org/index.php/bpi/catalog/book/190