scholarly journals C-C Chemokine Receptor Type 5 Links COVID-19, Rheumatoid Arthritis, and Hydroxychloroquine

2020 ◽  
Author(s):  
Mahmood Yaseen HACHIM ◽  
Ibrahim Y. Hachim ◽  
Kashif Naeem ◽  
Haifa Hannawi ◽  
Issa Al Salmi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Molecular Mechanisms ◽  
Immune Cell ◽  
Severe Form ◽  
Cell Recruitment ◽  
Beneficial Effects ◽  
Increased Risk ◽  
Patient Groups ◽  
Chemotactic Factors ◽  
Immune Cell Recruitment

Abstract Background: Patients with rheumatoid arthritis (RA) represent one of the fragile patient groups that might be susceptible to coronavirus disease -19 (COVID-19) and its severe form. On the other side, RA patients have been found not to have an increased risk of COVID19 infection. Moreover, some of the Disease-Modifying Anti-Rheumatic Drugs (DMARDS) commonly used to treat rheumatic diseases like Hydroxychloroquine (HCQ) were proposed as a potential therapy for COVID19 with a lack of full understanding of their molecular mechanisms. This highlights the need for the discovery of common pathways that may link both diseases at the molecular side Methods: We used the in silico approach to investigate the transcriptomic profile of RA synovium compared to osteoarthritis and healthy controls to identify RA specific molecular pathways shared with that of severe acute respiratory syndrome-corona virus-2 (SARS-COV-2) infected lung tissue. Results: Our results showed upregulation of chemotactic factors, including CCL4, CCL8, and CCL11, that all shared CCR5 as their receptor, as a common derangement observed in both diseases; RA and COVID-19. Moreover, our results also highlighted that HCQ might interfere with the COVID-19 infection through its ability to upregulate specific immune cell populations like activated natural killer (NK) cells, besides blocking CCR5 rich immune cell recruitment to the SARS-COV-2 infected lungs Conclusion: Our results might explain some of the reports that showed beneficial effects and indicate the need for proper patients stratification on their immune profile before selecting the therapeutic protocol or clinical trial enrollment. Keyword COVID-19, SARS-COV-2, Hydroxychloroquine, rheumatoid arthritis

scholarly journals C-C chemokine receptor type 5 links COVID-19, Rheumatoid arthritis, and Hydroxychloroquine

2020 ◽  
Author(s):  
Mahmood Yaseen Hachim ◽  
Ibrahim Hachim ◽  
Kashif Naeem ◽  
Haifa Hannawi ◽  
Issa Al Salmi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Molecular Mechanisms ◽  
Immune Cell ◽  
Severe Form ◽  
Cell Recruitment ◽  
Beneficial Effects ◽  
Increased Risk ◽  
Patient Groups ◽  
Chemotactic Factors ◽  
Immune Cell Recruitment

Abstract Background: Patients with rheumatoid arthritis (RA) represent one of the fragile patient groups that might be susceptible to coronavirus disease -19 (COVID-19) and its severe form. On the other side, RA patients have been found not to have an increased risk of COVID19 infection. Moreover, some of the Disease-Modifying Anti-Rheumatic Drugs (DMARDS) commonly used to treat rheumatic diseases like Hydroxychloroquine (HCQ) were proposed as a potential therapy for COVID19 with a lack of full understanding of their molecular mechanisms. This highlights the need for the discovery of common pathways that may link both diseases at the molecular side Methods: We used the in silico approach to investigate the transcriptomic profile of RA synovium compared to osteoarthritis and healthy controls to identify RA specific molecular pathways shared with that of severe acute respiratory syndrome-corona virus-2 (SARS-COV-2) infected lung tissue. Results: Our results showed upregulation of chemotactic factors, including CCL4, CCL8, and CCL11, that all shared CCR5 as their receptor, as a common derangement observed in both diseases; RA and COVID-19. Moreover, our results also highlighted that HCQ might interfere with the COVID-19 infection through its ability to upregulate specific immune cell populations like activated natural killer (NK) cells, besides blocking CCR5 rich immune cell recruitment to the SARS-COV-2 infected lungs Conclusion: Our results might explain some of the reports that showed beneficial effects and indicate the need for proper patients stratification on their immune profile before selecting the therapeutic protocol or clinical trial enrollment. Keyword COVID-19, SARS-COV-2, Hydroxychloroquine, rheumatoid arthritis

scholarly journals C-C chemokine receptor type 5 links COVID-19, Rheumatoid arthritis, and Hydroxychloroquine: In silico analysis 

2020 ◽  
Author(s):  
MAHMOOD Yaseen HACHIM ◽  
Ibrahim Hachim ◽  
Kashif Naeem ◽  
Haifa Hannawi ◽  
Issa Al Salmi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
In Silico ◽  
Molecular Mechanisms ◽  
Immune Cell ◽  
In Silico Analysis ◽  
Cell Recruitment ◽  
Beneficial Effects ◽  
Increased Risk ◽  
Patient Groups ◽  
Chemotactic Factors

Abstract Patients with rheumatoid arthritis (RA) represent one of the fragile patient groups that might be susceptible to the critical form of the coronavirus disease -19 (COVID-19) . On the other side, RA patients have been found not to have an increased risk of COVID-19 infection. Moreover, some of the Disease-Modifying Anti-Rheumatic Drugs (DMARDS) commonly used to treat rheumatic diseases like Hydroxychloroquine (HCQ) were proposed as a potential therapy for COVID-19 with a lack of full understanding of their molecular mechanisms. This highlights the need for the discovery of common pathways that may link both diseases at the molecular side. In this research, we used the in silico approach to investigate the transcriptomic profile of RA synovium to identify shared molecular pathways with that of severe acute respiratory syndrome-corona virus-2 (SARS-COV-2) infected lung tissue. Our results showed upregulation of chemotactic factors, including CCL4, CCL8, and CCL11, that all shared CCR5 as their receptor, as a common derangement observed in both diseases; RA and COVID-19. Moreover, our results also highlighted a possible mechanism through which HCQ, which can be used as a monotherapy in mild RA or as one of the triple-DMARDs therapy (tDMARDs; methotrexate, sulphasalazine, and HCQ), might interfere with the COVID-19 infection. This might be achieved through the ability of HCQ to upregulate specific immune cell populations like activated natural killer (NK) cells, which were found to be significantly reduced in COVID-19 infection. In addition to its ability to block CCR5 rich immune cell recruitment that also was upregulated in the SARS-COV-2 infected lungs. This might explain some of the reports that showed beneficial effects.

scholarly journals C-C chemokine receptor type 5 links COVID-19, rheumatoid arthritis, and Hydroxychloroquine: in silico analysis

2020 ◽  
Vol 5 (1) ◽  
Author(s):  
Mahmood Y. Hachim ◽  
Ibrahim Y. Hachim ◽  
Kashif Bin Naeem ◽  
Haifa Hannawi ◽  
Issa Al Salmi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
In Silico ◽  
Molecular Mechanisms ◽  
Immune Cell ◽  
In Silico Analysis ◽  
Cell Recruitment ◽  
Beneficial Effects ◽  
Increased Risk ◽  
Patient Groups ◽  
Chemotactic Factors

Abstract Patients with rheumatoid arthritis (RA) represent one of the fragile patient groups that might be susceptible to the critical form of the coronavirus disease − 19 (COVID-19). On the other side, RA patients have been found not to have an increased risk of COVID-19 infection. Moreover, some of the Disease-Modifying Anti-Rheumatic Drugs (DMARDS) commonly used to treat rheumatic diseases like Hydroxychloroquine (HCQ) were proposed as a potential therapy for COVID-19 with a lack of full understanding of their molecular mechanisms. This highlights the need for the discovery of common pathways that may link both diseases at the molecular side. In this research, we used the in silico approach to investigate the transcriptomic profile of RA synovium to identify shared molecular pathways with that of severe acute respiratory syndrome-corona virus-2 (SARS-COV-2) infected lung tissue. Our results showed upregulation of chemotactic factors, including CCL4, CCL8, and CCL11, that all shared CCR5 as their receptor, as a common derangement observed in both diseases; RA and COVID-19. Moreover, our results also highlighted a possible mechanism through which HCQ, which can be used as a monotherapy in mild RA or as one of the triple-DMARDs therapy (tDMARDs; methotrexate, sulphasalazine, and HCQ), might interfere with the COVID-19 infection. This might be achieved through the ability of HCQ to upregulate specific immune cell populations like activated natural killer (NK) cells, which were found to be significantly reduced in COVID-19 infection. In addition to its ability to block CCR5 rich immune cell recruitment that also was upregulated in the SARS-COV-2 infected lungs. This might explain some of the reports that showed beneficial effects.

scholarly journals Alpha-Synuclein to the Rescue: Immune Cell Recruitment by Alpha-Synuclein during Gastrointestinal Infection

2017 ◽  
Vol 9 (5) ◽  
pp. 437-440 ◽  
Author(s):  
Viviane Labrie ◽  
Patrik Brundin
Keyword(s):  
Immune Cell ◽  
Point Mutations ◽  
Alpha Synuclein ◽  
Cell Recruitment ◽  
Normal Functions ◽  
Intestinal Infections ◽  
Increased Risk ◽  
Or Gene ◽  
Immune Cell Recruitment

Intraneuronal accumulation of misfolded alpha-synuclein in the central and peripheral nervous systems is strongly linked to Parkinson disease (PD) and other related synucleinopathies. In rare inherited forms of PD, point mutations or gene multiplications mediate the formation of alpha-synuclein protein aggregates. However, in most PD cases it is presumed that the combined effects of ageing and environmental factors drive the formation of alpha-synuclein aggregates. Despite advances regarding alpha-synuclein pathobiology, the normal functions of this protein and factors that regulate its expression are not well understood. We discuss a recent study reporting that viral infection induces alpha-synuclein expression in neurons of the gastrointestinal tract. Alpha-synuclein levels increased during norovirus infection in the duodenum of children. In an in vitro paradigm, monomeric and oligomeric alpha-synuclein acted as chemoattractants for neutrophils and monocytes, and promoted the maturation of dendritic cells. This suggests that alpha-synuclein facilitates immune responses to infection. We explore the possibility that intestinal infections, and associated inflammation, place individuals at increased risk of PD by increasing alpha-synuclein levels and promoting the formation of alpha-synuclein aggregates that propagate in a prion-like fashion via the vagal nerve to the brainstem.

scholarly journals A Missing Link: Engagements of Dendritic Cells in the Pathogenesis of SARS-CoV-2 Infections

2021 ◽  
Vol 22 (3) ◽  
pp. 1118
Author(s):  
Abdulaziz Alamri ◽  
Derek Fisk ◽  
Deepak Upreti ◽  
Sam K. P. Kung
Keyword(s):  
Dendritic Cells ◽  
Severe Acute Respiratory Syndrome ◽  
Immune Responses ◽  
Immune Cell ◽  
Inflammatory Responses ◽  
Viral Disease ◽  
Cell Recruitment ◽  
Cross Presentation ◽  
Cell Immunity ◽  
Immune Cell Recruitment

Dendritic cells (DC) connect the innate and adaptive arms of the immune system and carry out numerous roles that are significant in the context of viral disease. Their functions include the control of inflammatory responses, the promotion of tolerance, cross-presentation, immune cell recruitment and the production of antiviral cytokines. Based primarily on the available literature that characterizes the behaviour of many DC subsets during Severe acute respiratory syndrome (SARS) and coronavirus disease 2019 (COVID-19), we speculated possible mechanisms through which DC could contribute to COVID-19 immune responses, such as dissemination of Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) to lymph nodes, mounting dysfunctional inteferon responses and T cell immunity in patients. We highlighted gaps of knowledge in our understanding of DC in COVID-19 pathogenesis and discussed current pre-clinical development of therapies for COVID-19.

scholarly journals Interleukin-17D and Nrf2 mediate initial innate immune cell recruitment and restrict MCMV infection

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Ruth Seelige ◽  
Robert Saddawi-Konefka ◽  
Nicholas M. Adams ◽  
Gaëlle Picarda ◽  
Joseph C. Sun ◽  
...  
Keyword(s):  
Immune Cell ◽  
Innate Immune ◽  
Innate Immune Cell ◽  
Mcmv Infection ◽  
Cell Recruitment ◽  
Immune Cell Recruitment

scholarly journals Non-Coding RNAs in COVID-19: Emerging Insights and Current Questions

2021 ◽  
Vol 7 (3) ◽  
pp. 54
Author(s):  
Tobias Plowman ◽  
Dimitris Lagos
Keyword(s):  
Immune Response ◽  
Severe Acute Respiratory Syndrome ◽  
Immune Cell ◽  
Cytokine Storm ◽  
Cell Recruitment ◽  
Vascular Dysregulation ◽  
Virus Rna ◽  
Growing Body ◽  
Non Coding Rnas ◽  
Immune Cell Recruitment

The highly infectious severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged as the causative agent of coronavirus disease 2019 (COVID-19) in late 2019, igniting an unprecedented pandemic. A mechanistic picture characterising the acute immunopathological disease in severe COVID-19 is developing. Non-coding RNAs (ncRNAs) constitute the transcribed but un-translated portion of the genome and, until recent decades, have been undiscovered or overlooked. A growing body of research continues to demonstrate their interconnected involvement in the immune response to SARS-CoV-2 and COVID-19 development by regulating several of its pathological hallmarks: cytokine storm syndrome, haemostatic alterations, immune cell recruitment, and vascular dysregulation. There is also keen interest in exploring the possibility of host–virus RNA–RNA and RNA–RBP interactions. Here, we discuss and evaluate evidence demonstrating the involvement of short and long ncRNAs in COVID-19 and use this information to propose hypotheses for future mechanistic and clinical studies.

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