Impact of Azithromycin and 8-Hydroxychloroquine in 2019 Novel Coronavirus (COVID-19) Pandemic: A Systematic Review

2021 ◽  
Vol 11 (3) ◽  
Author(s):  
Srikanta Chandra ◽  
Preeta Bose ◽  
Jyoti Saxena ◽  
Muniraj Bhattacharya ◽  
Arun dutta ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Bacterial Protein ◽  
Lysosomal Ph ◽  
Inflammatory Conditions ◽  
Corona Virus ◽  
Novel Coronavirus ◽  
Antigen Presenting ◽  
Bacterial Protein Synthesis ◽  
Modern Era

As we know novel coronavirus is an emergent nuisance in this stipulated period. Corona virus is a group of enveloped viruses, with non-segmented, single stranded & positive sense RNA genomes. Human Corona virus is mainly subdivided into four categories such as 229E, NL63, OC43, HKU1. Epidemiologically it has a greater prevalence in the modern era. The features encountered in the clinical course of the disease are multifarious spanning from cough, sneezing, fever, breathlessness. It may take 2-14 days for a person to notice symptoms after infection. Azithromycin and 8 Hydroxychloroquine both plays an instrumental role for management of COVID-19. Azithromycin is a macrolide antibiotic and it binds with a 50s ribosome then inhibits bacterial protein synthesis. On the other hand 8-Hydroxychloroquine was approved by United State in the year of 1955 .Basically it is used as a antimalarial drugs . Briefly, in inflammatory conditions it binds with toll like receptor & blocks them. 8- hydroxychloroquine increases lysosomal pH in antigen presenting cells . In inflammatory conditions it blocks toll like receptors on plasmacytoid dendritic cells. In our review we focused on the role of Azithromycin, and 8-hydroxychloroquine in Covid-19 .

scholarly journals Genes Involved in Formation and Attachment of a Two-Carbon Chain as a Component of Eurekanate, a Branched-Chain Sugar Moiety of Avilamycin A

2005 ◽  
Vol 71 (1) ◽  
pp. 400-406 ◽  
Author(s):  
Irina Treede ◽  
Gerd Hauser ◽  
Agnes M�hlenweg ◽  
Carsten Hofmann ◽  
Maraike Schmidt ◽  
...  
Keyword(s):  
Potent Inhibitor ◽  
Ribosomal Subunit ◽  
Carbon Chain ◽  
Biosynthetic Gene Cluster ◽  
Bacterial Protein ◽  
Structure Modification ◽  
Experimental Proof ◽  
Branched Chain ◽  
Bacterial Protein Synthesis

ABSTRACT Eurekanate belongs to the important class of branched-chain carbohydrates present in a wide variety of natural sources. It is a component of avilamycin A, a potent inhibitor of bacterial protein synthesis targeting the 50S ribosomal subunit. The present work provides experimental proof for the function of two genes of the avilamycin biosynthetic gene cluster, aviB1 and aviO2, that are both involved in avilamycin structure modification. The functions of both genes were identified by gene inactivation experiments and nuclear magnetic resonance analyses of extracts produced by the mutants. We suggest that both AviO2 and AviB1 are involved in the biosynthesis of eurekanate within avilamycin biosynthesis. Moreover, two other genes (aviO1 and aviO3) have been inactivated, resulting in a breakdown of avilamycin production in the mutants ITO1 and ITO3, which clearly shows the essential role of both enzymes in avilamycin biosynthesis. The exact functions of both aviO1 and aviO3 remained unknown.

scholarly journals Development of a Secondary Immune Response toMycobacterium tuberculosisIs Independent of Toll-Like Receptor 2

2010 ◽  
Vol 79 (3) ◽  
pp. 1118-1123 ◽  
Author(s):  
Amanda McBride ◽  
Kamlesh Bhatt ◽  
Padmini Salgame
Keyword(s):  
Immune Response ◽  
T Cells ◽  
Host Resistance ◽  
Toll Like Receptor ◽  
Response Phenotype ◽  
Toll Like Receptor 2 ◽  
Antigen Presenting ◽  
Memory Immune Response

ABSTRACTPublished work indicates that the contribution of Toll-like receptor 2 (TLR2) to host resistance during acuteMycobacterium tuberculosisinfection is marginal. However, in these studies, TLR2 participation in the memory immune response toM. tuberculosiswas not determined. The substantialin vitroevidence thatM. tuberculosisstrongly triggers TLR2 on dendritic cells and macrophages to bring about either activation or inhibition of antigen-presenting cell (APC) functions, along with accumulating evidence that memory T cell development can be calibrated by TLR signals, led us to question the role of TLR2 in host resistance to secondary challenge withM. tuberculosis. To address this question, a memory immunity model was employed, and the response of TLR2-deficient (TLR2 knockout [TLR2KO]) mice following a secondary exposure toM. tuberculosiswas compared to that of wild-type (WT) mice based on assessment of the bacterial burden, recall response, phenotype of recruited T cells, and granulomatous response. We found that upon rechallenge withM. tuberculosis, both WT and TLR2KO immune mice displayed similarly enhanced resistance to infection in comparison to their naïve counterparts. The frequencies ofM. tuberculosis-specific gamma interferon (IFN-γ)-producing T cells, the phenotypes of recruited T cells, and the granulomatous responses were also similar between WT and TLR2KO immune mice. Together, the findings from this study indicate that TLR2 signaling does not influence memory immunity toM. tuberculosis.

scholarly journals Toll-Like Receptor 3 in Solid Cancer and Therapy Resistance

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3227
Author(s):  
Ximena Maria Muresan ◽  
Jan Bouchal ◽  
Zoran Culig ◽  
Karel Souček
Keyword(s):  
Tumor Regression ◽  
Current Knowledge ◽  
Therapy Resistance ◽  
Solid Cancer ◽  
Type I ◽  
Toll Like Receptor ◽  
Cytokines And Chemokines ◽  
Antiviral Function ◽  
Antigen Presenting

Toll-like receptor 3 (TLR3) is a member of the TLR family, which has been extensively studied for its antiviral function. It is highly expressed in the endosomes of antigen-presenting immune cells and epithelial cells. TLR3 binds specifically double-strand RNAs (dsRNAs), leading to the activation of mainly two downstream pathways: the phosphorylation of IRF3, with subsequent production of type I interferon, and the activation of NF-κB, which drives the production of inflammatory cytokines and chemokines. Several studies have demonstrated TLR3 expression in multiple neoplasia types including breast, prostate, and lung cancer. Most studies were focused on the beneficial role of TLR3 activation in tumor cells, which leads to the production of cytotoxic cytokines and interferons and promotes caspase-dependent apoptosis. Indeed, ligands of this receptor were proposed for the treatment of cancer, also in combination with conventional chemotherapy. In contrast to these findings, recent evidence showed a link between TLR3 and tumor progression, metastasis, and therapy resistance. In the present review, we summarize the current knowledge of the mechanisms through which TLR3 can either lead to tumor regression or promote carcinogenesis as well as the potential of TLR-based therapies in resistant cancer.

scholarly journals Role of microRNAs in the Regulation of Dendritic Cell Generation and Function

2020 ◽  
Vol 21 (4) ◽  
pp. 1319 ◽  
Author(s):  
Viviana Scalavino ◽  
Marina Liso ◽  
Grazia Serino
Keyword(s):  
Adaptive Systems ◽  
Intrinsic Factors ◽  
Inflammatory Conditions ◽  
Inflammatory Processes ◽  
Plasmacytoid Dcs ◽  
Non Coding Rnas ◽  
And Function ◽  
Antigen Presenting ◽  
Mirna Deregulation

Dendritic cells (DCs) are antigen-presenting cells with a key role in immune responses. They act as a link between the innate and adaptive systems and they can induce and maintain immunologic tolerance. DCs are subdivided into conventional and plasmacytoid DCs. These cell subsets originate from the same bone marrow precursors and their differentiation process is determined by several extrinsic and intrinsic factors, such as cytokines, transcription factors, and miRNAs. miRNAs are small non-coding RNAs that play a crucial role in modulating physiological and pathological processes mediated by DCs. miRNA deregulation affects many inflammatory conditions and diseases. The aim of this review was to underline the importance of miRNAs in inflammatory processes mediated by DCs in physiological and pathological conditions and to highlight their potential application for future therapies.

Toll-like receptor 4 regulates colitis-associated adenocarcinoma development in interleukin-10-deficient (IL-10−/−) mice

2007 ◽  
Vol 35 (5) ◽  
pp. 1375-1376 ◽  
Author(s):  
R. Zhang ◽  
Y. Li ◽  
P.L. Beck ◽  
D.-M. McCafferty
Keyword(s):  
Interleukin 10 ◽  
Bacterial Toxins ◽  
Deficient Mouse ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Inflammatory Conditions ◽  
Increased Risk ◽  
Growing Body ◽  
Leucocyte Recruitment

Chronic inflammatory conditions such as ulcerative colitis and Crohn's disease are associated with an increased risk of developing adenocarcinoma. It has been hypothesized that this increased risk may be related to soluble mediators present in the inflammatory environment and that factors involved in exacerbating the inflammatory response could increase the risk of developing colitis-associated cancer. There is a growing body of evidence from both clinical studies and animal models which suggests that colitis occurs due to an aberrant immune response to enteric flora in genetically susceptible individuals. It is well documented that bacterial toxins such as endotoxin have potent pro-inflammatory effects through activation of TLR4 (Toll-like receptor 4) and therefore this molecule could potentially play a prominent role in the initiation/exacerbation of colitis and adenocarcinoma development. Using genetic mutant mice, we have examined the role of TLR4 in a spontaneously developing mouse model of colitis-associated adenocarcinoma: the IL-10−/− (interleukin-10-deficient) mouse. Surprisingly, our evidence suggests that the absence of TLR4 promotes colitis-associated adenocarcinoma in IL-10−/− mice. TLR4-dependent chemokine induction may play a part in modulating the development of colitis-associated neoplasia through altered leucocyte recruitment.

scholarly journals Toll-Like Receptor 2-Mediated Signaling Requirements for Francisella tularensis Live Vaccine Strain Infection of Murine Macrophages

2007 ◽  
Vol 75 (8) ◽  
pp. 4127-4137 ◽  
Author(s):  
Leah E. Cole ◽  
Kari Ann Shirey ◽  
Eileen Barry ◽  
Araceli Santiago ◽  
Prasad Rallabhandi ◽  
...  
Keyword(s):  
Protein Synthesis ◽  
Francisella Tularensis ◽  
Vaccine Strain ◽  
Live Vaccine Strain ◽  
Toll Like Receptor ◽  
Bacterial Protein ◽  
Wild Type ◽  
Murine Macrophages ◽  
Toll Like Receptor 2 ◽  
Bacterial Protein Synthesis

ABSTRACT Francisella tularensis, an aerobic, non-spore-forming, gram-negative coccobacillus, is the causative agent of tularemia. We reported previously that F. tularensis live vaccine strain (LVS) elicited strong, dose-dependent NF-κB reporter activity in Toll-like receptor 2 (TLR2)-expressing HEK293T cells and proinflammatory gene expression in primary murine macrophages. Herein, we report that F. tularensis LVS-induced murine macrophage proinflammatory cytokine gene and protein expression are overwhelmingly TLR2 dependent, as evidenced by the abrogated responses of TLR2−/− macrophages. F. tularensis LVS infection also increased expression of TLR2 both in vitro, in mouse macrophages, and in vivo, in livers from F. tularensis LVS-infected mice. Colocalization of intracellular F. tularensis LVS, TLR2, and MyD88 was visualized by confocal microscopy. Signaling was abrogated if the F. tularensis LVS organisms were heat or formalin killed or treated with chloramphenicol, indicating that the TLR2 agonist activity is dependent on new bacterial protein synthesis. F. tularensis LVS replicates in macrophages; however, bacterial replication was not required for TLR2 signaling because LVSΔguaA, an F. tularensis LVS guanine auxotroph that fails to replicate in the absence of exogenous guanine, activated NF-κB in TLR2-transfected HEK293T cells and induced cytokine expression in wild-type macrophages comparably to wild-type F. tularensis LVS. Collectively, these data indicate that the primary macrophage response to F. tularensis LVS is overwhelmingly TLR2 dependent, requires de novo bacterial protein synthesis, and is independent of intracellular F. tularensis replication.

scholarly journals Macrophages and Uveitis in Experimental Animal Models

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Salvador Mérida ◽  
Elena Palacios ◽  
Amparo Navea ◽  
Francisco Bosch-Morell
Keyword(s):  
Animal Models ◽  
Experimental Animal ◽  
Macrophage Polarization ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Experimental Animal Models ◽  
Leading Role ◽  
Antigen Presenting ◽  
Experimental Autoimmune

Resident and infiltrated macrophages play relevant roles in uveitis as effectors of innate immunity and inductors of acquired immunity. They are major effectors of tissue damage in uveitis and are also considered to be potent antigen-presenting cells. In the last few years, experimental animal models of uveitis have enabled us to enhance our understanding of the leading role of macrophages in eye inflammation processes, including macrophage polarization in experimental autoimmune uveoretinitis and the major role of Toll-like receptor 4 in endotoxin-induced uveitis. This improved knowledge should guide advantageous iterative research to establish mechanisms and possible therapeutic targets for human uveitis resolution.

scholarly journals Lactoferrin retargets adenoviruses to TLR4 to induce an abortive NLRP3-associated pyroptotic response in human dendritic cells

2020 ◽  
Author(s):  
Coraline Chéneau ◽  
Karsten Eichholz ◽  
Tuan Hiep Tran ◽  
Thi Thu Phuong Tran ◽  
Océane Paris ◽  
...  
Keyword(s):  
Inflammatory Cytokine ◽  
Membrane Integrity ◽  
Human Adenovirus ◽  
Mononuclear Phagocyte ◽  
Cytokine Release ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Human Dendritic Cells ◽  
Antigen Presenting

AbstractDespite decades of investigations, we still poorly grasp the immunogenicity of human adenovirus (HAdV)-based vaccines in humans. In this study, we explored the role of lactoferrin, which belong to the alarmin subset of antimicrobial peptides that provide immediate direct and indirect activity against a range of pathogens following a breach in tissue homeostasis. Lactoferrin is a globular, iron-sequestering, glycoprotein that can increase HAdV infection and maturation of antigen-presenting cells. However, the mechanism by which HAdV-lactoferrin complexes induce maturation is unknown. We show that lactoferrin redirects HAdVs from species B, C, and D to toll-like receptor 4 (TLR4) complexes on human mononuclear phagocyte. TLR4-mediated internalization induces an abortive NLRP3-associated pyroptotic response inducing pro-inflammatory cytokine release and disrupting plasma membrane integrity without cell death. These data impact our understanding of the immunogenicity of HAdV-based vaccines and may provide ways to increase their efficacy.

Impaired Toll-like receptor 8–mediated IL-6 and TNF-α production in antigen-presenting cells from patients with X-linked agammaglobulinemia

Blood ◽  
2006 ◽  
Vol 109 (6) ◽  
pp. 2553-2556 ◽  
Author(s):  
Klára Sochorová ◽  
Rudolf Horváth ◽  
Daniela Rožková ◽  
Jiří Litzman ◽  
Jiřina Bartůňková ◽  
...  
Keyword(s):  
Critical Role ◽  
Toll Like Receptor ◽  
Normal Numbers ◽  
Tlr Signaling ◽  
Tlr Agonists ◽  
Tnf Α ◽  
Bruton Tyrosine Kinase ◽  
Antigen Presenting ◽  
Stimulation Of

Abstract The critical role of Bruton tyrosine kinase (Btk) in B cells has been documented by the block of B-cell development in X-linked agammaglobulinemia (XLA). Less is known about Btk function in myeloid cells. Several pieces of evidence indicate that Btk is a component of Toll-like receptor (TLR) signaling. We analyzed whether Btk deficiency in XLA is associated with an impaired dendritic cell (DC) compartment or defective TLR signaling. We analyzed the expression of TLRs 1 to 9 on myeloid DCs generated from XLA patients and evaluated their response to activation by specific TLR agonists. We show that XLA patients have normal numbers of circulating DCs. Btk-deficient DCs have no defect in response to stimulation of TLRs 1/2, 2/6, 3, 4, and 5 but display a profound impairment of IL-6 and TNF-α production in response to stimulation by TLR-8 cognate agonist, ssRNA. These findings may provide an explanation for the susceptibility to enteroviral infections in XLA patients.

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