scholarly journals Can Salivary Innate Immune Molecules Provide Clue on Taste Dysfunction in COVID-19?

2021 ◽  
Vol 12 ◽  
Author(s):  
Aaron Ermel ◽  
Thankam Paul Thyvalikakath ◽  
Tatiana Foroud ◽  
Babar Khan ◽  
Mythily Srinivasan
Keyword(s):  
Innate Immune ◽  
Host Responses ◽  
Long Term Effects ◽  
Toll Like Receptor 4 ◽  
Angiotensin Converting Enzyme 2 ◽  
Peptidoglycan Recognition Protein ◽  
Recognition Protein ◽  
Taste Dysfunction ◽  
Entry Receptor

Emerging concerns following the severe acute respiratory syndrome coronavirus-2 (SARS-CoV2) pandemic are the long-term effects of coronavirus disease (COVID)-19. Dysgeusia in COVID-19 is supported by the abundant expression of the entry receptor, angiotensin-converting enzyme-2 (ACE2), in the oral mucosa. The invading virus perturbs the commensal biofilm and regulates the host responses that permit or suppress viral infection. We correlated the microbial recognition receptors and soluble ACE2 (sACE2) with the SARS-CoV2 measures in the saliva of COVID-19 patients. Data indicate that the toll-like receptor-4, peptidoglycan recognition protein, and sACE2 are elevated in COVID-19 saliva and correlate moderately with the viral load.

scholarly journals Short- and Long-Term Effects of Weaning Age on Pig Innate Immune Status

2018 ◽  
Vol 08 (02) ◽  
pp. 137-150
Author(s):  
Janeen L. Salak-Johnson ◽  
Sherrie R. Webb
Keyword(s):  
Immune Status ◽  
Innate Immune ◽  
Long Term Effects ◽  
Weaning Age ◽  
Short And Long Term

scholarly journals Short-Term Versus Long-Term Effects of Adipocyte Toll-Like Receptor 4 Activation on Insulin Resistance in Male Mice

Endocrinology ◽  
2017 ◽  
Vol 158 (5) ◽  
pp. 1260-1270 ◽  
Author(s):  
Caroline Tao ◽  
William L. Holland ◽  
Qiong A. Wang ◽  
Mengle Shao ◽  
Lin Jia ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Male Mice ◽  
Toll Like Receptor ◽  
Long Term Effects ◽  
Short Term ◽  
Toll Like Receptor 4

scholarly journals Weevilpgrp-lbprevents endosymbiont TCT dissemination and chronic host systemic immune activation

2019 ◽  
Vol 116 (12) ◽  
pp. 5623-5632 ◽  
Author(s):  
Justin Maire ◽  
Carole Vincent-Monégat ◽  
Séverine Balmand ◽  
Agnès Vallier ◽  
Mireille Hervé ◽  
...  
Keyword(s):  
Immune Responses ◽  
Differential Regulation ◽  
Molecular Processes ◽  
Independent Manner ◽  
Peptidoglycan Recognition Protein ◽  
Systemic Immune Activation ◽  
Recognition Protein ◽  
Context Specific ◽  
Encoding Genes

Long-term intracellular symbiosis (or endosymbiosis) is widely distributed across invertebrates and is recognized as a major driving force in evolution. However, the maintenance of immune homeostasis in organisms chronically infected with mutualistic bacteria is a challenging task, and little is known about the molecular processes that limit endosymbiont immunogenicity and host inflammation. Here, we investigated peptidoglycan recognition protein (PGRP)-encoding genes in the cereal weevilSitophilus zeamais’s association withSodalis pierantoniusendosymbiont. We discovered that weevilpgrp-lbgenerates three transcripts via alternative splicing and differential regulation. A secreted isoform is expressed in insect tissues under pathogenic conditions through activation of the PGRP-LC receptor of the immune deficiency pathway. In addition, cytosolic and transmembrane isoforms are permanently produced within endosymbiont-bearing organ, the bacteriome, in a PGRP-LC–independent manner. Bacteriome isoforms specifically cleave the tracheal cytotoxin (TCT), a peptidoglycan monomer released by endosymbionts.pgrp-lbsilencing by RNAi results in TCT escape from the bacteriome to other insect tissues, where it chronically activates the host systemic immunity through PGRP-LC. While such immune deregulations did not impact endosymbiont load, they did negatively affect host physiology, as attested by a diminished sexual maturation of adult weevils. Whereaspgrp-lbwas first described in pathogenic interactions, this work shows that, in an endosymbiosis context, specific bacteriome isoforms have evolved, allowing endosymbiont TCT scavenging and preventing chronic endosymbiont-induced immune responses, thus promoting host homeostasis.

scholarly journals A human secretome library screen reveals a role for Peptidoglycan Recognition Protein 1 in Lyme borreliosis

2020 ◽  
Vol 16 (11) ◽  
pp. e1009030
Author(s):  
Akash Gupta ◽  
Gunjan Arora ◽  
Connor E. Rosen ◽  
Zachary Kloos ◽  
Yongguo Cao ◽  
...  
Keyword(s):  
Extracellular Proteins ◽  
Host Responses ◽  
Yeast Display ◽  
Biologically Relevant ◽  
Peptidoglycan Recognition Protein ◽  
Library Screen ◽  
Recognition Protein ◽  
Vector Borne ◽  
Vertebrate Hosts ◽  
Serum Igg Levels

Lyme disease, the most common vector-borne illness in North America, is caused by the spirochete Borrelia burgdorferi. Infection begins in the skin following a tick bite and can spread to the hearts, joints, nervous system, and other organs. Diverse host responses influence the level of B. burgdorferi infection in mice and humans. Using a systems biology approach, we examined potential molecular interactions between human extracellular and secreted proteins and B. burgdorferi. A yeast display library expressing 1031 human extracellular proteins was probed against 36 isolates of B. burgdorferi sensu lato. We found that human Peptidoglycan Recognition Protein 1 (PGLYRP1) interacted with the vast majority of B. burgdorferi isolates. In subsequent experiments, we demonstrated that recombinant PGLYRP1 interacts with purified B. burgdorferi peptidoglycan and exhibits borreliacidal activity, suggesting that vertebrate hosts may use PGLYRP1 to identify B. burgdorferi. We examined B. burgdorferi infection in mice lacking PGLYRP1 and observed an increased spirochete burden in the heart and joints, along with splenomegaly. Mice lacking PGLYRP1 also showed signs of immune dysregulation, including lower serum IgG levels and higher levels of IFNγ, CXCL9, and CXCL10.Taken together, our findings suggest that PGLYRP1 plays a role in the host’s response to B. burgdorferi and further demonstrate the utility of expansive yeast display screening in capturing biologically relevant interactions between spirochetes and their hosts.

scholarly journals Recognition of Staphylococcus aureus by the Innate Immune System

2005 ◽  
Vol 18 (3) ◽  
pp. 521-540 ◽  
Author(s):  
Bénédicte Fournier ◽  
Dana J. Philpott
Keyword(s):  
Staphylococcus Aureus ◽  
Cell Wall ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Protein A ◽  
Lipoteichoic Acid ◽  
Innate Immune ◽  
Peptidoglycan Recognition Protein ◽  
Recognition Protein ◽  
Necrosis Factor

SUMMARY The gram-positive bacterium Staphylococcus aureus is a major pathogen responsible for a variety of diseases ranging from minor skin infections to life-threatening conditions such as sepsis. Cell wall-associated and secreted proteins (e.g., protein A, hemolysins, and phenol-soluble modulin) and cell wall components (e.g., peptidoglycan and alanylated lipoteichoic acid) have been shown to be inflammatory, and these staphylococcal components may contribute to sepsis. On the host side, many host factors have been implicated in the innate detection of staphylococcal components. One class of pattern recognition molecules, Toll-like receptor 2, has been shown to function as the transmembrane component involved in the detection of staphylococcal lipoteichoic acid and phenol-soluble modulin and is involved in the synthesis of inflammatory cytokines by monocytes/macrophages in response to these components. Nod2 (nucleotide-binding oligomerization domain 2) is the intracellular sensor for muramyl dipeptide, the minimal bioactive structure of peptidoglycan, and it may contribute to the innate immune defense against S. aureus. The staphylococcal virulence factor protein A was recently shown to interact directly with tumor necrosis factor receptor 1 in airway epithelium and to reproduce the effects of tumor necrosis factor alpha. Finally, peptidoglycan recognition protein L is an amidase that inactivates the proinflammatory activities of peptidoglycan. However, peptidoglycan recognition protein L probably plays a minor role in the innate immune response to S. aureus. Thus, several innate immunity receptors may be implicated in host defense against S. aureus.

Perspectives into the possible effects of the B.1.1.7 variant of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on spermatogenesis

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Andrea M. T. Kallumadyil ◽  
Tess McClenahan ◽  
Samantha De Filippis ◽  
Ananya Vungarala ◽  
Nihal Satyadev ◽  
...  
Keyword(s):  
Severe Acute Respiratory Syndrome ◽  
Type Ii ◽  
Long Term Effects ◽  
Serum Samples ◽  
Infected Male ◽  
Angiotensin Converting Enzyme 2 ◽  
Renal Tubular Cells ◽  
Type Ii Pneumocytes ◽  
Renal Tubular

Abstract B.1.1.7 is a recently discovered variant of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) associated with increased transmissibility. Recent findings indicate that this variant has a propensity to infect adolescents and children at higher rates than adults. The virus gains entry into various body cells utilizing angiotensin-converting enzyme 2 (ACE-2) and basigin (CD147) as receptors. The virus mainly affects type II pneumocytes of lungs, endothelial cells, enterocytes, and renal tubular cells. It is reported to affect testes, causing testicular pain, and producing histopathological changes, as observed in some autopsies. The B.1.1.7 variant can also affect various cells in the testes. This raises a major concern regarding the long-term effects of the viral infection on spermatogenesis and highlights the pressing need for a robust database of serum samples from infected male children.

scholarly journals Toll and IMD Pathways Synergistically Activate an Innate Immune Response in Drosophila melanogaster

2007 ◽  
Vol 27 (12) ◽  
pp. 4578-4588 ◽  
Author(s):  
Takahiro Tanji ◽  
Xiaodi Hu ◽  
Alexander N. R. Weber ◽  
Y. Tony Ip
Keyword(s):  
Drosophila Melanogaster ◽  
Target Genes ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Peptidoglycan Recognition Protein ◽  
Synergistic Activation ◽  
Independent Functions ◽  
Recognition Protein ◽  
Dual Activation ◽  
Specific Ligand

ABSTRACT The inducible expression of antimicrobial peptide genes in Drosophila melanogaster is regulated by the conserved Toll and peptidoglycan recognition protein LC/immune deficiency (PGRP-LC/IMD) signaling pathways. It has been proposed that the two pathways have independent functions and mediate the specificity of innate immune responses towards different microorganisms. Scattered evidence also suggests that some antimicrobial target genes can be activated by both Toll and IMD, albeit to different extents. This dual activation can be mediated by independent stimulation or by cross-regulation of the two pathways. We show in this report that the Toll and IMD pathways can interact synergistically, demonstrating that cross-regulation occurs. The presence of Spätzle (the Toll ligand) and gram-negative peptidoglycan (the PGRP-LC ligand) together caused synergistic activation of representative target genes of the two pathways, including Drosomycin, Diptericin, and AttacinA. Constitutive activation of Toll and PGRP-LC/IMD could mimic the synergistic stimulation. RNA interference assays and promoter analyses demonstrate that cooperation of different NF-κB-related transcription factors mediates the synergy. These results illustrate how specific ligand binding by separate upstream pattern recognition receptors can be translated into a broad-spectrum host response, a hallmark of innate immunity.

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