Ellagic acid modulates the expression of oral innate immune mediators: potential role in mucosal protection

2014 ◽  
Vol 44 (3) ◽  
pp. 214-221 ◽  
Author(s):  
Aornrutai Promsong ◽  
Whasun Oh Chung ◽  
Surada Satthakarn ◽  
Wipawee Nittayananta
Keyword(s):  
Ellagic Acid ◽  
Potential Role ◽  
Innate Immune ◽  
Mucosal Protection ◽  
Immune Mediators

Houttuynia cordatamodulates oral innate immune mediators: potential role of herbal plant on oral health

Oral Diseases ◽  
2015 ◽  
Vol 21 (4) ◽  
pp. 512-518 ◽  
Author(s):  
S Satthakarn ◽  
WO Chung ◽  
A Promsong ◽  
W Nittayananta
Keyword(s):  
Oral Health ◽  
Potential Role ◽  
Innate Immune ◽  
Immune Mediators ◽  
Herbal Plant

scholarly journals Contributions of Electron Microscopy to Understand Secretion of Immune Mediators by Human Eosinophils

2010 ◽  
Vol 16 (6) ◽  
pp. 653-660 ◽  
Author(s):  
Rossana C.N. Melo ◽  
Ann M. Dvorak ◽  
Peter F. Weller
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Immune Responses ◽  
Innate Immune System ◽  
Innate Immune ◽  
Cell Secretion ◽  
The Past ◽  
Functional Capabilities ◽  
Immune Mediators ◽  
Transmission Electron

AbstractMechanisms governing secretion of proteins underlie the biologic activities and functions of human eosinophils, leukocytes of the innate immune system, involved in allergic, inflammatory, and immunoregulatory responses. In response to varied stimuli, eosinophils are recruited from the circulation into inflammatory foci, where they modulate immune responses through the release of granule-derived products. Transmission electron microscopy (TEM) is the only technique that can clearly identify and distinguish between different modes of cell secretion. In this review, we highlight the advances in understanding mechanisms of eosinophil secretion, based on TEM findings, that have been made over the past years and that have provided unprecedented insights into the functional capabilities of these cells.

scholarly journals Borrelia burgdorferi Resistance to a Major Skin Antimicrobial Peptide Is Independent of Outer Surface Lipoprotein Content

2009 ◽  
Vol 53 (10) ◽  
pp. 4490-4494 ◽  
Author(s):  
Amit Sarkar ◽  
Kit Tilly ◽  
Philip Stewart ◽  
Aaron Bestor ◽  
James M. Battisti ◽  
...  
Keyword(s):  
Borrelia Burgdorferi ◽  
Antimicrobial Peptide ◽  
Immune Evasion ◽  
Essential Role ◽  
Potential Role ◽  
Innate Immune ◽  
Initial Stage ◽  
Mammalian Infection ◽  
Innate Immune Evasion

ABSTRACT We hypothesize a potential role for Borrelia burgdorferi OspC in innate immune evasion at the initial stage of mammalian infection. We demonstrate that B. burgdorferi is resistant to high levels (>200 μg/ml) of cathelicidin and that this antimicrobial peptide exhibits limited binding to the spirochetal outer membrane, irrespective of OspC or other abundant surface lipoproteins. We conclude that the essential role of OspC is unrelated to resistance to this component of innate immunity.

scholarly journals Plasma levels of innate immune mediators are associated with liver fibrosis in low parasite burden Schistosoma mansoni- infected individuals

2018 ◽  
Vol 87 (3) ◽  
pp. e12642 ◽  
Author(s):  
J. L. Rodrigues Oliveira ◽  
M. M. Teixeira ◽  
J. R. Lambertucci ◽  
C. M. F. Antunes ◽  
M. Carneiro ◽  
...  
Keyword(s):  
Liver Fibrosis ◽  
Schistosoma Mansoni ◽  
Plasma Levels ◽  
Parasite Burden ◽  
Innate Immune ◽  
Immune Mediators

scholarly journals Antiviral immunity is impaired in COPD patients with frequent exacerbations

2019 ◽  
Vol 317 (6) ◽  
pp. L893-L903 ◽  
Author(s):  
Aran Singanayagam ◽  
Su-Ling Loo ◽  
Maria Calderazzo ◽  
Lydia J. Finney ◽  
Maria-Belen Trujillo Torralbo ◽  
...  
Keyword(s):  
Epithelial Cells ◽  
Treatment Options ◽  
Stable State ◽  
Innate Immune ◽  
Chronic Obstructive ◽  
Type I ◽  
Obstructive Pulmonary Disease ◽  
Immune Mediators ◽  
Copd Patients

Patients with frequent exacerbations represent a chronic obstructive pulmonary disease (COPD) subgroup requiring better treatment options. The aim of this study was to determine the innate immune mechanisms that underlie susceptibility to frequent exacerbations in COPD. We measured sputum expression of immune mediators and bacterial loads in samples from patients with COPD at stable state and during virus-associated exacerbations. In vitro immune responses to rhinovirus infection in differentiated primary bronchial epithelial cells (BECs) sampled from patients with COPD were additionally evaluated. Patients were stratified as frequent exacerbators (≥2 exacerbations in the preceding year) or infrequent exacerbators (<2 exacerbations in the preceding year) with comparisons made between these groups. Frequent exacerbators had reduced sputum cell mRNA expression of the antiviral immune mediators type I and III interferons and reduced interferon-stimulated gene (ISG) expression when clinically stable and during virus-associated exacerbation. A role for epithelial cell-intrinsic innate immune dysregulation was identified: induction of interferons and ISGs during in vitro rhinovirus (RV) infection was also impaired in differentiated BECs from frequent exacerbators. Frequent exacerbators additionally had increased sputum bacterial loads at 2 wk following virus-associated exacerbation onset. These data implicate deficient airway innate immunity involving epithelial cells in the increased propensity to exacerbations observed in some patients with COPD. Therapeutic approaches to boost innate antimicrobial immunity in the lung could be a viable strategy for prevention and treatment of frequent exacerbations.

Antimicrobial proteins and peptides of blood: templates for novel antimicrobial agents

Blood ◽  
2000 ◽  
Vol 96 (8) ◽  
pp. 2664-2672 ◽  
Author(s):  
Ofer Levy
Keyword(s):  
Host Defense ◽  
Blood Cells ◽  
Antimicrobial Agents ◽  
Severe Infection ◽  
Innate Immune ◽  
Antimicrobial Proteins ◽  
Microbial Invasion ◽  
Immune Mediators ◽  
Rapid Responses ◽  
Proteins And Peptides

Abstract The innate immune system provides rapid and effective host defense against microbial invasion in a manner that is independent of prior exposure to a given pathogen.1 It has long been appreciated that the blood contains important elements that mediate rapid responses to infection. Thus, anatomic compartments with ample blood supply are less frequently infected and recover more readily once infected, whereas regions with poor perfusion are prone to severe infection and may require surgical débridement. Blood-borne innate immune mediators are either carried in circulating blood cells (ie, leukocytes and platelets) or in plasma after release from blood cells or on secretion by the liver.

scholarly journals The Role of Monocytes and Macrophages in Human Atherosclerosis, Plaque Neoangiogenesis, and Atherothrombosis

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Francesco Moroni ◽  
Enrico Ammirati ◽  
Giuseppe Danilo Norata ◽  
Marco Magnoni ◽  
Paolo G. Camici
Keyword(s):  
Animal Studies ◽  
Arterial Wall ◽  
Causes Of Death ◽  
Complex Disease ◽  
Potential Role ◽  
Innate Immune ◽  
Pathogenic Role ◽  
Monocytes And Macrophages ◽  
Human Atherosclerosis

Atherosclerosis is one of the leading causes of death and disability worldwide. It is a complex disease characterized by lipid accumulation within the arterial wall, inflammation, local neoangiogenesis, and apoptosis. Innate immune effectors, in particular monocytes and macrophages, play a pivotal role in atherosclerosis initiation and progression. Although most of available evidence on the role of monocytes and macrophages in atherosclerosis is derived from animal studies, a growing body of evidence elucidating the role of these mononuclear cell subtypes in human atherosclerosis is currently accumulating. A novel pathogenic role of monocytes and macrophages in terms of atherosclerosis initiation and progression, in particular concerning the role of these cell subsets in neovascularization, has been discovered. The aim of the present article is to review currently available evidence on the role of monocytes and macrophages in human atherosclerosis and in relation to plaque characteristics, such as plaque neoangiogenesis, and patients’ prognosis and their potential role as biomarkers.

Antimicrobial proteins and peptides of blood: templates for novel antimicrobial agents

Blood ◽  
2000 ◽  
Vol 96 (8) ◽  
pp. 2664-2672 ◽  
Author(s):  
Ofer Levy
Keyword(s):  
Host Defense ◽  
Blood Cells ◽  
Antimicrobial Agents ◽  
Severe Infection ◽  
Innate Immune ◽  
Antimicrobial Proteins ◽  
Microbial Invasion ◽  
Immune Mediators ◽  
Rapid Responses ◽  
Proteins And Peptides

The innate immune system provides rapid and effective host defense against microbial invasion in a manner that is independent of prior exposure to a given pathogen.1 It has long been appreciated that the blood contains important elements that mediate rapid responses to infection. Thus, anatomic compartments with ample blood supply are less frequently infected and recover more readily once infected, whereas regions with poor perfusion are prone to severe infection and may require surgical débridement. Blood-borne innate immune mediators are either carried in circulating blood cells (ie, leukocytes and platelets) or in plasma after release from blood cells or on secretion by the liver.

scholarly journals Discordant transcriptional signatures of mitochondrial genes in Parkinson’s disease human myeloid cells

2020 ◽  
Author(s):  
Elisa Navarro ◽  
Evan Udine ◽  
Katia de Paiva Lopes ◽  
Madison Parks ◽  
Giulietta Riboldi ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Potential Role ◽  
Risk Allele ◽  
Myeloid Cells ◽  
Mitochondrial Genes ◽  
Innate Immune ◽  
Primary Microglia ◽  
Mitochondrial Alterations ◽  
And Control

AbstractAn increasing number of identified Parkinson’s disease (PD) risk loci contain genes highly expressed in innate immune cells, yet their potential role in pathological mechanisms is not obvious. We have generated transcriptomic profiles of CD14+ monocytes from 230 individuals with sporadic PD and age-matched healthy subjects. We identified dysregulation of genes involved in mitochondrial and proteasomal function. We also generated transcriptomic profiles of primary microglia from autopsied brains of 55 PD and control subjects and observed discordant transcriptomic signatures of mitochondrial genes in PD monocytes and microglia. We further identified PD susceptibility genes, whose expression, relative to each risk allele, is altered in monocytes. These findings reveal that transcriptomic mitochondrial alterations are detectable in PD monocytes and are distinct from brain microglia, and facilitates efforts to understand the roles of myeloid cells in PD.

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