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
2009 ◽  
Vol 53 (10) ◽  
pp. 4490-4494 ◽  
Author(s):  
Amit Sarkar ◽  
Kit Tilly ◽  
Philip Stewart ◽  
Aaron Bestor ◽  
James M. Battisti ◽  
...  

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.


2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Francesco Moroni ◽  
Enrico Ammirati ◽  
Giuseppe Danilo Norata ◽  
Marco Magnoni ◽  
Paolo G. Camici

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.


Endocrinology ◽  
2020 ◽  
Vol 161 (11) ◽  
Author(s):  
Gabrielle P Huizinga ◽  
Benjamin H Singer ◽  
Kanakadurga Singer

Abstract The coronavirus disease 2019 (COVID-19) pandemic has forced us to consider the physiologic role of obesity in the response to infectious disease. There are significant disparities in morbidity and mortality by sex, weight, and diabetes status. Numerous endocrine changes might drive these varied responses to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, including hormone and immune mediators, hyperglycemia, leukocyte responses, cytokine secretion, and tissue dysfunction. Studies of patients with severe COVID-19 disease have revealed the importance of innate immune responses in driving immunopathology and tissue injury. In this review we will describe the impact of the metabolically induced inflammation (meta-inflammation) that characterizes obesity on innate immunity. We consider that obesity-driven dysregulation of innate immune responses may drive organ injury in the development of severe COVID-19 and impair viral clearance.


2014 ◽  
Vol 44 (3) ◽  
pp. 214-221 ◽  
Author(s):  
Aornrutai Promsong ◽  
Whasun Oh Chung ◽  
Surada Satthakarn ◽  
Wipawee Nittayananta

2021 ◽  
Vol 12 ◽  
Author(s):  
Anton Früh ◽  
Katharina Tielking ◽  
Felix Schoknecht ◽  
Shuheng Liu ◽  
Ulf C. Schneider ◽  
...  

Background: Subarachnoid hemorrhage (SAH) caused by rupture of an intracranial aneurysm, is a life-threatening emergency that is associated with substantial morbidity and mortality. Emerging evidence suggests involvement of the innate immune response in secondary brain injury, and a potential role of neutrophil extracellular traps (NETs) for SAH-associated neuroinflammation. In this study, we investigated the spatiotemporal patterns of NETs in SAH and the potential role of the RNase A (the bovine equivalent to human RNase 1) application on NET burden.Methods: A total number of n=81 male C57Bl/6 mice were operated utilizing a filament perforation model to induce SAH, and Sham operation was performed for the corresponding control groups. To confirm the bleeding and exclude stroke and intracerebral hemorrhage, the animals received MRI after 24h. Mice were treated with intravenous injection of RNase A (42μg/kg body weight) or saline solution for the control groups, respectively. Quadruple-immunofluorescence (IF) staining for cell nuclei (DAPI), F-actin (phalloidin), citrullinated H3, and neurons (NeuN) was analyzed by confocal imaging and used to quantify NET abundance in the subarachnoid space (SAS) and brain parenchyma. To quantify NETs in human SAH patients, cerebrospinal spinal fluid (CSF) and blood samples from day 1, 2, 7, and 14 after bleeding onset were analyzed for double-stranded DNA (dsDNA) via Sytox Green.Results: Neutrophil extracellular traps are released upon subarachnoid hemorrhage in the SAS on the ipsilateral bleeding site 24h after ictus. Over time, NETs showed progressive increase in the parenchyma on both ipsi- and contralateral site, peaking on day 14 in periventricular localization. In CSF and blood samples of patients with aneurysmal SAH, NETs also increased gradually over time with a peak on day 7. RNase application significantly reduced NET accumulation in basal, cortical, and periventricular areas.Conclusion: Neutrophil extracellular trap formation following SAH originates in the ipsilateral SAS of the bleeding site and spreads gradually over time to basal, cortical, and periventricular areas in the parenchyma within 14days. Intravenous RNase application abrogates NET burden significantly in the brain parenchyma, underpinning a potential role in modulation of the innate immune activation after SAH.


2019 ◽  
Vol 10 ◽  
Author(s):  
Shikha Negi ◽  
Deepjyoti Kumar Das ◽  
Susanta Pahari ◽  
Sajid Nadeem ◽  
Javed N. Agrewala

2006 ◽  
Vol 8 (9-10) ◽  
pp. 1573-1582 ◽  
Author(s):  
Kazuhito Rokutan ◽  
Tsukasa Kawahara ◽  
Yuki Kuwano ◽  
Kumiko Tominaga ◽  
Atsuo Sekiyama ◽  
...  

2020 ◽  
Vol 8 (1) ◽  
pp. e000576
Author(s):  
Nausheen Ahmed ◽  
Mahmoud Ghannoum ◽  
Molly Gallogly ◽  
Marcos de Lima ◽  
Ehsan Malek

Multiple myeloma (MM) is a malignancy of terminally differentiated plasma cells, which typically evolves over time from its precursor, monoclonal gammopathy of undetermined significance. While the underlying mechanisms of this evolution remain elusive, immunomodulatory factors affecting the bone marrow (BM) microenvironment are suspected to play a role. There is an increasing evidence that the gut microbiome exerts an influence on its host’s adaptive and innate immune systems, inflammatory pathways and the BM microenvironment. Dysbiosis, therefore, may impact tumorigenesis in MM. This article gives an overview of potential mechanisms by which the microbiome may influence the pathogenesis of MM, MM patients’ responses to treatment and toxicities experienced by MM patients undergoing autologous transplant. It also discusses the potential role of the mycobiome in MM, a less studied component of the microbiome.


2021 ◽  
pp. 107385842098722
Author(s):  
Mingchao Shi ◽  
Fengna Chu ◽  
Xiaoping Tian ◽  
Qiaolifan Aerqin ◽  
Feiqi Zhu ◽  
...  

The pathogenesis of Alzheimer’s disease (AD) is complex. Still it remains unclear, which resulted in all efforts for AD treatments with targeting the pathogenic factors unsuccessful over past decades. It has been evidenced that the innate immune is strongly implicated in the pathogenesis of AD. However, the role of adaptive immune in AD remains mostly unknown and the results obtained were controversial. In the review, we summarized recent studies and showed that the molecular and cellular alterations in AD patients and its animal models involving T cells and B cells as well as immune mediators of adaptive immune occur not only in the peripheral blood but also in the brain and the cerebrospinal fluid. The risk factors that cause AD contribute to AD progress by affecting the adaptive immune, indicating that adaptive immunity proposes a pivotal role in this disease. It may provide a possible basis for applying immunotherapy in AD and further investigates whether the immunotherapies are effective or off-target?


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