scholarly journals Nanomaterial Exposure Induced Neutrophil Extracellular Traps: A New Target in Inflammation and Innate Immunity

2019 ◽  
Vol 2019 ◽  
pp. 1-8 ◽  
Author(s):  
Hang Yang ◽  
Tony N. Marion ◽  
Yi Liu ◽  
Lingshu Zhang ◽  
Xue Cao ◽  
...  
Keyword(s):  
Drug Delivery ◽  
Immune Responses ◽  
Myeloid Cell ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Cell Type ◽  
Extracellular Traps ◽  
Pharmaceutical Industries ◽  
The Relationship

Nanotechnology has become a novel subject with impact in many research and technology areas. Nanoparticles (NPs), as a key component in nanotechnology, are widely used in many areas such as optical, magnetic, electrical, and mechanical engineering. The biomedical and pharmaceutical industries have embraced NPs as a viable drug delivery modality. As such, the potential for NP-induced cytotoxicity has emerged as a major concern for NP drug delivery systems. Thus, it is important to understand how NPs affect the innate immune system. As the most abundant myeloid cell type in innate immune responses, neutrophils are critical for concerns about potentially toxic side effects of NPs. When activated by innate immune stimuli, neutrophils may initiate NETosis to release neutrophil extracellular traps (NETs). Herein, we have reviewed the relationship between NPs and the induction of NETosis and release of NETs.

scholarly journals Intestinal infection results in impaired lung innate immunity to secondary respiratory infection

2020 ◽  
Author(s):  
Shubhanshi Trivedi ◽  
Allie H. Grossmann ◽  
Owen Jensen ◽  
Mark J. Cody ◽  
Kristi J. Warren ◽  
...  
Keyword(s):  
Immune Responses ◽  
Causes Of Death ◽  
Neutrophil Extracellular Traps ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Bacterial Burden ◽  
Intestinal Infection ◽  
Extracellular Traps ◽  
Lung Immunity ◽  
Increased Susceptibility

AbstractPneumonia and diarrhea are among the leading causes of death worldwide, and epidemiological studies have demonstrated that diarrhea is associated with an increased risk of subsequent pneumonia. Our aim was to determine the impact of intestinal infection on innate immune responses in the lung. Using a mouse model of intestinal infection by Salmonella enterica serovar Typhimurium (S. Typhimurium), we investigated how infection in the gut compartment can modulate immunity in the lungs and impact susceptibility to bacterial (Klebsiella pneumoniae) challenge. We found alterations in frequencies of innate immune cells in lungs of intestinally-infected mice compared to uninfected mice. On subsequent challenge with K. pneumoniae we found that mice with prior intestinal infection have higher lung bacterial burden and inflammation, increased neutrophil margination, and neutrophil extracellular traps (NETs), but lower overall numbers of neutrophils, compared to mice without prior intestinal infection. Together, these results suggest that intestinal infection impacts lung innate immune responses, most notably neutrophil characteristics, potentially resulting in increased susceptibility to secondary pneumonia.Author summaryInfections of the lung and gut are among the leading causes of death worldwide. Human studies have shown that children with diarrhea are at higher risk of subsequent lung infection. How intestinal infections impact lung immunity is not well known. In the present study, we reveal that bacterial infection of the intestinal mucosa may compromise lung immunity, offering new insights into increased susceptibility to respiratory infections. We found that upon respiratory infection, mice with prior intestinal infection are more moribund and despite having higher bacterial burden, they show reduced numbers of neutrophils in the lung compared to mice without prior intestinal infection. We also found excessive neutrophil extracellular traps formation in the lungs of mice with prior intestinal infection, providing evidence of increased pulmonary tissue damage. Collectively, these data identify a direct link between pulmonary and enteric infection and suggests gut infections impair neutrophils responses in the lungs.

scholarly journals Geometrical reorganization of Dectin-1 and TLR2 on single phagosomes alters their synergistic immune signaling

2019 ◽  
Vol 116 (50) ◽  
pp. 25106-25114 ◽  
Author(s):  
Wenqian Li ◽  
Jun Yan ◽  
Yan Yu
Keyword(s):  
Immune Responses ◽  
Immune Regulation ◽  
Spatial Organization ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Membrane Composition ◽  
Intracellular Compartments ◽  
Synergistic Regulation ◽  
The Relationship

Receptors of innate immune cells function synergistically to detect pathogens and elicit appropriate immune responses. Many receptor pairs also appear “colocalized” on the membranes of phagosomes, the intracellular compartments for pathogen ingestion. However, the nature of the seemingly receptor colocalization and the role it plays in immune regulation are unclear, due to the inaccessibility of intracellular phagocytic receptors. Here, we report a geometric manipulation technique to directly probe the role of phagocytic receptor “colocalization” in innate immune regulation. Using particles with spatially patterned ligands as phagocytic targets, we can decouple the receptor pair, Dectin-1 and Toll-like receptor (TLR)2, to opposite sides on a single phagosome or bring them into nanoscale proximity without changing the overall membrane composition. We show that Dectin-1 enhances immune responses triggered predominantly by TLR2 when their centroid-to-centroid proximity is <500 nm, but this signaling synergy diminishes upon receptor segregation beyond this threshold distance. Our results demonstrate that nanoscale proximity, not necessarily colocalization, between Dectin-1 and TLR2 is required for their synergistic regulation of macrophage immune responses. This study elucidates the relationship between the spatial organization of phagocytic receptors and innate immune responses. It showcases a technique that allows spatial manipulation of receptors and their signal cross-talk on phagosomes inside living cells.

scholarly journals TANK-binding kinase 1-dependent or -independent signaling elicits the cell-type-specific innate immune responses induced by the adenovirus vector

2015 ◽  
Vol 28 (3) ◽  
pp. 105-115 ◽  
Author(s):  
Sayaka Tsuzuki ◽  
Masashi Tachibana ◽  
Masahisa Hemmi ◽  
Tomoko Yamaguchi ◽  
Masaki Shoji ◽  
...  
Keyword(s):  
Immune Responses ◽  
Adenovirus Vector ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Cell Type ◽  
Cell Type Specific

scholarly journals Toll-like receptor-induced innate immune responses in non-parenchymal liver cells are cell type-specific

Immunology ◽  
2010 ◽  
Vol 129 (3) ◽  
pp. 363-374 ◽  
Author(s):  
Jun Wu ◽  
Zhongji Meng ◽  
Min Jiang ◽  
Ejuan Zhang ◽  
Martin Trippler ◽  
...  
Keyword(s):  
Immune Responses ◽  
Liver Cells ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Cell Type ◽  
Parenchymal Liver ◽  
Cell Type Specific

scholarly journals An Update on Innate Immune Responses during SARS-CoV-2 Infection

Viruses ◽  
2021 ◽  
Vol 13 (10) ◽  
pp. 2060
Author(s):  
Yu Zhang ◽  
Shuaiyin Chen ◽  
Yuefei Jin ◽  
Wangquan Ji ◽  
Weiguo Zhang ◽  
...  
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Type I Interferons ◽  
Organ Injury ◽  
Type I ◽  
Innate Immune Responses ◽  
Innate Immune Signaling ◽  
Viral Proteases ◽  
Viral Components ◽  
The Relationship

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a member of the Coronaviridae family, which is responsible for the COVID-19 pandemic followed by unprecedented global societal and economic disruptive impact. The innate immune system is the body’s first line of defense against invading pathogens and is induced by a variety of cellular receptors that sense viral components. However, various strategies are exploited by SARS-CoV-2 to disrupt the antiviral innate immune responses. Innate immune dysfunction is characterized by the weak generation of type I interferons (IFNs) and the hypersecretion of pro-inflammatory cytokines, leading to mortality and organ injury in patients with COVID-19. This review summarizes the existing understanding of the mutual effects between SARS-CoV-2 and the type I IFN (IFN-α/β) responses, emphasizing the relationship between host innate immune signaling and viral proteases with an insight on tackling potential therapeutic targets.

scholarly journals Length of dsRNA (poly I:C) drives distinct innate immune responses, depending on the cell type

2013 ◽  
Vol 94 (5) ◽  
pp. 1025-1036 ◽  
Author(s):  
M. Firoz Mian ◽  
Amna N. Ahmed ◽  
Mehrnaz Rad ◽  
Artem Babaian ◽  
Dawn Bowdish ◽  
...  
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Poly I:C ◽  
Innate Immune Responses ◽  
Cell Type

scholarly journals Environment impacts innate immune ontogeny

2016 ◽  
Vol 23 (1) ◽  
pp. 3-10 ◽  
Author(s):  
Mathieu Garand ◽  
Bing Cai ◽  
Tobias R Kollmann
Keyword(s):  
Immune Responses ◽  
Immune Modulation ◽  
Mononuclear Cells ◽  
Innate Immune ◽  
Racial Groups ◽  
Innate Immune Responses ◽  
Susceptibility To Infection ◽  
Cytokine Responses ◽  
Underlying Mechanisms ◽  
The Relationship

Susceptibility to infection and response to vaccination differ between populations and as a function of age. The underlying mechanisms for this age- and population-dependent variation are not known. Specifically, it is unclear if these variations are due to differences in genetically encoded host programs or driven by environmental influences or a combination of both. To address the relationship between gene and environment regarding immune ontogeny, we determined the innate cytokine responses following PRR stimulation of blood mononuclear cells at birth, 1, and 2 yr of age in infants from Caucasian vs . Asian parents and were raised in the same city. At birth, we found that innate cytokine responses were significantly elevated in Asian compared with Caucasian infants. However, these differences waned and responses became more similar over the course of 1–2 yr of living in a similar environment. Our observations that innate response differences present at birth subsequently equalized rather than diverged suggest a key role for environmental effects common to both racial groups in shaping the innate immune responses early in life. Delineating the underlying environmental factors that modulate innate immune responses early in life could provide avenues for targeted beneficial immune modulation.

scholarly journals Vpx enhances innate immune responses independently of SAMHD1 during HIV-1 infection

Retrovirology ◽  
2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Oya Cingöz ◽  
Nicolas D. Arnow ◽  
Mireia Puig Torrents ◽  
Norbert Bannert
Keyword(s):  
Immune Responses ◽  
Cell Lines ◽  
Myeloid Cells ◽  
Adaptor Protein ◽  
Myeloid Cell ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Accessory Gene ◽  
Monocytic Cell ◽  
Hiv 1

Abstract Background The genomes of HIV-2 and some SIV strains contain the accessory gene vpx, which carries out several functions during infection, including the downregulation of SAMHD1. Vpx is also commonly used in experiments to increase HIV-1 infection efficiency in myeloid cells, particularly in studies that investigate the activation of antiviral pathways. However, the potential effects of Vpx on cellular innate immune signaling is not completely understood. We investigated whether and how Vpx affects ISG responses in monocytic cell lines and MDMs during HIV-1 infection. Results HIV-1 infection at excessively high virus doses can induce ISG activation, although at the expense of high levels of cell death. At equal infection levels, the ISG response is potentiated by the presence of Vpx and requires the initiation of reverse transcription. The interaction of Vpx with the DCAF1 adaptor protein is important for the enhanced response, implicating Vpx-mediated degradation of a host factor. Cells lacking SAMHD1 show similarly augmented responses, suggesting an effect that is independent of SAMHD1 degradation. Overcoming SAMHD1 restriction in MDMs to reach equal infection levels with viruses containing and lacking Vpx reveals a novel function of Vpx in elevating innate immune responses. Conclusions Vpx likely has as yet undefined roles in infected cells. Our results demonstrate that Vpx enhances ISG responses in myeloid cell lines and primary cells independently of its ability to degrade SAMHD1. These findings have implications for innate immunity studies in myeloid cells that use Vpx delivery with HIV-1 infection.

Sign in / Sign up

Export Citation Format

Share Document