Granulocyte apoptosis in the pathogenesis and resolution of lung disease

2006 ◽  
Vol 110 (3) ◽  
pp. 293-304 ◽  
Author(s):  
Stephen M. Bianchi ◽  
David H. Dockrell ◽  
Stephen A. Renshaw ◽  
Ian Sabroe ◽  
Moira K. B. Whyte
Keyword(s):  
Immune Responses ◽  
Lung Disease ◽  
Inflammatory Cell ◽  
Control Point ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Potential Control ◽  
Cellular Processes ◽  
Cell Type Specific ◽  
Eosinophil Granulocytes

Apoptosis, programmed cell death, of neutrophil and eosinophil granulocytes is a potential control point in the physiological resolution of innate immune responses. There is also increasing evidence that cellular processes of apoptosis can be dysregulated by pathogens as a mechanism of immune evasion and that delayed apoptosis, resulting in prolonged inflammatory cell survival, is important in persistence of tissue inflammation. The identification of cell-type specific pathways to apoptosis may allow the design of novel anti-inflammatory therapies or agents to augment the innate immune responses to infection. This review will explore the physiological roles of granulocyte apoptosis and their importance in infectious and non-infectious lung disease.

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 Fibrotic lung disease inhibits innate immune responses to Staphylococcal pneumonia via impaired neutrophil and macrophage function

JCI Insight ◽  
2022 ◽  
Author(s):  
Helen I. Warheit-Niemi ◽  
Summer J. Edwards ◽  
Shuvasree SenGupta ◽  
Carole A. Parent ◽  
Xiaofeng Zhou ◽  
...  
Keyword(s):  
Immune Responses ◽  
Lung Disease ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Macrophage Function ◽  
Staphylococcal Pneumonia ◽  
Fibrotic Lung Disease

scholarly journals Circadian regulation of the Drosophila astrocyte transcriptome

PLoS Genetics ◽  
2021 ◽  
Vol 17 (9) ◽  
pp. e1009790
Author(s):  
Samantha You ◽  
Alder M. Yu ◽  
Mary A. Roberts ◽  
Ivanna J. Joseph ◽  
F. Rob Jackson
Keyword(s):  
Immune Responses ◽  
Transcriptional Profiling ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Sleep Behavior ◽  
Circadian Control ◽  
Number Of Genes ◽  
Cell Type Specific ◽  
Normal Sleep ◽  
The Brain

Recent studies have demonstrated that astrocytes cooperate with neurons of the brain to mediate circadian control of many rhythmic processes including locomotor activity and sleep. Transcriptional profiling studies have described the overall rhythmic landscape of the brain, but few have employed approaches that reveal heterogeneous, cell-type specific rhythms of the brain. Using cell-specific isolation of ribosome-bound RNAs in Drosophila, we constructed the first circadian “translatome” for astrocytes. This analysis identified 293 “cycling genes” in astrocytes, most with mammalian orthologs. A subsequent behavioral genetic screen identified a number of genes whose expression is required in astrocytes for normal sleep behavior. In particular, we show that certain genes known to regulate fly innate immune responses are also required for normal sleep patterns.

scholarly journals Great balls of fire: activation and signalling of inflammatory caspases

2021 ◽  
Author(s):  
Georgia Bateman ◽  
Benjamin Hill ◽  
Ryan Knight ◽  
Dave Boucher
Keyword(s):  
Immune Responses ◽  
Inflammatory Cell ◽  
Current Knowledge ◽  
Cysteine Proteases ◽  
Innate Immune ◽  
Caspase Activity ◽  
Innate Immune Responses ◽  
Caspase Activation ◽  
Biochemical Processes ◽  
Inflammatory Caspases

Innate immune responses are tightly regulated by various pathways to control infections and maintain homeostasis. One of these pathways, the inflammasome pathway, activates a family of cysteine proteases called inflammatory caspases. They orchestrate an immune response by cleaving specific cellular substrates. Canonical inflammasomes activate caspase-1, whereas non-canonical inflammasomes activate caspase-4 and -5 in humans and caspase-11 in mice. Caspases are highly specific enzymes that select their substrates through diverse mechanisms. During inflammation, caspase activity is responsible for the secretion of inflammatory cytokines and the execution of a form of lytic and inflammatory cell death called pyroptosis. This review aims to bring together our current knowledge of the biochemical processes behind inflammatory caspase activation, substrate specificity, and substrate signalling.

scholarly journals Cell-type specific innate immune responses shape rabies virus tropism

2021 ◽  
Author(s):  
Lena Feige ◽  
Tatsuya Kozaki ◽  
Guilherme Dias de Melo ◽  
Vincent Guillemot ◽  
Florence Larrous ◽  
...  
Keyword(s):  
Immune Responses ◽  
Rabies Virus ◽  
Matrix Protein ◽  
Innate Immune ◽  
Janus Kinase ◽  
Innate Immune Responses ◽  
Cell Type ◽  
Viral Spread ◽  
Cell Type Specific

Viral tropism, or the specificity of a particular virus to infect a certain cell type, is crucial in determining virus replication, viral spread, and ultimately host survival. Rabies, one of the deadliest known zoonotic diseases, is still causing 60.000 human deaths annually. Upon central nervous system (CNS) entry, neurotropic rabies virus (RABV) preserves the neural network by limiting apoptosis and inflammation. To date, we do not fully understand the factors determining RABV tropism and why glial cells are unable to clear RABV from the infected brain. Here, we compare susceptibilities and innate immune responses of CNS cell types towards infection with virulent dog RABV Tha and less virulent Th2P-4M in vitro , highlighting differences in cellular susceptibility and antiviral responses. Less virulent Th2P-4M bears mutations introduced in viral phosphoprotein (P-protein) and matrix protein (M-protein) thereby hindering viral immune evasion of the host nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and Janus kinase (JAK) - signal transducer and activator of transcription protein (STAT) pathways. Our results reveal that human neural stem cell (hNSC)-derived neurons and astrocytes, in contrast to human iPSC-derived microglia, are highly susceptible to Tha and Th2P-4M infection in vitro . Surprisingly, Th2P-4M presents a stronger neurotropism in hNSC-derived CNS cultures compared to Tha suggesting that NF-κB- and JAK-STAT-mediated antiviral host responses are defining RABV replication and thereby its tropism. Further, we show that astrocyte-like (SVGp12) and microglia-like (HMC3) cells protect neuroblastoma cells (SK-N-SH) from Tha infection in vitro . Transcription profiles and quantification of intracellular protein levels revealed major differences in antiviral immune responses mediated by neurons, astrocytes ( IFN B1 , CCL5 , CXCL10 , IL1 B , IL6 , LIF ), and microglia ( CCL5 , CXCL10 , ISG15 , MX1 , IL6 ) upon virulent Tha infection. Overall, we provide evidence that RABV tropism depends on its capability to evade cell-type specific immune responses via P- and M-proteins.

532 TLR-INDUCED AND CELL TYPE-SPECIFIC INNATE IMMUNE RESPONSES IN NON-PARENCHYMAL LIVER CELLS

2008 ◽  
Vol 48 ◽  
pp. S200
Author(s):  
J. Wu ◽  
Z. Meng ◽  
M. Trippler ◽  
R. Broering ◽  
A. Szczeponek ◽  
...  
Keyword(s):  
Immune Responses ◽  
Liver Cells ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Cell Type ◽  
Parenchymal Liver ◽  
Cell Type Specific

scholarly journals Comprehensive comparison of transcriptomes in SARS-CoV-2 infection: alternative entry routes and innate immune responses

2021 ◽  
Author(s):  
Yingying Cao ◽  
Daniel Hoffmann ◽  
Pei Hao ◽  
Xintian Xu ◽  
Lina Song ◽  
...  
Keyword(s):  
Immune Responses ◽  
Viral Entry ◽  
A549 Cells ◽  
Innate Immune ◽  
Cell Entry ◽  
Innate Immune Responses ◽  
Cell Type ◽  
Cellular Processes ◽  
Virus Dose ◽  
Comprehensive Comparison

The pathogenesis of COVID-19 emerges as complex, with multiple factors leading to injury of different organs. Several studies on underlying cellular processes have produced contradictory claims, e.g. on SARS-CoV-2 cell entry or innate immune responses. However, clarity in these matters is imperative for therapy development. We therefore performed a meta-study with a diverse set of transcriptomes under infections with SARS-CoV-2, SARS-CoV and MERS-CoV, including data from different cells and COVID-19 patients. Using these data, we investigated viral entry routes and innate immune responses. First, our analyses support the existence of cell entry mechanisms for SARS and SARS-CoV-2 other than the ACE2 route with evidence of inefficient infection of cells without expression of ACE2; expression of TMPRSS2/TPMRSS4 is unnecessary for efficient SARS-CoV-2 infection with evidence of efficient infection of A549 cells transduced with a vector expressing human ACE2. Second, we find that innate immune responses in terms of interferons and interferon simulated genes are strong in relevant cells, for example Calu3 cells, but vary markedly with cell type, virus dose, and virus type.

scholarly journals The Effects of CFTR and Mucoid Phenotype on Susceptibility and Innate Immune Responses in a Mouse Model of Pneumococcal Lung Disease

PLoS ONE ◽  
2015 ◽  
Vol 10 (10) ◽  
pp. e0140335 ◽  
Author(s):  
Evida A. Dennis ◽  
Mamie T. Coats ◽  
Sarah E. Griffin ◽  
Joanetha Y. Hale ◽  
Lea Novak ◽  
...  
Keyword(s):  
Mouse Model ◽  
Immune Responses ◽  
Lung Disease ◽  
Innate Immune ◽  
Innate Immune Responses
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