Going further post-RNA-seq: In silico functional analyses revealing candidate genes and regulatory elements related to mastitis in dairy cattle

2021 ◽  
pp. 1-7
Author(s):  
Hyago Passe Pereira ◽  
Lucas Lima Verardo ◽  
Mayara Morena Del Cambre Amaral Weller ◽  
Ana Paula Sbardella ◽  
Danísio Prado Munari ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Immune Responses ◽  
Streptococcus Agalactiae ◽  
Gene Networks ◽  
Regulatory Elements ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Rna Seq ◽  
Functional Analyses ◽  
The Relationship

Abstract This study aimed to obtain a better understanding of the regulatory genes and molecules involved in the development of mastitis. For this purpose, the transcription factors (TF) and MicroRNAs (miRNA) related to differentially expressed genes previously found in extracorporeal udders infected with Streptococcus agalactiae were investigated. The Gene-TF network highlighted LOC515333, SAA3, CD14, NFKBIA, APOC2 and LOC100335608 and genes that encode the most representative transcription factors STAT3, PPARG, EGR1 and NFKB1 for infected udders. In addition, it was possible to highlight, through the analysis of the gene-miRNA network, genes that could be post-transcriptionally regulated by miRNAs, such as the relationship between the CCL5 gene and the miRNA bta-miR-363. Overall, our data demonstrated genes and regulatory elements (TF and miRNA) that can play an important role in mastitis resistance. The results provide new insights into the first functional pathways and the network of genes that orchestrate the innate immune responses to infection by Streptococcus agalactiae. Our results will increase the general knowledge about the gene networks, transcription factors and miRNAs involved in fighting intramammary infection and maintaining tissue during infection and thus enable a better understanding of the pathophysiology of mastitis.

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 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 A Blueprint for Cancer-Related Inflammation and Host Innate Immunity

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3211
Author(s):  
Lucia García-López ◽  
Isabel Adrados ◽  
Dolors Ferres-Marco ◽  
Maria Dominguez
Keyword(s):  
Drosophila Melanogaster ◽  
Immune Responses ◽  
Gene Networks ◽  
Cost Effective ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Host Interactions ◽  
Powerful Means ◽  
Adult Drosophila

Both in situ and allograft models of cancer in juvenile and adult Drosophila melanogaster fruit flies offer a powerful means for unravelling cancer gene networks and cancer–host interactions. They can also be used as tools for cost-effective drug discovery and repurposing. Moreover, in situ modeling of emerging tumors makes it possible to address cancer initiating events—a black box in cancer research, tackle the innate antitumor immune responses to incipient preneoplastic cells and recurrent growing tumors, and decipher the initiation and evolution of inflammation. These studies in Drosophila melanogaster can serve as a blueprint for studies in more complex organisms and help in the design of mechanism-based therapies for the individualized treatment of cancer diseases in humans. This review focuses on new discoveries in Drosophila related to the diverse innate immune responses to cancer-related inflammation and the systemic effects that are so detrimental to the host.

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 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 Human nasal wash RNA-seq reveals distinct cell-specific innate immune responses between influenza and SARS-CoV-2

JCI Insight ◽  
2021 ◽  
Author(s):  
Kevin M. Gao ◽  
Alan G. Derr ◽  
Zhiru Guo ◽  
Kerstin Nundel ◽  
Ann Marshak-Rothstein ◽  
...  
Keyword(s):  
Immune Responses ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Rna Seq ◽  
Nasal Wash ◽  
Distinct Cell

scholarly journals Transcriptome analysis based on RNA-seq of common innate immune responses of flounder cells to IHNV, VHSV, and HIRRV

PLoS ONE ◽  
2020 ◽  
Vol 15 (9) ◽  
pp. e0239925
Author(s):  
Kwang Il Kim ◽  
Unn Hwa Lee ◽  
Miyoung Cho ◽  
Sung-Hee Jung ◽  
Eun Young Min ◽  
...  
Keyword(s):  
Immune Responses ◽  
Transcriptome Analysis ◽  
Innate Immune ◽  
Innate Immune Responses ◽  
Rna Seq

scholarly journals Toll-like Receptors Induce a Phagocytic Gene Program through p38

2003 ◽  
Vol 199 (1) ◽  
pp. 81-90 ◽  
Author(s):  
Sean E. Doyle ◽  
Ryan M. O'Connell ◽  
Gustavo A. Miranda ◽  
Sagar A. Vaidya ◽  
Edward K. Chow ◽  
...  
Keyword(s):  
Immune Responses ◽  
Interleukin 1 ◽  
Innate Immune ◽  
Myeloid Differentiation ◽  
Innate Immune Responses ◽  
Toll Like Receptor ◽  
Evolutionarily Conserved ◽  
Myeloid Differentiation Factor ◽  
The Relationship ◽  
Number Of Bacteria

Toll-like receptor (TLR) signaling and phagocytosis are hallmarks of macrophage-mediated innate immune responses to bacterial infection. However, the relationship between these two processes is not well established. Our data indicate that TLR ligands specifically promote bacterial phagocytosis, in both murine and human cells, through induction of a phagocytic gene program. Importantly, TLR-induced phagocytosis of bacteria was found to be reliant on myeloid differentiation factor 88–dependent signaling through interleukin-1 receptor–associated kinase-4 and p38 leading to the up-regulation of scavenger receptors. Interestingly, individual TLRs promote phagocytosis to varying degrees with TLR9 being the strongest and TLR3 being the weakest inducer of this process. We also demonstrate that TLR ligands not only amplify the percentage of phagocytes uptaking Escherichia coli, but also increase the number of bacteria phagocytosed by individual macrophages. Taken together, our data describe an evolutionarily conserved mechanism by which TLRs can specifically promote phagocytic clearance of bacteria during infection.

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