The gene expression profile of porcine alveolar macrophages infected with a highly pathogenic porcine reproductive and respiratory syndrome virus indicates overstimulation of the innate immune system by the virus

2014 ◽  
Vol 160 (3) ◽  
pp. 649-662 ◽  
Author(s):  
Yan Xiao ◽  
Tong-Qing An ◽  
Zhi-Jun Tian ◽  
Tian-Chao Wei ◽  
Yi-Feng Jiang ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Alveolar Macrophages ◽  
Innate Immune System ◽  
Innate Immune ◽  
Respiratory Syndrome Virus ◽  
Highly Pathogenic

scholarly journals Bacillus anthracis Spores Stimulate Cytokine and Chemokine Innate Immune Responses in Human Alveolar Macrophages through Multiple Mitogen-Activated Protein Kinase Pathways

2006 ◽  
Vol 74 (8) ◽  
pp. 4430-4438 ◽  
Author(s):  
Kaushik Chakrabarty ◽  
Wenxin Wu ◽  
J. Leland Booth ◽  
Elizabeth S. Duggan ◽  
K. Mark Coggeshall ◽  
...  
Keyword(s):  
Immune System ◽  
Bacillus Anthracis ◽  
Alveolar Macrophages ◽  
Innate Immune System ◽  
Innate Immune ◽  
Mitogen Activated Protein Kinase ◽  
Tnf Α ◽  
Human Alveolar Macrophages ◽  
Mitogen Activated Protein ◽  
Multiple Signaling

ABSTRACT Contact with the human alveolar macrophage plays a key role in the innate immune response to Bacillus anthracis spores. Because there is a significant delay between the initial contact of the spore with the host and clinical evidence of disease, there appears to be temporary containment of the pathogen by the innate immune system. Therefore, the early macrophage response to Bacillus anthracis exposure is important in understanding the pathogenesis of this disease. In this paper, we studied the initial events after exposure to spores, beginning with the rapid internalization of spores by the macrophages. Spore exposure rapidly activated the mitogen-activated protein kinase signaling pathways extracellular signal-regulated kinase, c-Jun-NH2-terminal kinase, and p38. This was followed by the transcriptional activation of cytokine and primarily monocyte chemokine genes as determined by RNase protection assays. Transcriptional induction is reflected at the translational level, as interleukin-1α (IL-1α), IL-1β, IL-6, and tumor necrosis factor alpha (TNF-α) cytokine protein levels were markedly elevated as determined by enzyme-linked immunosorbent assay. Induction of IL-6 and TNF-α, and, to a lesser extent, IL-1α and IL-1β, was partially inhibited by the blockade of individual mitogen-activated protein kinases, while the complete inhibition of cytokine induction was achieved when multiple signaling pathway inhibitors were used. Taken together, these data clearly show activation of the innate immune system in human alveolar macrophages by Bacillus anthracis spores. The data also show that multiple signaling pathways are involved in this cytokine response. This report is the first comprehensive examination of this process in primary human alveolar macrophages.

scholarly journals Gene expression analysis of the innate immune system during early rearing and weaning of meagre (Argyrosomus regius)

2019 ◽  
Vol 94 ◽  
pp. 819-832
Author(s):  
Cindy Campoverde ◽  
Douglas J. Milne ◽  
Christopher J. Secombes ◽  
Alicia Estévez ◽  
Enric Gisbert ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Expression Analysis ◽  
Innate Immune System ◽  
Gene Expression Analysis ◽  
Innate Immune ◽  
Argyrosomus Regius ◽  
Early Rearing

scholarly journals Candidate innate immune system gene expression in the ecological model Daphnia

2011 ◽  
Vol 35 (10) ◽  
pp. 1068-1077 ◽  
Author(s):  
Ellen Decaestecker ◽  
Pierrick Labbé ◽  
Kirsten Ellegaard ◽  
Judith E. Allen ◽  
Tom J. Little
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Innate Immune System ◽  
Ecological Model ◽  
Innate Immune

Inflammation of the cystic fibrosis mouse small intestine

2004 ◽  
Vol 286 (6) ◽  
pp. G1032-G1041 ◽  
Author(s):  
Oxana Norkina ◽  
Simran Kaur ◽  
Donna Ziemer ◽  
Robert C. De Lisle
Keyword(s):  
Gene Expression ◽  
Cystic Fibrosis ◽  
Small Intestine ◽  
Immune System ◽  
Mast Cells ◽  
Innate Immune System ◽  
Innate Immune ◽  
Serum Amyloid ◽  
Mouse Small Intestine ◽  
Cytochrome P 450

The CFTR null mouse [cystic fibrosis (CF) mouse] has a severe intestinal phenotype that serves as a model for CF-related growth deficiency, meconium ileus, and distal intestinal obstructive syndrome. DNA microarray analysis was used to investigate gene expression in the CF mouse small intestine. Sixty-one genes exhibited a statistically significant twofold or greater increase in expression, and 98 genes were downregulated twofold or greater. Of the upregulated genes, most were associated with inflammation and included markers for cells of the innate immune system (mast cells and neutrophils) and for acute-phase genes (serum amyloid A and complement factors). The downregulated genes include 10 cytochrome P-450 genes; several are involved in lipid metabolism, and several are involved in various transport processes. Confirmation by quantitative RT-PCR showed gene expression was significantly increased for mast cell protease 2 (27-fold), hematopoietic cell transcript 1 (17-fold), serum amyloid A3 (2.9-fold), suppressor of cytokine signaling 3 (2.0-fold), leucine-rich α2-glycoprotein (21-fold), resistin-like molecule-β (49-fold), and Muclin (2.5-fold) and was significantly decreased for cytochrome P-450 4a10 (28-fold) and cubilin (114-fold). Immune cell infiltration was confirmed histologically by staining for mast cells and neutrophils. These data demonstrate that the CF intestine exhibits an inflammatory state with upregulation of components of the innate immune system.

scholarly journals Genome-wide transcriptional response of primary alveolar macrophages following infection with porcine reproductive and respiratory syndrome virus

2008 ◽  
Vol 89 (10) ◽  
pp. 2550-2564 ◽  
Author(s):  
Sem Genini ◽  
Peter L. Delputte ◽  
Roberto Malinverni ◽  
Maria Cecere ◽  
Alessandra Stella ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alveolar Macrophages ◽  
Time Course ◽  
Viral Infections ◽  
Interleukin 10 ◽  
Innate Immune ◽  
Differentially Expressed ◽  
Respiratory Syndrome Virus ◽  
Swine Industry

Porcine reproductive and respiratory syndrome is a major cause of economic loss for the swine industry worldwide. Porcine reproductive and respiratory syndrome virus (PRRSV) triggers weak and atypical innate immune responses, but key genes and mechanisms by which the virus interferes with the host innate immunity have not yet been elucidated. In this study, genes that control the response of the main target of PRRSV, porcine alveolar macrophages (PAMs), were profiled in vitro with a time-course experiment spanning the first round of virus replication. PAMs were obtained from six piglets and challenged with the Lelystad PRRSV strain, and gene expression was investigated using Affymetrix microarrays and real-time PCR. Of the 1409 differentially expressed transcripts identified by analysis of variance, two, five, 25, 16 and 100 differed from controls by a minimum of 1.5-fold at 1, 3, 6, 9 and 12 h post-infection (p.i.), respectively. A PRRSV infection effect was detectable between 3 and 6 h p.i., and was characterized by a consistent downregulation of gene expression, followed by the start of the host innate immune response at 9 h p.i. The expression of beta interferon 1 (IFN-β), but not of IFN-α, was strongly upregulated, whilst few genes commonly expressed in response to viral infections and/or induced by interferons were found to be differentially expressed. A predominance of anti-apoptotic transcripts (e.g. interleukin-10), a shift towards a T-helper cell type 2 response and a weak upregulation of tumour necrosis factor-α expression were observed within 12 h p.i., reinforcing the hypotheses that PRRSV has developed sophisticated mechanisms to escape the host defence.

scholarly journals Brain Death Enhances Activation of the Innate Immune System and Leads to Reduced Renal Metabolic Gene Expression

2019 ◽  
Vol 103 (9) ◽  
pp. 1821-1833 ◽  
Author(s):  
Laura J. Zitur ◽  
Peter J. Chlebeck ◽  
Scott K. Odorico ◽  
Juan S. Danobeitia ◽  
Tiffany J. Zens ◽  
...  
Keyword(s):  
Gene Expression ◽  
Immune System ◽  
Brain Death ◽  
Innate Immune System ◽  
Innate Immune ◽  
Metabolic Gene ◽  
Metabolic Gene Expression

scholarly journals The heterogeneity of lung macrophages in the susceptibility to disease

2015 ◽  
Vol 24 (137) ◽  
pp. 505-509 ◽  
Author(s):  
Luisa Morales-Nebreda ◽  
Alexander V. Misharin ◽  
Harris Perlman ◽  
G.R. Scott Budinger
Keyword(s):  
Gene Expression ◽  
Alveolar Macrophage ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Alveolar Macrophages ◽  
Tissue Injury ◽  
Local Environment ◽  
Specific Gene ◽  
Injured Lung ◽  
Cellular Defence

Alveolar macrophages are specialised resident phagocytes in the alveolus, constituting the first line of immune cellular defence in the lung. As the lung microenvironment is challenged and remodelled by inhaled pathogens and air particles, so is the alveolar macrophage pool altered by signals that maintain and/or replace its composition. The signals that induce the recruitment of circulating monocytes to the injured lung, as well as their distinct gene expression profile and susceptibility to epigenetic reprogramming by the local environment remain unclear. In this review, we summarise the unique characteristics of the alveolar macrophage pool ontogeny, phenotypic heterogeneity and plasticity during homeostasis, tissue injury and normal ageing. We also discuss new evidence arising from recent studies where investigators described how the epigenetic landscape drives the specific gene expression profile of alveolar macrophages. Altogether, new analysis of macrophages by means of “omic” technologies will allow us to identify key pathways by which these cells contribute to the development and resolution of lung disease in both mice and humans.

scholarly journals CREB pathway links PGE2 signaling with macrophage polarization

2015 ◽  
Vol 112 (51) ◽  
pp. 15642-15647 ◽  
Author(s):  
Bing Luan ◽  
Young-Sil Yoon ◽  
John Le Lay ◽  
Klaus H. Kaestner ◽  
Susan Hedrick ◽  
...  
Keyword(s):  
Gene Expression ◽  
Insulin Resistance ◽  
Adipose Tissue ◽  
Immune System ◽  
Insulin Sensitivity ◽  
Innate Immune System ◽  
Marker Gene ◽  
Innate Immune ◽  
M2 Polarization ◽  
Marker Gene Expression

Obesity is thought to promote insulin resistance in part via activation of the innate immune system. Increases in proinflammatory cytokine production by M1 macrophages inhibit insulin signaling in white adipose tissue. In contrast, M2 macrophages have been found to enhance insulin sensitivity in part by reducing adipose tissue inflammation. The paracrine hormone prostaglandin E2 (PGE2) enhances M2 polarization in part through activation of the cAMP pathway, although the underlying mechanism is unclear. Here we show that PGE2 stimulates M2 polarization via the cyclic AMP-responsive element binding (CREB)-mediated induction of Krupple-like factor 4 (KLF4). Targeted disruption of CREB or the cAMP-regulated transcriptional coactivators 2 and 3 (CRTC2/3) in macrophages down-regulated M2 marker gene expression and promoted insulin resistance in the context of high-fat diet feeding. As re-expression of KLF4 rescued M2 marker gene expression in CREB-depleted cells, our results demonstrate the importance of the CREB/CRTC pathway in maintaining insulin sensitivity in white adipose tissue via its effects on the innate immune system.

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