scholarly journals Gene expression profiling of the effects of organic dust in lung epithelial and THP-1 cells reveals inductive effects on inflammatory and immune response genes

2016 ◽  
Vol 48 (4) ◽  
pp. 281-289 ◽  
Author(s):  
Vijay Boggaram ◽  
David S. Loose ◽  
Koteswara R. Gottipati ◽  
Kartiga Natarajan ◽  
Courtney T. Mitchell
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Organic Dust ◽  
Monocytic Cells ◽  
Lung Epithelial ◽  
Poultry Dust ◽  
Induced Changes ◽  
Dust Extract

The intensification and concentration of animal production operations expose workers to high levels of organic dusts in the work environment. Exposure to organic dusts is a risk factor for the development of acute and chronic respiratory symptoms and diseases. Lung epithelium plays important roles in the control of immune and inflammatory responses to environmental agents to maintain lung health. To better understand the effects of organic dust on lung inflammatory responses, we characterized the gene expression profiles of A549 alveolar and Beas2B bronchial epithelial and THP-1 monocytic cells influenced by exposure to poultry dust extract by DNA microarray analysis using Illumina Human HT-12 v4 Expression BeadChip. We found that A549 alveolar and Beas2B bronchial epithelial and THP-1 cells responded with unique changes in the gene expression profiles with regulation of genes encoding inflammatory cytokines, chemokines, and other inflammatory proteins being common to all the three cells. Significantly induced genes included IL-8, IL-6, IL-1β, ICAM-1, CCL2, CCL5, TLR4, and PTGS2. Validation by real-time qRT-PCR, ELISA, Western immunoblotting, and immunohistochemical staining of lung sections from mice exposed to dust extract validated DNA microarray results. Pathway analysis indicated that dust extract induced changes in gene expression influenced functions related to cellular growth and proliferation, cell death and survival, and cellular development. These data show that a broad range of inflammatory mediators produced in response to poultry dust exposure can modulate lung immune and inflammatory responses. This is the first report on organic dust induced changes in expression profiles in lung epithelial and THP-1 monocytic cells.

scholarly journals Transcriptional mechanisms and protein kinase signaling mediate organic dust induction of IL-8 expression in lung epithelial and THP-1 cells

2015 ◽  
Vol 308 (1) ◽  
pp. L11-L21 ◽  
Author(s):  
Koteswara R. Gottipati ◽  
Shiva Kumar Bandari ◽  
Matthew W. Nonnenmann ◽  
Jeffrey L. Levin ◽  
Gregory P. Dooley ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Inflammatory Responses ◽  
Dust Exposure ◽  
Kinase Signaling ◽  
Organic Dust ◽  
Chronic Lung Diseases ◽  
Lung Epithelial ◽  
Poultry Dust ◽  
Protein Kinase Signaling ◽  
Dust Extract

Exposure to the agricultural work environment is a risk factor for the development of respiratory symptoms and chronic lung diseases. Inflammation is an important contributor to the pathogenesis of tissue injury and disease. Cellular and molecular mechanisms mediating lung inflammatory responses to agricultural dust are not yet fully understood. We studied the effects of poultry dust extract on molecular regulation of interleukin-8 (IL-8), a proinflammatory cytokine, in A549 and Beas2B lung epithelial and THP-1 monocytic cells. Our findings indicate that poultry dust extract potently induces IL-8 levels by increasing IL-8 gene transcription without altering IL-8 mRNA stability. Increase in IL-8 promoter activity was due to enhanced binding of activator protein 1 and NF-κB. IL-8 induction was associated with protein kinase C (PKC) and mitogen-activated protein kinase (MAPK) activation and inhibited by PKC and MAPK inhibitors. IL-8 increase was not inhibited by polymyxin B or l-nitroarginine methyl ester, indicating lack of involvement of lipopolysaccharide and nitric oxide in the induction. Lung epithelial and THP-1 cells share common mechanisms for induction of IL-8 levels. Our findings identify key roles for transcriptional mechanisms and protein kinase signaling pathways for IL-8 induction and provide insights into the mechanisms regulating lung inflammatory responses to organic dust exposure.

scholarly journals Age and Vitamin E-Induced Changes in Gene Expression Profiles of T Cells

2006 ◽  
Vol 177 (9) ◽  
pp. 6052-6061 ◽  
Author(s):  
Sung Nim Han ◽  
Oskar Adolfsson ◽  
Cheol-Koo Lee ◽  
Tomas A. Prolla ◽  
Jose Ordovas ◽  
...  
Keyword(s):  
Gene Expression ◽  
T Cells ◽  
Vitamin E ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Induced Changes

Whole blood genome-wide gene expression profile in males after prolonged wakefulness and sleep recovery

2012 ◽  
Vol 44 (21) ◽  
pp. 1003-1012 ◽  
Author(s):  
R. Pellegrino ◽  
D. Y. Sunaga ◽  
C. Guindalini ◽  
R. C. S. Martins ◽  
D. R. Mazzotti ◽  
...  
Keyword(s):  
Gene Expression ◽  
Whole Blood ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Killer Cell ◽  
Gene Expression Profiles ◽  
Sleep Loss ◽  
The Body ◽  
Dna Damage And Repair ◽  
Peripheral Tissues

Although the specific functions of sleep have not been completely elucidated, the literature has suggested that sleep is essential for proper homeostasis. Sleep loss is associated with changes in behavioral, neurochemical, cellular, and metabolic function as well as impaired immune response. Using high-resolution microarrays we evaluated the gene expression profiles of healthy male volunteers who underwent 60 h of prolonged wakefulness (PW) followed by 12 h of sleep recovery (SR). Peripheral whole blood was collected at 8 am in the morning before the initiation of PW (Baseline), after the second night of PW, and one night after SR. We identified over 500 genes that were differentially expressed. Notably, these genes were related to DNA damage and repair and stress response, as well as diverse immune system responses, such as natural killer pathways including killer cell lectin-like receptors family, as well as granzymes and T-cell receptors, which play important roles in host defense. These results support the idea that sleep loss can lead to alterations in molecular processes that result in perturbation of cellular immunity, induction of inflammatory responses, and homeostatic imbalance. Moreover, expression of multiple genes was downregulated following PW and upregulated after SR compared with PW, suggesting an attempt of the body to re-establish internal homeostasis. In silico validation of alterations in the expression of CETN3, DNAJC, and CEACAM genes confirmed previous findings related to the molecular effects of sleep deprivation. Thus, the present findings confirm that the effects of sleep loss are not restricted to the brain and can occur intensely in peripheral tissues.

Distinct gene expression profiles provoked by polyacrylamide beads (Biogel) during chronic and acute inflammation in mice selected for maximal and minimal inflammatory responses

2016 ◽  
Vol 65 (4) ◽  
pp. 313-323 ◽  
Author(s):  
Jussara Gonçalves Fernandes ◽  
Tatiane Canhamero ◽  
Andrea Borrego ◽  
José Ricardo Jensen ◽  
Wafa Hanna Cabrera ◽  
...  
Keyword(s):  
Gene Expression ◽  
Acute Inflammation ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Distinct Gene

454 pyrosequencing-based analysis of gene expression profiles in the amphipod Melita plumulosa: Transcriptome assembly and toxicant induced changes

2014 ◽  
Vol 153 ◽  
pp. 73-88 ◽  
Author(s):  
Sharon E. Hook ◽  
Natalie A. Twine ◽  
Stuart L. Simpson ◽  
David A. Spadaro ◽  
Philippe Moncuquet ◽  
...  
Keyword(s):  
Gene Expression ◽  
454 Pyrosequencing ◽  
Transcriptome Assembly ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Induced Changes

scholarly journals Variability in statin-induced changes in gene expression profiles of pancreatic cancer

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Helena Gbelcová ◽  
Silvie Rimpelová ◽  
Tomáš Ruml ◽  
Marie Fenclová ◽  
Vítek Kosek ◽  
...  
Keyword(s):  
Gene Expression ◽  
Pancreatic Cancer ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Induced Changes

scholarly journals Single-Cell Transcript Profiling of Barley Attacked by the Powdery Mildew Fungus

2007 ◽  
Vol 20 (3) ◽  
pp. 235-246 ◽  
Author(s):  
Torben Gjetting ◽  
Peter H. Hagedorn ◽  
Patrick Schweizer ◽  
Hans Thordal-Christensen ◽  
Timothy L. W. Carver ◽  
...  
Keyword(s):  
Gene Expression ◽  
Powdery Mildew ◽  
Expression Profiles ◽  
Cdna Array ◽  
Gene Expression Profiles ◽  
Powdery Mildew Fungus ◽  
Nonspecific Resistance ◽  
Susceptible Host ◽  
Leaf Epidermal Cell ◽  
Induced Changes

In many plant-pathogen interactions, there are several possible outcomes for simultaneous attacks on the same leaf. For instance, an attack by the powdery mildew fungus on one barley leaf epidermal cell may succeed in infection and formation of a functional haustorium, whereas a neighboring cell attacked at the same time may resist fungal penetration. To date, the mixed cellular responses seen even in susceptible host leaves have made it difficult to relate induced changes in gene expression to resistance or susceptibility in bulk leaf samples. By microextraction of cell-specific mRNA and subsequent cDNA array analysis, we have successfully obtained separate gene expression profiles for specific mildew-resistant and -infected barley cells. Thus, for the first time, it is possible to identify genes that are specifically regulated in infected cells and, presumably, involved in fungal establishment. Further, although much is understood about the genetic basis of effective papilla resistance associated with mutant mlo barley, we provide here the first evidence for gene regulation associated with effective papilla-based nonspecific resistance expressed in nominally “susceptible” wild-type barley.

Prednisolone-induced changes in gene-expression profiles in healthy volunteers

2011 ◽  
Vol 12 (7) ◽  
pp. 985-998 ◽  
Author(s):  
Erik JM Toonen ◽  
Wilco WM Fleuren ◽  
Ulla Nässander ◽  
Marie-José C van Lierop ◽  
Susanne Bauerschmidt ◽  
...  
Keyword(s):  
Gene Expression ◽  
Healthy Volunteers ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Induced Changes

Abstract 149: Regulation of Pathogen-Associated Molecular Pattern Recognition by the Apo A-I Mimetic Peptide 4F

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Geeta Datta ◽  
David K Crossman ◽  
Lesley E Smythies ◽  
M N Palgunachari ◽  
Manjula Chaddha ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Responses ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
Rna Isolation ◽  
Mimetic Peptide ◽  
M1 Macrophage ◽  
Vehicle Treatment ◽  
Anti Inflammatory ◽  
Pre Treatment

The apolipoprotein A-I (apoA-I) mimetic peptide 4F displays prominent anti-inflammatory properties, including the ability to reduce vascular macrophage content. Macrophages are a heterogenous group of cells that are represented by two principal phenotypes, the classically-activated M1 macrophage and an alternatively-activated M2 phenotype. We previously reported that apoA-I and 4F favor the differentiation of human monocytes to an anti-inflammatory phenotype similar to that displayed by M2 macrophages. Further, 4F treatment attenuated LPS-induced inflammatory responses in monocyte-derived macrophages (MDMs). In the current study, we investigated effects of 4F and vehicle on LPS-induced gene expression in human MDMs by microarray analysis. RNA isolation, labeling and hybridization were performed, and the transcriptional profile was examined using the Human Gene ST 1.0 Affymetrix chip. Analysis of MDM gene expression profiles revealed that 4F modulated mRNA expression for 1099 genes (± 2-fold change, p<0.05), of which 149 genes regulated inflammatory responses. LPS treatment of MDMs significantly up-regulated genes encoding Toll-like receptors (TLR1, 2, 4, 6, and 8) compared to vehicle treatment. These responses were attenuated by 4F treatment. MyD88, CD14, IRAK4, TRAF6, TRAF3, MALT1 and IKBKB, genes that modulate NF-κB activation and subsequent cytokine synthesis, were also reduced by 4F. Corroborating this, FACS analyses showed that pre-treatment of MDMs with 4F reduced the LPS-dependent phosphorylation of NF-κB by 70% compared to vehicle treatment. These 4F-induced responses were also associated with a reduction in TNF-α and IL-6 secretion. These data suggest that an important anti-inflammatory mechanism of 4F action may be to down-regulate genes involved in the TLR signaling pathway, thus attenuating the responsiveness of macrophages to LPS and other pathogen-associated molecular patterns (PAMPs).

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