Inflammatory responses to secondary organic aerosols (SOA) generated from biogenic and anthropogenic precursors

Abstract. Cardiopulmonary health implications resulting from exposure to secondary organic aerosols (SOA), which comprise a significant fraction of ambient particulate matter (PM), have received increasing interest in recent years. In this study, alveolar macrophages were exposed to SOA generated from the photooxidation of biogenic and anthropogenic precursors (isoprene, α-pinene, β-caryophyllene, pentadecane, m-xylene, and naphthalene) under different formation conditions (RO2 + HO2 vs. RO2 + NO dominant, dry vs. humid). Various cellular responses were measured, including reactive oxygen and nitrogen species (ROS/RNS) production and secreted levels of cytokines, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). SOA precursor identity and formation condition affected all measured responses in a hydrocarbon-specific manner. With the exception of naphthalene SOA, cellular responses followed a trend where TNF-α levels reached a plateau with increasing IL-6 levels. ROS/RNS levels were consistent with relative levels of TNF-α and IL-6, due to their respective inflammatory and anti-inflammatory effects. Exposure to naphthalene SOA, whose aromatic-ring-containing products may trigger different cellular pathways, induced higher levels of TNF-α and ROS/RNS than suggested by the trend. Distinct cellular response patterns were identified for hydrocarbons whose photooxidation products shared similar chemical functionalities and structures, which suggests that the chemical structure (carbon chain length and functionalities) of photooxidation products may be important for determining cellular effects. A positive nonlinear correlation was also detected between ROS/RNS levels and previously measured DTT (dithiothreitol) activities for SOA samples. In the context of ambient samples collected during summer and winter in the greater Atlanta area, all laboratory-generated SOA produced similar or higher levels of ROS/RNS and DTT activities. These results suggest that the health effects of SOA are important considerations for understanding the health implications of ambient aerosols.

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Inflammatory responses to secondary organic aerosols (SOA) generated from biogenic and anthropogenic precursors

10.5194/acp-2017-262 ◽

2017 ◽

Cited By ~ 2

Author(s):

Wing Y. Tuet ◽

Yunle Chen ◽

Shierly Fok ◽

Julie A. Champion ◽

Nga L. Ng

Keyword(s):

Cellular Response ◽

Secondary Organic Aerosols ◽

Inflammatory Responses ◽

Organic Aerosols ◽

Cellular Responses ◽

Formation Condition ◽

Ambient Aerosols ◽

Health Implications ◽

Cellular Effects ◽

Tnf Α

Abstract. Cardiopulmonary health implications resulting from exposure to secondary organic aerosols (SOA), which comprise a significant fraction of ambient particulate matter (PM), have received increasing interest in recent years. In this study, alveolar macrophages were exposed to SOA generated from the photooxidation of biogenic and anthropogenic precursors (isoprene, α-pinene, β-caryophyllene, pentadecane, m-xylene, and naphthalene) under different formation conditions (RO2 + HO2 vs. RO2 + NO dominant, dry vs. humid). Various cellular responses were measured, including reactive oxygen/nitrogen species (ROS/RNS) production and secreted levels of cytokines, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6). SOA precursor identity and formation condition affected all measured responses in a hydrocarbon-specific manner. With the exception of naphthalene SOA, cellular responses followed a trend where TNF-α levels reached a plateau with increasing IL-6 levels. ROS/RNS levels were consistent with relative levels of TNF-α and IL-6, due to their respective inflammatory and anti-inflammatory effects. Exposure to naphthalene SOA, whose aromatic ring-containing products may trigger different cellular pathways, induced higher levels of TNF-α and ROS/RNS than suggested by the trend. Distinct cellular response patterns were identified for hydrocarbons whose photooxidation products shared similar chemical functionalities and structures, which suggests that the carbon backbone may be important for determining cellular effects. A positive nonlinear correlation was also detected between ROS/RNS levels and previously measured DTT activities for SOA samples. In the context of ambient samples collected during summer and winter in the greater Atlanta area, all laboratory-generated SOA produced similar or higher levels of ROS/RNS and DTT activities. These results suggest that the health effects of SOA are important considerations for understanding the health implications of ambient aerosols.

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Enhanced expression and activation of pro-inflammatory transcription factors distinguish aneurysmal from atherosclerotic aorta: IL-6- and IL-8-dominated inflammatory responses prevail in the human aneurysm

Clinical Science ◽

10.1042/cs20070352 ◽

2008 ◽

Vol 114 (11) ◽

pp. 687-697 ◽

Cited By ~ 73

Author(s):

Jan H. N. Lindeman ◽

Hazem Abdul-Hussien ◽

Alexander F. M. Schaapherder ◽

J. Hajo VAN Bockel ◽

Jan H. VON DER Thüsen ◽

...

Keyword(s):

Transcription Factors ◽

Cellular Response ◽

Target Genes ◽

Inflammatory Responses ◽

Interleukin 2 ◽

Cellular Responses ◽

Vasa Vasorum ◽

Inflammatory Factors ◽

Inflammatory Parameters ◽

Enhanced Expression

Inflammation plays a key role in the pathogenesis of an AAA (abdominal aortic aneurysm); however, the nature of the inflammatory factors and cellular response(s) involved in AAA growth is controversial. In the present study, we set out to determine the aortic levels of inflammatory cytokines in relation to downstream inflammatory transcription factors and cellular responses. A comparison of AAA wall samples with atherosclerotic wall samples taken from the same aortic region allowed AAA-specific inflammatory parameters to be identified that distinguish AAAs from ASD (aortic atherosclerotic disease). RT-PCR (real-time PCR), ELISA, Western blotting and immunohistochemistry were combined to assess cytokines and transcription factors at the mRNA and protein level, and their activation status. Compared with ASD, inflammatory parameters associated with Th1-type [T-bet, IL (interleukin)-2, IFN-γ (interferon-γ), TNF-α (tumour necrosis factor-α), IL-1α and cytotoxic T-cells] and Th2-type [GATA3, IL-4, IL-10, IL-13 and B-cells] responses were all increased in AAA samples. Evaluation of major downstream inflammatory transcription factors revealed higher baseline levels of C/EBP (CCAAT/enhancer-binding protein) α, β and δ in the AAA samples. Baseline p65 NF-κB (nuclear factor κB) and c-Jun [AP-1 (activator protein-1)] levels were comparable, but their activated forms were strongly increased in the AAA samples. Downstream target genes of p65 NF-κB, c-Jun, IL-6 and IL-8 were hyperexpressed. Molecular and cellular processes associated with IL-6 and IL-8 hyperactivation were enhanced in the AAA samples, i.e. the expression of phospho-STAT-3 (signal transducer and activator of transcription-3) and perforin were elevated, and the content of plasma cells, neutrophils and vasa vasorum was increased. In conclusion, our findings demonstrate that an AAA is a general inflammatory condition which is characterized by enhanced expression and activation of pro-inflammatory transcription factors, accompanied by IL-6 and IL-8 hyperexpression and exaggerated downstream cellular responses, which together clearly distinguish an AAA from ASD.

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Modeling SOA formation from the oxidation of intermediate volatility <i>n</i>-alkanes

Atmospheric Chemistry and Physics ◽

10.5194/acp-12-7577-2012 ◽

2012 ◽

Vol 12 (16) ◽

pp. 7577-7589 ◽

Cited By ~ 58

Author(s):

B. Aumont ◽

R. Valorso ◽

C. Mouchel-Vallon ◽

M. Camredon ◽

J. Lee-Taylor ◽

...

Keyword(s):

Organic Compounds ◽

Dimensional Space ◽

Organic Aerosols ◽

Organic Aerosol ◽

Carbon Chain ◽

Chemical Mechanism ◽

Carbon Chain Length ◽

Successive Formation ◽

Formation And Evolution ◽

Lower Vapor Pressure

Abstract. The chemical mechanism leading to SOA formation and ageing is expected to be a multigenerational process, i.e. a successive formation of organic compounds with higher oxidation degree and lower vapor pressure. This process is here investigated with the explicit oxidation model GECKO-A (Generator of Explicit Chemistry and Kinetics of Organics in the Atmosphere). Gas phase oxidation schemes are generated for the C8–C24 series of n-alkanes. Simulations are conducted to explore the time evolution of organic compounds and the behavior of secondary organic aerosol (SOA) formation for various preexisting organic aerosol concentration (COA). As expected, simulation results show that (i) SOA yield increases with the carbon chain length of the parent hydrocarbon, (ii) SOA yield decreases with decreasing COA, (iii) SOA production rates increase with increasing COA and (iv) the number of oxidation steps (i.e. generations) needed to describe SOA formation and evolution grows when COA decreases. The simulated oxidative trajectories are examined in a two dimensional space defined by the mean carbon oxidation state and the volatility. Most SOA contributors are not oxidized enough to be categorized as highly oxygenated organic aerosols (OOA) but reduced enough to be categorized as hydrocarbon like organic aerosols (HOA), suggesting that OOA may underestimate SOA. Results show that the model is unable to produce highly oxygenated aerosols (OOA) with large yields. The limitations of the model are discussed.

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Modeling SOA formation from the oxidation of intermediate volatility <i>n</i>-alkanes

Atmospheric Chemistry and Physics Discussions ◽

10.5194/acpd-12-14447-2012 ◽

2012 ◽

Vol 12 (6) ◽

pp. 14447-14482

Author(s):

B. Aumont ◽

R. Valorso ◽

C. Mouchel-Vallon ◽

M. Camredon ◽

J. Lee-Taylor ◽

...

Keyword(s):

Organic Compounds ◽

Dimensional Space ◽

Organic Aerosols ◽

Organic Aerosol ◽

Carbon Chain ◽

Chemical Mechanism ◽

Carbon Chain Length ◽

Successive Formation ◽

Formation And Evolution ◽

Lower Vapor Pressure

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Supplementary material to "Inflammatory responses to secondary organic aerosols (SOA) generated from biogenic and anthropogenic precursors"

10.5194/acp-2017-262-supplement ◽

2017 ◽

Author(s):

Wing Y. Tuet ◽

Yunle Chen ◽

Shierly Fok ◽

Julie A. Champion ◽

Nga L. Ng

Keyword(s):

Secondary Organic Aerosols ◽

Inflammatory Responses ◽

Organic Aerosols ◽

Supplementary Material

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Anti-β2 Glycoprotein I Antibodies Cause Inflammation and Recruit Dendritic Cells in Platelet Clearance

Thrombosis and Haemostasis ◽

10.1055/s-0037-1616059 ◽

2001 ◽

Vol 86 (11) ◽

pp. 1257-1263 ◽

Cited By ~ 6

Author(s):

Attilio Bondanza ◽

Angelo Manfredi ◽

Valérie Zimmermann ◽

Matteo Iannacone ◽

Angela Tincani ◽

...

Keyword(s):

Dendritic Cells ◽

Inflammatory Responses ◽

Glycoprotein I ◽

Activated Platelets ◽

Tnf Α ◽

Per Se ◽

Antigen Presenting ◽

Antiinflammatory Cytokine

SummaryScavenger phagocytes are mostly responsible for the in vivo clearance of activated or senescent platelets. In contrast to other particulate substrates, the phagocytosis of platelets does not incite pro-inflammatory responses in vivo. This study assessed the contribution of macrophages and dendritic cells (DCs) to the clearance of activated platelets. Furthermore, we verified whether antibodies against the β2 Glycoprotein I (β2GPI), which bind to activated platelets, influence the phenomenon. DCs did not per se internalise activated platelets. In contrast, macrophages efficiently phagocytosed platelets. In agreement with the uneventful nature of the clearance of platelets in vivo, phagocytosing macrophages did not release IL-1β, TNF-α or IL-10. β2GPI bound to activated platelets and was required for their recognition by anti-ββ2GPI antibodies. DCs internalised platelets opsonised by anti-ββ2GPI antibodies. The phagocytosis of opsonised platelets determined the release of TNF-α and IL-1β by DCs and macrophages. Phagocytosing macrophages, but not DCs, secreted the antiinflammatory cytokine IL-1β0. We conclude that anti-ββ2GPI antibodies cause inflammation during platelet clearance and shuttle platelet antigens to antigen presenting DCs.

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Punicalagin Prevents Inflammation in LPS-Induced RAW264.7 Macrophages by Inhibiting FoxO3a/Autophagy Signaling Pathway

Nutrients ◽

10.3390/nu11112794 ◽

2019 ◽

Vol 11 (11) ◽

pp. 2794 ◽

Cited By ~ 8

Author(s):

Cao ◽

Chen ◽

Ren ◽

Zhang ◽

Tan ◽

...

Keyword(s):

Western Blot ◽

Signaling Pathway ◽

Inflammatory Cytokines ◽

Blot Analysis ◽

Western Blot Analysis ◽

Inflammatory Responses ◽

Raw264.7 Macrophages ◽

Tnf Α ◽

Autophagy Inhibition ◽

Pro Inflammatory Cytokines

Punicalagin, a hydrolysable tannin of pomegranate juice, exhibits multiple biological effects, including inhibiting production of pro-inflammatory cytokines in macrophages. Autophagy, an intracellular self-digestion process, has been recently shown to regulate inflammatory responses. In this study, we investigated the anti-inflammatory potential of punicalagin in lipopolysaccharide (LPS) induced RAW264.7 macrophages and uncovered the underlying mechanisms. Punicalagin significantly attenuated, in a concentration-dependent manner, LPS-induced release of NO and decreased pro-inflammatory cytokines TNF-α and IL-6 release at the highest concentration. We found that punicalagin inhibited NF-κB and MAPK activation in LPS-induced RAW264.7 macrophages. Western blot analysis revealed that punicalagin pre-treatment enhanced LC3II, p62 expression, and decreased Beclin1 expression in LPS-induced macrophages. MDC assays were used to determine the autophagic process and the results worked in concert with Western blot analysis. In addition, our observations indicated that LPS-induced releases of NO, TNF-α, and IL-6 were attenuated by treatment with autophagy inhibitor chloroquine, suggesting that autophagy inhibition participated in anti-inflammatory effect. We also found that punicalagin downregulated FoxO3a expression, resulting in autophagy inhibition. Overall these results suggested that punicalagin played an important role in the attenuation of LPS-induced inflammatory responses in RAW264.7 macrophages and that the mechanisms involved downregulation of the FoxO3a/autophagy signaling pathway.

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