Parainfluenza Virus Type 1 Induces Epithelial IL-8 Production via p38-MAPK Signalling

Morales, Miguel A.; Gutiérrez, Carlos Cabello; Nepomuceno, Fidencio Mejía; Peralta, Leticia Valle; Maqueda, Elba Valencia; Zavala, María Eugenia Manjarrez

doi:10.1155/2014/515984

Cited by 10 publications

(7 citation statements)

References 45 publications

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“…As shown in Figure 6 , PM alone triggered the activation of ERK and JNK by 1.6 and 1.2 folds (both p < 0.05) respectively compared to untreated control, whereas p38 was not affected. Moreover, we detected 46 kDa isoform of p-JNK in MLE-12 cells as observed similarly by Morales et al, 2014 [ 22 ] in A549 lung epithelial cells. Interestingly, however, MC dose dependently inhibited the phosphorylation of ERK (by 1.4-fold at 31.3 μg/mL and by 1.7-fold at 62.5 μg/mL, respectively (both p < 0.05)) and JNK (by 1.4-fold at 31.3 and 62.5 μg/mL, respectively (both p < 0.05)) to the level similar in untreated control, validating MC’s potential in suppressing PM-triggered MAPK signaling by repressing ERK and JNK.…”

Section: Resultssupporting

confidence: 89%

Mojabanchromanol Isolated from Sargassum horneri Attenuates Particulate Matter Induced Inflammatory Responses via Suppressing TLR2/4/7-MAPK Signaling in MLE-12 Cells

et al. 2020

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Chromanols from marine algae are studied for drug development due to its prominent bioactive properties, and mojabanchromanol (MC), a chromanol isolated from a brown algae Sargassum horneri, is found to possess anti-oxidant potential. In this study, we hypothesized MC may attenuate particulate matter (PM)-induced and reactive oxygen species (ROS)-mediated inflammatory responses in airways and tried to identify its potential and underlying mechanism against PM (majority <2.5 µm in diameter)-induced inflammatory responses in a lung type II alveolar epithelial cell line, MLE-12. MC attenuated PM-induced malondialdehyde (MDA), a lipid peroxidation end product, and 8-hydroxydeoxyguanosine (8-OHdG), the most representative DNA oxidative damage product, further validating MC’s potential in attenuating PM-induced oxidative stress. MC also suppressed PM-triggered TLR2/4/7 activation in MLE-12 cells. Moreover, MC reduced ROS-mediated phosphorylation of mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase 1/2 (Erk1/2) and c-Jun NH (2)-terminal kinase (JNK) that were also activated in PM exposed cells. MC further inhibited the secretion of pro-inflammatory cytokines (IL-6, IL-1β and IL-33) in MLE-12 cells exposed to PM. These results provide a clear evidence for MC’s potential in attenuating PM-triggered inflammatory responses in MLE-12 cells via repressing TLR2/4/7 and MAPK signaling. Therefore, MC can be developed as a therapeutic agent against PM induced airway inflammatory responses.

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Section: Resultssupporting

confidence: 89%

Mojabanchromanol Isolated from Sargassum horneri Attenuates Particulate Matter Induced Inflammatory Responses via Suppressing TLR2/4/7-MAPK Signaling in MLE-12 Cells

et al. 2020

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“…Inhibitors of p38 have also been used to highlight its importance in inflammatory cytokine production in response to other respiratory viruses. Treatment of A549 cells with SB203580 decreased release of CCL5 in response to RSV infection, and CXCL8 in response to parainfluenza virus infection [29,30]. Supporting this, inhibition of p38 in primary bronchial epithelial cells reduced mRNA production of IL-1β and TNF-α in response to RSV infection [31].…”

Section: The Epithelial Response To Respiratory Viral Infectionmentioning

confidence: 96%

Emerging Regulatory Roles of Dual-Specificity Phosphatases in Inflammatory Airway Disease

Manley

Parker

Zhang

2019

IJMS

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Inflammatory airway disease, such as asthma and chronic obstructive pulmonary disease (COPD), is a major health burden worldwide. These diseases cause large numbers of deaths each year due to airway obstruction, which is exacerbated by respiratory viral infection. The inflammatory response in the airway is mediated in part through the MAPK pathways: p38, JNK and ERK. These pathways also have roles in interferon production, viral replication, mucus production, and T cell responses, all of which are important processes in inflammatory airway disease. Dual-specificity phosphatases (DUSPs) are known to regulate the MAPKs, and roles for this family of proteins in the pathogenesis of airway disease are emerging. This review summarizes the function of DUSPs in regulation of cytokine expression, mucin production, and viral replication in the airway. The central role of DUSPs in T cell responses, including T cell activation, differentiation, and proliferation, will also be highlighted. In addition, the importance of this protein family in the lung, and the necessity of further investigation into their roles in airway disease, will be discussed.

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“…Our analysis also identified many enzymes involved in nucleic acid metabolism and energy production, such as DEAD box helicases. Kinases identified as uniquely phosphorylated during IAV infection included mitogen-activated protein kinases (MAPKs), as well as several members of CDK, Ca 2ϩ /calmodulin-dependent kinase (CaMK) and cAMP-dependent protein kinase (PKA) families, which are known to be activated by various viruses (45)(46)(47)(48)(49). Transporters are involved in the movement of ions, small molecules, or macromolecules across biological membranes.…”

Section: Phosphoproteomic Analysis Of Influenza Infectionmentioning

confidence: 99%

Phosphoproteomics to Characterize Host Response During Influenza A Virus Infection of Human Macrophages

Söderholm

Kainov

Öhman

et al. 2016

Molecular & Cellular Proteomics

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Influenza A viruses cause infections in the human respiratory tract and give rise to annual seasonal outbreaks, as well as more rarely dreaded pandemics. Influenza A viruses become quickly resistant to the virus-directed antiviral treatments, which are the current main treatment options. A promising alternative approach is to target host cell factors that are exploited by influenza viruses. To this end, we characterized the phosphoproteome of influenza A virus infected primary human macrophages to elucidate the intracellular signaling pathways and critical host factors activated upon influenza infection. We identified 1675 phosphoproteins, 4004 phosphopeptides and 4146 nonredundant phosphosites. The phosphorylation of 1113 proteins (66%) was regulated upon infection, highlighting the importance of such global phosphoproteomic profiling in primary cells. Notably, 285 of the identified phosphorylation sites have not been previously described in publicly available phosphorylation databases, despite many published large-scale phosphoproteome studies using human and mouse cell lines. Systematic bioinformatics analysis of the phosphoproteome data indicated that the phosphorylation of proteins involved in the ubiquitin/proteasome pathway (such as TRIM22 and TRIM25) and antiviral responses (such as MAVS) changed in infected macrophages. Proteins known to play roles in small GTPase-, mitogen-activated protein kinase-, and cyclin-dependent kinase- signaling were also regulated by phosphorylation upon infection. In particular, the influenza infection had a major influence on the phosphorylation profiles of a large number of cyclin-dependent kinase substrates. Functional studies using cyclin-dependent kinase inhibitors showed that the cyclin-dependent kinase activity is required for efficient viral replication and for activation of the host antiviral responses. In addition, we show that cyclin-dependent kinase inhibitors protect IAV-infected mice from death. In conclusion, we provide the first comprehensive phosphoproteome characterization of influenza A virus infection in primary human macrophages, and provide evidence that cyclin-dependent kinases represent potential therapeutic targets for more effective treatment of influenza infections.

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Parainfluenza Virus Type 1 Induces Epithelial IL-8 Production via p38-MAPK Signalling

Cited by 10 publications

References 45 publications

Mojabanchromanol Isolated from Sargassum horneri Attenuates Particulate Matter Induced Inflammatory Responses via Suppressing TLR2/4/7-MAPK Signaling in MLE-12 Cells

Mojabanchromanol Isolated from Sargassum horneri Attenuates Particulate Matter Induced Inflammatory Responses via Suppressing TLR2/4/7-MAPK Signaling in MLE-12 Cells

Emerging Regulatory Roles of Dual-Specificity Phosphatases in Inflammatory Airway Disease

Phosphoproteomics to Characterize Host Response During Influenza A Virus Infection of Human Macrophages

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