scholarly journals Dibutyltin alters immune cell production of the pro‐inflammatory cytokines interleukin (IL) 1β and IL‐6: role of mitogen‐activated protein kinases and changes in mRNA

2020 ◽  
Vol 40 (8) ◽  
pp. 1047-1059
Author(s):  
Linda Sushak ◽  
Sahra Gabure ◽  
JaQuel Maise ◽  
Jessica Arnett ◽  
Margaret M. Whalen
Keyword(s):  
Protein Kinases ◽  
Inflammatory Cytokines ◽  
Immune Cell ◽  
Mitogen Activated Protein Kinases ◽  
Cell Production ◽  
Mitogen Activated Protein ◽  
Pro Inflammatory Cytokines

scholarly journals Cell Intrinsic Roles of Apoptosis-Associated Speck-Like Protein in Regulating Innate and Adaptive Immune Responses

2011 ◽  
Vol 11 ◽  
pp. 2418-2423 ◽  
Author(s):  
Hoda Hassan ◽  
Amal O. Amer
Keyword(s):  
Immune Responses ◽  
Protein Kinases ◽  
Inflammatory Cytokines ◽  
Adaptor Protein ◽  
Adaptive Immune Responses ◽  
Mitogen Activated Protein Kinases ◽  
Adaptive Immune ◽  
Mitogen Activated Protein ◽  
Intrinsic Roles

The role of apoptosis-associated speck-Like protein (ASC) in the assembly of the inflammasome complex within macrophages has been elucidated in several studies. In this particular role, ASC functions as an adaptor protein by linking nod-like receptors (NLRs) and procaspase-1, thereby leading to the activation of caspase-1 to cleave inflammatory cytokines IL-1βand IL-18 and inducing pyroptosis. It has been noted that ASC maintains inflammasome-independent roles, including but not limited to controlling the expression of Dock2 and mitogen-activated protein kinases (MAPK/ERK2) and regulating the NF-κB pathway. This paper will emphasize the major roles of ASC during pathogen infection, the mechanisms by which it mediates inflammation, and discuss its more recently discovered functions.

scholarly journals Role of Mitogen-Activated Protein Kinases and NF-κB in the Regulation of Proinflammatory and Anti-Inflammatory Cytokines by Porphyromonas gingivalis Hemagglutinin B

2005 ◽  
Vol 73 (7) ◽  
pp. 3990-3998 ◽  
Author(s):  
Ping Zhang ◽  
Michael Martin ◽  
Suzanne M. Michalek ◽  
Jannet Katz
Keyword(s):  
Signaling Pathways ◽  
Protein Kinases ◽  
Porphyromonas Gingivalis ◽  
Inflammatory Cytokines ◽  
Mitogen Activated Protein Kinases ◽  
Mitogen Activated Protein ◽  
Ifn Γ ◽  
Anti Inflammatory ◽  
Stimulation Of

ABSTRACT Hemagglutinin B (HagB) is a nonfimbrial adhesin expressed on the surface of Porphyromonas gingivalis and has been implicated as a potential virulence factor involved in mediating the attachment of the bacteria to host cells. However, the molecular mechanisms underlying host responses to HagB and their roles in pathogenesis have yet to be elucidated. Mitogen-activated protein kinases (MAPKs) are activated following engagement of a variety of cell surface receptors via dual tyrosine and threonine phosphorylation and are thought to be involved in various cellular responses. The purpose of this study was to determine the role of intracellular signaling pathways including the MAPKs and NF-κB in regulating the production of proinflammatory and anti-inflammatory cytokines following stimulation of murine macrophages with recombinant HagB (rHagB). Stimulation of peritoneal macrophages with rHagB resulted in the production of the proinflammatory cytokines interleukin-12p40 (IL-12p40), gamma interferon (IFN-γ), and tumor necrosis factor alpha, as well as the anti-inflammatory cytokine IL-10. We also demonstrated the activation of extracellular signal-related kinase (ERK), c-Jun NH2-terminal protein kinase (JNK), and p38 MAPKs by rHagB-stimulated macrophages. Furthermore, blocking of the ERK and p38 signaling pathways by using specific inhibitors revealed differential regulatory roles in the rHagB-mediated production of proinflammatory and anti-inflammatory cytokines. ERK and p38 were important in down-regulation of IL-12p40 and IFN-γ production and up-regulation of IL-10 production. The enhanced levels of IL-12p40 in rHagB-stimulated macrophages by inhibition of ERK or p38 activity were partially attributable to the inhibition of IL-10 production. Moreover, NF-κB was found to be critical for up-regulation of IL-12p40 and down-regulation of IL-10 production in rHagB-stimulated macrophages. Taken together, our results demonstrate a role for the p38 and ERK pathways and the transcription factor NF-κB in modulating key immunoregulatory cytokines involved in the development of immune responses to P. gingivalis HagB.

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