scholarly journals Kupffer Cells Interact With Hepatitis B Surface Antigen In Vivo and In Vitro, Leading to Proinflammatory Cytokine Production and Natural Killer Cell Function

2014 ◽  
Vol 211 (8) ◽  
pp. 1268-1278 ◽  
Author(s):  
Arjan Boltjes ◽  
Nadine van Montfoort ◽  
Paula J. Biesta ◽  
Marjoleine L. Op den Brouw ◽  
Jaap Kwekkeboom ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Proinflammatory Cytokine ◽  
Cytokine Production ◽  
Cell Function ◽  
Hepatitis B Surface Antigen ◽  
Killer Cell ◽  
Proinflammatory Cytokine Production ◽  
Natural Killer Cell Function

scholarly journals Renal Transplant Immunosuppression Impairs Natural Killer Cell Function In Vitro and In Vivo

PLoS ONE ◽  
2010 ◽  
Vol 5 (10) ◽  
pp. e13294 ◽  
Author(s):  
Olivier Morteau ◽  
Samkeliso Blundell ◽  
Aron Chakera ◽  
Sophia Bennett ◽  
Charita M. Christou ◽  
...  
Keyword(s):  
Renal Transplant ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Cell Function ◽  
Killer Cell ◽  
Natural Killer Cell Function

scholarly journals In-vivo administration of histone deacetylase inhibitors does not impair natural killer cell function in HIV+ individuals

AIDS ◽  
2019 ◽  
Vol 33 (4) ◽  
pp. 605-613 ◽  
Author(s):  
Carolina Garrido ◽  
Martin Tolstrup ◽  
Ole S. Søgaard ◽  
Thomas A. Rasmussen ◽  
Brigitte Allard ◽  
...  
Keyword(s):  
Natural Killer Cell ◽  
Natural Killer ◽  
Histone Deacetylase ◽  
Histone Deacetylase Inhibitors ◽  
Cell Function ◽  
Killer Cell ◽  
Natural Killer Cell Function ◽  
In Vivo Administration

scholarly journals Abnormal Natural Killer Cell Function in Systemic Sclerosis: Altered Cytokine Production and Defective Killing Activity

2005 ◽  
Vol 125 (4) ◽  
pp. 731-737 ◽  
Author(s):  
Mayuka Horikawa ◽  
Minoru Hasegawa ◽  
Kazuhiro Komura ◽  
Ikuko Hayakawa ◽  
Koichi Yanaba ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Natural Killer Cell ◽  
Natural Killer ◽  
Cytokine Production ◽  
Cell Function ◽  
Killer Cell ◽  
Natural Killer Cell Function ◽  
Killing Activity

scholarly journals Corticotropin-Releasing Hormone Augments Proinflammatory Cytokine Production from Macrophages In Vitro and in Lipopolysaccharide-Induced Endotoxin Shock in Mice

2002 ◽  
Vol 70 (11) ◽  
pp. 6068-6074 ◽  
Author(s):  
Sofia Agelaki ◽  
Christos Tsatsanis ◽  
Achille Gravanis ◽  
Andrew N. Margioris
Keyword(s):  
Proinflammatory Cytokine ◽  
Cytokine Production ◽  
Endotoxin Shock ◽  
Proinflammatory Cytokine Production ◽  
Corticotropin Releasing Hormone ◽  
Necrosis Factor Alpha ◽  
Releasing Hormone ◽  
Tnf Α

ABSTRACT Corticotropin-releasing hormone (CRH) exerts an anti-inflammatory effect indirectly, via cortisole production, and a proinflammatory effect directly on immune cells. The aim of the present work was to examine the effect of CRH on macrophage-derived cytokines both in vitro and in vivo. For the in vitro experiments we used two types of macrophages: (i) the RAW264.7 monocyte/macrophage cell line and (ii) thioglycolate-elicited peritoneal macrophages from BALB/c mice. We have found that CRH enhanced lipopolysaccharide (LPS)-induced tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), and IL-6 production. For the in vivo experiments we have used the LPS-induced endotoxin shock model in BALB/c mice, an established model for systemic inflammation in which macrophages are the major source of the proinflammatory cytokines responsible for the development of the shock. Administration of antalarmin, a synthetic CRH receptor 1 (CRHR1) antagonist, prior to LPS prolonged survival in a statistically significant manner. The effect was more evident at the early stages of endotoxin shock. CRHR1 blockade suppressed LPS-induced elevation of the macrophage-derived cytokines TNF-α, IL-1β, and IL-6, confirming the role of CRH signals in cytokine expression. In conclusion, our data suggest that CRH signals play an early and crucial role in augmenting LPS-induced proinflammatory cytokine production by macrophages. Our data suggest that the diffuse neuroendocrine system via CRH directly affects the immune system at the level of macrophage activation and cytokine production.

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