scholarly journals Impact of class A, B and C CpG-oligodeoxynucleotides on in vitro activation of innate immune cells in human immunodeficiency virus-1 infected individuals

Immunology ◽  
2007 ◽  
Vol 120 (4) ◽  
pp. 526-535 ◽  
Author(s):  
Jeffrey A. Martinson ◽  
Allan R. Tenorio ◽  
Carlos J. Montoya ◽  
Lena Al-Harthi ◽  
Carolyne N. Gichinga ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Immune Cells ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Cpg Oligodeoxynucleotides ◽  
Class A ◽  
Immunodeficiency Virus ◽  
In Vitro Activation ◽  
Human Immunodeficiency Virus 1

scholarly journals Oral Exposure to House Dust Mite Activates Intestinal Innate Immunity

Foods ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 561
Author(s):  
Sara Benedé ◽  
Leticia Pérez-Rodríguez ◽  
Mónica Martínez-Blanco ◽  
Elena Molina ◽  
Rosina López-Fandiño
Keyword(s):  
House Dust ◽  
House Dust Mite ◽  
Immune Cells ◽  
Oral Route ◽  
Innate Immune ◽  
Oral Exposure ◽  
Lymphoid Tissues ◽  
Innate Immune Cells ◽  
Dust Mite

Scope: House dust mite (HDM) induces Th2 responses in lungs and skin, but its effects in the intestine are poorly known. We aimed to study the involvement of HDM in the initial events that would promote sensitization through the oral route and eventually lead to allergy development. Methods and results: BALB/c mice were exposed intragastrically to proteolytically active and inactive HDM, as such, or in combination with egg white (EW), and inflammatory and type 2 responses were evaluated. Oral administration of HDM, by virtue of its proteolytic activity, promoted the expression, in the small intestine, of genes encoding tight junction proteins, proinflammatory and Th2-biasing cytokines, and it caused expansion of group 2 innate immune cells, upregulation of Th2 cytokines, and dendritic cell migration and activation. In lymphoid tissues, its proteolytically inactivated counterpart also exerted an influence on the expression of surface DC molecules involved in interactions with T cells and in Th2 cell differentiation, which was confirmed in in vitro experiments. However, in our experimental setting we did not find evidence for the promotion of sensitization to coadministered EW. Conclusion: Orally administered HDM upregulates tissue damage factors and also acts as an activator of innate immune cells behaving similarly to potent oral Th2 adjuvants.

Abstract 1772: Cardiomyocyte Damage-Released S100A1 Protein Evokes A Proinflammatory Phenotype In Cardiac Fibroblasts

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
David Rohde ◽  
Melanie Boerries ◽  
Herzog Nicole ◽  
Gang Qiu ◽  
Philipp Ehlermann ◽  
...  
Keyword(s):  
Western Blotting ◽  
Immune Cells ◽  
Nuclear Translocation ◽  
Cardiac Fibroblasts ◽  
Innate Immune ◽  
Host Cells ◽  
Boyden Chamber ◽  
Innate Immune Cells ◽  
Danger Signal

Background: S100A1, a cardiomyocyte specific inotropic calcium sensor protein, is released from infarcted human myocardium in the extracellular environment and circulation, reaching peak serum levels (1–2 μM) 8–9 hours after clinical onset. As growing evidence indicates that S100 proteins can act as pre-existing danger signals triggering the innate immune system into action upon release from injured host cells, we hypothesized that damage-released S100A1 can act as a cardiac danger signal alerting innate immune cells. Methods and Results: Here we report for the first time that necrotic cardiomyocytes release S100A1 protein in vitro, which is exclusively internalized by cardiac fibroblasts (CFs) in a clathrin- and caveolin-independent manner as shown by IF. Internalized S100A1 specifically activated MAPKs/SAPKs (p38, ERK1/2 and JNK) resulting in nuclear translocation of p65 (NF-kB) as assessed by Western blotting, EMSA and IF. In turn, S100A1 triggered an inflammatory gene program in CFs including enhanced expression of adhesion molecules, integrins, chemokines and cytokines including I-CAM, V-CAM, CD11b/18, IL1-alpha, MCP-1, TNF-alpha, SDF-1 among others as obtained by RT-PCR, Western blotting and ELISA. This resulted in enhanced chemoattraction and adhesion of monocytotic and stem cells to S100A1-activated CF as shown by Boyden-chamber and adhesion assays. In line with their proinflammatory transition, S100A1-activated CFs exhibited decreased collagen-1/-3 expression and de-novo collagen production, enhanced collagenolytic MMP-9 abundance and activity and increased levels of the antiangiogenic matricellular factor thrombospondin-2 reflecting extracellular matrix net degradation. Importantly, the immun-modulatory and antifibrotic actions of S100A1 protein in vitro were restricted to CFs, RAGE independent and occurred at concentrations (0.1–1 μM) that were found in patients after AMI. Conclusion: Our in vitro results indicate that S100A1 has the properties of a pre-exisiting endogenous cardiomyocyte danger signal transforming cardiac fibroblasts into immunmodulatory cells that might recruit innate immune cells to the site of cardiac injury and link cardiomyocyte damage to post-MI inflammation.

scholarly journals Hyperglycemic Memory of Innate Immune Cells Promotes In Vitro Proinflammatory Responses of Human Monocytes and Murine Macrophages

2021 ◽  
pp. ji1901348
Author(s):  
Kathrin Thiem ◽  
Samuel T. Keating ◽  
Mihai G. Netea ◽  
Niels P. Riksen ◽  
Cees J. Tack ◽  
...  
Keyword(s):  
Immune Cells ◽  
Innate Immune ◽  
Innate Immune Cells ◽  
Human Monocytes ◽  
Murine Macrophages ◽  
Proinflammatory Responses

scholarly journals Synergistic neurotoxicity of opioids and human immunodeficiency virus-1 Tat protein in striatal neurons in vitro

Neuroscience ◽  
2001 ◽  
Vol 102 (3) ◽  
pp. 555-563 ◽  
Author(s):  
J.A. Gurwell ◽  
A. Nath ◽  
Q. Sun ◽  
J. Zhang ◽  
K.M. Martin ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Tat Protein ◽  
Striatal Neurons ◽  
Immunodeficiency Virus ◽  
Human Immunodeficiency Virus 1

scholarly journals HIV-1LAI Nef blocks the development of hematopoietic stem/progenitor cells into myeloid-erythroid lineage cells

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Wei Zou ◽  
Juanjuan Xing ◽  
Shijie Zou ◽  
Mei Jiang ◽  
Xinping Chen ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Progenitor Cells ◽  
Cell Loss ◽  
Underlying Mechanism ◽  
Humanized Mice ◽  
Hematopoietic Stem ◽  
Immunodeficiency Virus ◽  
Hiv 1 ◽  
Human Immunodeficiency Virus 1

Abstract Background A variety of hematopoietic abnormalities are commonly seen in human immunodeficiency virus-1 (HIV-1) infected individuals despite antiviral therapy, but the underlying mechanism remains elusive. Nef plays an important role in HIV-1 induced T cell loss and disease progression, but it is not known whether Nef participates in other hematopoietic abnormalities associated with infection. Results In the current study we investigated the influence of HIV-1LAI Nef (LAI Nef) on the development of hematopoietic stem/progenitor cells (HSPCs) into myeloid-erythroid lineage cells, and found that nef expression in HSPCs blocked their differentiation both in vitro and in humanized mice reconstituted with nef-expressing HSPCs. Conclusions Our novel findings demonstrate LAI Nef compromised the development of myeloid-erythroid lineage cells, and therapeutics targeting Nef would be promising in correcting HIV-1 associated hematopoietic abnormalities.

scholarly journals Replication of the human immunodeficiency virus 1 and impaired differentiation of T cells after in vitro infection of bone marrow immature T cells.

1989 ◽  
Vol 83 (2) ◽  
pp. 610-615 ◽  
Author(s):  
Y Lunardi-Iskandar ◽  
M T Nugeyre ◽  
V Georgoulias ◽  
F Barré-Sinoussi ◽  
C Jasmin ◽  
...  
Keyword(s):  
Bone Marrow ◽  
Human Immunodeficiency Virus ◽  
T Cells ◽  
Immunodeficiency Virus ◽  
Human Immunodeficiency Virus 1
Sign in / Sign up

Export Citation Format

Share Document