scholarly journals Faculty Opinions recommendation of Inhibition of aquaporin-3 in macrophages by a monoclonal antibody as potential therapy for liver injury.

2021 ◽  
Author(s):  
Wendy Bollag
Keyword(s):  
Monoclonal Antibody ◽  
Liver Injury ◽  
Aquaporin 3

scholarly journals Inhibition of aquaporin-3 in macrophages by a monoclonal antibody as potential therapy for liver injury

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Mariko Hara-Chikuma ◽  
Manami Tanaka ◽  
Alan S. Verkman ◽  
Masato Yasui
Keyword(s):  
Monoclonal Antibody ◽  
Liver Injury ◽  
Macrophage Activation ◽  
Cell Activation ◽  
Stellate Cell ◽  
Nuclear Factor Κb ◽  
Activated Macrophages ◽  
Aquaporin 3 ◽  
Glycerol Transport ◽  
Water Glycerol

Abstract Aquaporin 3 (AQP3) is a transporter of water, glycerol and hydrogen peroxide (H2O2) that is expressed in various epithelial cells and in macrophages. Here, we developed an anti-AQP3 monoclonal antibody (mAb) that inhibited AQP3-facilitated H2O2 and glycerol transport, and prevented liver injury in experimental animal models. Using AQP3 knockout mice in a model of liver injury and fibrosis produced by CCl4, we obtained evidence for involvement of AQP3 expression in nuclear factor-κB (NF-κB) cell signaling, hepatic oxidative stress and inflammation in macrophages during liver injury. The activated macrophages caused stellate cell activation, leading to liver injury, by a mechanism involving AQP3-mediated H2O2 transport. Administration of an anti-AQP3 mAb, which targeted an extracellular epitope on AQP3, prevented liver injury by inhibition of AQP3-mediated H2O2 transport and macrophage activation. These findings implicate the involvement of macrophage AQP3 in liver injury, and provide evidence for mAb inhibition of AQP3-mediated H2O2 transport as therapy for macrophage-dependent liver injury.

Attenuation of Ischemic liver injury in monkeys by anti-LFA1 monoclonal antibody therapy

1999 ◽  
Vol 67 (7) ◽  
pp. S31
Author(s):  
J. Klupp ◽  
G. Puhl ◽  
J. Tiollier ◽  
C. Radke ◽  
C. Lojewski ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Liver Injury ◽  
Antibody Therapy ◽  
Monoclonal Antibody Therapy

scholarly journals Overexpression of Interleukin-15 Increases Susceptibility to Lipopolysaccharide-Induced Liver Injury in Mice Primed with Mycobacterium bovis Bacillus Calmette-Guérin

2004 ◽  
Vol 72 (7) ◽  
pp. 3855-3862 ◽  
Author(s):  
Toshiki Yajima ◽  
Hitoshi Nishimura ◽  
Kimika Saito ◽  
Hiroyuki Kuwano ◽  
Yasunobu Yoshikai
Keyword(s):  
Monoclonal Antibody ◽  
T Cells ◽  
Liver Injury ◽  
Mycobacterium Bovis ◽  
Bystander Activation ◽  
Highly Sensitive ◽  
Interleukin 15 ◽  
Ifn Γ

ABSTRACT Mice primed with Mycobacterium bovis bacillus Calmette-Guérin (BCG) are highly sensitive to lipopolysaccharide (LPS)-induced liver injury and lethality. We found that interleukin-15 (IL-15) transgenic (Tg) mice primed with BCG were more susceptible to LPS-induced liver injury than non-Tg mice. The numbers of CD44+ CD8+ T cells expressing intracellular gamma interferon (IFN-γ) significantly increased in the livers of BCG-primed IL-15 Tg mice after LPS injection, and the depletion of CD8+ T cells from BCG-primed IL-15 Tg mice completely abolished the susceptibility to LPS-induced lethality. Liver T cells from BCG-primed IL-15 Tg mice produced IFN-γ in vitro in response to LPS, which was inhibited by the addition of anti-IL-12 monoclonal antibody (MAb). In vivo treatment with anti-IL-12 MAb inhibited the appearance of CD44+ CD8+ T cells expressing intracellular IFN-γ after LPS injection. These results suggest that the overexpression of IL-15 increases susceptibility to LPS-induced liver injury in BCG-primed mice via bystander activation of CD8+ T cells.

scholarly journals Orally administered anti-eotaxin-1 monoclonal antibody is biologically active in the gut and alleviates immune-mediated hepatitis: A novel anti-inflammatory personalized therapeutic approach

2021 ◽  
Vol 35 ◽  
pp. 205873842110212
Author(s):  
Tawfik Khoury ◽  
Dory Rotnemer-Golinkin ◽  
Lidya Zolotarev ◽  
Yaron Ilan
Keyword(s):  
Monoclonal Antibody ◽  
Biological Activity ◽  
Liver Injury ◽  
Oral Administration ◽  
Serum Levels ◽  
Liver Disorder ◽  
Vital Role ◽  
Biologically Active ◽  
Immunomodulatory Effect ◽  
Immune Mediated

Personalized therapies are designed to optimize the safety-to-efficacy ratio by selecting patients with higher response rates based on specific biomarkers. Inflammation plays a vital role in the pathogenesis of non-alcoholic steatohepatitis (NASH), a common liver disorder. Eotaxin-1 plays a role in innate and adaptive immune responses. High eotaxin-1 levels are associated with diabetes and fatty liver disease and, therefore, serves as a biomarker for patient selection. The anti-eotaxin-1 monoclonal antibody is tailored for the personalized therapy of patients with inflammatory conditions due to high levels of eotaxin-1. To evaluate the biological activity and immunomodulatory effect of orally administered anti-eotaxin-1. C57B1/6 mice were treated with either oral or intra-peritoneal anti-eotaxin-1 antibody before induction of immune-mediated hepatitis using an injection of concanavalin A (ConA) and checked for liver injury and eotaxin-1 serum levels. Oral administration of anti-eotaxin-1 alleviated the immune-mediated liver injury. Serum alanine aminotransferase levels decreased to 1807 U/L, compared with 19025 U/L in untreated controls and 3657 U/L in mice treated with parenteral anti-eotaxin-1 ( P < 0.005). A trend toward reduced serum eotaxin-1 levels was observed in treated mice, ranging from 594 pg/mL in the controls to 554 and 561 pg/mL in mice treated orally and intraperitoneally ( P = 0.08, P = 0.06, respectively). Oral administration of anti-eotaxin-1 antibody shows biological activity in the gut and exerts a systemic immunomodulatory effect to alleviate immune-mediated hepatitis. The data suggest that testing for eotaxin-1 serum levels may enable screening patients with high-eotaxin-1 levels-associated NASH.

THE F(ab???)2 FRAGMENT OF AN ANTI-ICAM-1 MONOCLONAL ANTIBODY ATTENUATES LIVER INJURY AFTER ORTHOTOPIC LIVER TRANSPLANTATION1

1996 ◽  
Vol 61 (1) ◽  
pp. 99-104 ◽  
Author(s):  
Yoshiya Nishimura ◽  
Yoshiyuki Takei ◽  
Sunao Kawano ◽  
Moritaka Goto ◽  
Kouichi Nagano ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Liver Injury

A novel CCL24 blocking monoclonal antibody ameliorates liver injury in experimental models of cholestasis

2018 ◽  
Vol 68 ◽  
pp. S451-S452
Author(s):  
M. Segal ◽  
A. Katav ◽  
S. Hashmueli ◽  
A. Aharon ◽  
M. Pinzani ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Liver Injury ◽  
Experimental Models

Effects of Steroids on Fetal Rat Liver

1969 ◽  
Vol 27 ◽  
pp. 350-351
Author(s):  
F. G. Zaki
Keyword(s):  
Liver Injury ◽  
Rat Liver ◽  
Fetal Liver ◽  
Dosage Level ◽  
Maternal Plasma ◽  
Methyl Prednisolone ◽  
Fetal Rat ◽  
Toxic Agents ◽  
Fetal Rat Liver ◽  
Neonatal Liver

Fetal and neonatal liver injury induced by agents circulating in maternal plasma, even though well recognized, its morphological manifestations are not yet established. As part of our studies of fetal and neonatal liver injury induced by maternal nutritional disorders, metabolic impairment and toxic agents, the effects of two anti-inflammatory steroids have been recently inves tigated.Triamcinolone and methyl prednisolone were injected each in a group of rats during pregnancy at a-dosage level of 2 mgm three times a week. Fetal liver was studied at 18 days of gestation. Litter size and weight markedly decreased than those of control rats. Stillbirths and resorption were of higher incidence in the triamcinolone group than in those given the prednisolone.

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