Quiescent mouse peritoneal macrophages which phagocytose, and which respond to phagocytosis with a sudden elevation in hexose monophosphate shunt activity, immediately release into the medium oxygen metabolites, arachidonic acid oxygenation products, and lysosomal hydrolases. Such cells subsequently differentiate and acquire the properties of inflammatory macrophages. The latter process appears to be under the control of prostaglandin E2 and possibly other cyclooxygenase products which are formed as a consequence of phagocytosis and seem to act as feed-back inhibitors.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/S0171-2985(82)80094-6 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
CD47 Expression Defines Efficacy of Rituximab with CHOP in Non-Germinal Center B-cell (Non-GCB) Diffuse Large B-cell Lymphoma Patients (DLBCL), but Not in GCB DLBCL.
Cancer Immunol Res
October 2019
University of Groningen, University Medical Center Groningen, Department of Hematology, Groningen, the Netherlands.
Addition of rituximab (R) to "CHOP" (cyclophosphamide, doxorubicin, vincristine, and prednisone) chemotherapy improved outcome for diffuse large B-cell lymphoma (DLBCL) patients. Approximately 40% of patients who receive R-CHOP still succumb to disease due to intrinsic resistance or relapse. A potential negative regulator of DLBCL treatment outcome is the CD47 "don't eat me" immune checkpoint.
View Article and Find Full Text PDF[Immunotropic activity of panaxans--bioglycans isolated from ginseng].
Antibiot Khimioter
December 2001
Research Institute of Epidemiology and Microbiology, Siberian Branch of the Russian Academy of Medical Sciences, Pacific Institute of Bioorganic Chemistry, Far East Branch of the Russian Academy of Sciences, Vladivostok.
Immunomodulating activity of panaxanes--polysaccharides isolated from the roots and culture of Panax ginseng was studied. Effects of both preparations were analogous. Profilaxy use of panaxanes provided increased resistance to coli-sepsis in mice, increased neutrophiles and macrophages phagocytosis, stimulated humoral and cell immune factors and induced important regulating cytokins--interferone gamma and tumor necrosis factor.
View Article and Find Full Text PDFBactericidal/permeability-increasing protein promotes complement activation for neutrophil-mediated phagocytosis on bacterial surface.
Immunology
August 2001
Department of Hygienic Chemistry, Graduate School of Pharmaceutical Sciences, Hokkaido University, Sapporo, Japan.
The neutrophil bactericidal/permeability-increasing protein (BPI) has both bactericidal and lipopolysaccharide-neutralizing activities. The present study suggests that BPI also plays an important role in phagocytosis of Escherichia coli by neutrophils through promotion of complement activation on the bacterial surface. Flow cytometric analysis indicated that fluorescein-labelled E.
View Article and Find Full Text PDFBacterial phagocytosis activates extracellular signal-regulated kinase and p38 mitogen-activated protein kinase cascades in human neutrophils.
J Leukoc Biol
December 1998
Department of Medicine, University of Louisville Health Sciences Center, Veterans Affairs Medical Center, Kentucky, USA.
The hypothesis that bacterial phagocytosis by human polymorphonuclear neutrophils (PMNs) stimulates MAPK cascades that regulate respiratory burst activation was tested. Extracellular response kinase (ERK) and p38 kinase, but not c-Jun NH2-terminal kinase, activities were increased within 5 min of phagocytosis of plasma-opsonized Staphylococcus aureus (S-SA), reached maximum at 20-30 min, and remained elevated through 60 min. The role of Fcy receptors was examined using gamma globulin-opsonized SA (IgG-SA), whereas CR3 receptors were activated by particulate beta-glucan.
View Article and Find Full Text PDFDefective neutrophil function in the autoimmune mouse strain MRL/lpr. Potential role of transforming growth factor-beta.
J Immunol
June 1991
Research Service, Harry S Truman VA Medical Center, Columbia, MO 65201.
Patients with systemic autoimmune diseases such as SLE and rheumatoid arthritis have increased rates of morbidity and mortality caused by infection. Although this increased risk of infection has been primarily attributed to therapeutic immuno-suppression, some reports exist of defective polymorphonuclear leukocytes (PMN) function in these patients. The purpose of the present work is to investigate the recruitment of PMN phagocytic function in a murine model of autoimmunity, the MRL/lpr mouse.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!