Bovine LF (bLF) at concentrations in the range of 50-250 micrograms/ml enhanced the phagocytic activity of human neutrophils as determined by measuring the incorporation of FITC-labeled latex beads by flow cytometry. The stimulatory effect of bLF was not abrogated by hydrolysis with pepsin. Bovine lactoferricin (bLFcin), which is a bactericidal fragment purified from a pepsin hydrolysate of bLF (bLFH), also enhanced the phagocytic activity, whereas, in contrast, the fraction of bLFH depleted of bLFcin showed no stimulatory effect. The phagocytosis-enhancing activity of bLF still remained after washing the neutrophils, following exposure to bLF. Also, bLF pretreatment of the latex beads stimulated their uptake. These results demonstrate that bLF is effective in promoting the phagocytic activity of human neutrophils. This activity appears to be due to its bLFcin domain and may involve dual mechanisms of direct binding to neutrophils and opsonin-like activity.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1006/cimm.1997.1246 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
SPeak to the heart.
Immunity
March 2025
Pediatric Translational Medicine Institute and Pediatric Congenital Heart Disease Institute, Shanghai Children's Medical Center, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China; Shanghai Collaborative Innovative Center of Intelligent Medical Device and Active Health, Shanghai University of Medicine & Health Sciences, Shanghai 201318, China. Electronic address:
Neuroimmune regulation modulates responses to cardiovascular stress and injury. In this issue of Immunity, Perrotta et al. delineate a heart-brain-spleen axis that induces adaptive cardiac remodeling in response to pressure overload, highlighting a SPeak mechanism (spleen-derived PlGF efflux activates cardiac macrophages).
View Article and Find Full Text PDFThe neurorepellent SLIT2 inhibits LPS-induced proinflammatory signaling in macrophages.
J Immunol
January 2025
Program in Cell Biology, The Hospital for Sick Children, Toronto, ON, Canada.
Macrophages are important mediators of immune responses with critical roles in the recognition and clearance of pathogens, as well as in the resolution of inflammation and wound healing. The neuronal guidance cue SLIT2 has been widely studied for its effects on immune cell functions, most notably directional cell migration. Recently, SLIT2 has been shown to directly enhance bacterial killing by macrophages, but the effects of SLIT2 on inflammatory activation of macrophages are less known.
View Article and Find Full Text PDFLipin-1 restrains macrophage lipid synthesis to promote inflammation resolution.
J Immunol
January 2025
Department of Microbiology and Immunology, Louisiana State University Health Sciences Center, Shreveport, LA, United States.
Macrophages are critical to maintaining and restoring tissue homeostasis during inflammation. The lipid metabolic state of macrophages influences their function and polarization, which is crucial to the resolution of inflammation. The contribution of lipid synthesis to proinflammatory macrophage responses is well understood.
View Article and Find Full Text PDFPlasmacytoid dendritic cell sensing of African swine fever virus-infected macrophages results in STING-dependent robust interferon-α production.
J Immunol
January 2025
Institute of Virology and Immunology, Mittelhäusern, Switzerland.
While several African swine fever virus (ASFV)-encoded proteins potently interfere with the cGAS-STING (cyclic GMP-AMP synthetase-stimulator of interferon genes) pathway at different levels to suppress interferon (IFN) type I production in infected macrophages, systemic IFN-α is induced during the early stages of AFSV infection in pigs. The present study elucidates a mechanism by which such responses can be triggered, at least in vitro. We demonstrate that infection of monocyte-derived macrophages (MDMs) by ASFV genotype 2 strains is highly efficient but immunologically silent with respect to IFN type I, IFN-stimulated gene induction, and tumor necrosis factor production.
View Article and Find Full Text PDFA human histidyl-tRNA synthetase splice variant therapeutic targets NRP2 to resolve lung inflammation and fibrosis.
Sci Transl Med
March 2025
Department of Molecular Medicine, Scripps Research Institute, La Jolla, CA 92037, USA.
Interstitial lung disease (ILD) consists of a group of immune-mediated disorders that can cause inflammation and progressive fibrosis of the lungs, representing an area of unmet medical need given the lack of disease-modifying therapies and toxicities associated with current treatment options. Tissue-specific splice variants (SVs) of human aminoacyl-tRNA synthetases (aaRSs) are catalytic nulls thought to confer regulatory functions. One example from human histidyl-tRNA synthetase (HARS), termed HARS because the splicing event resulted in a protein encompassing the WHEP-TRS domain of HARS (a structurally conserved domain found in multiple aaRSs), is enriched in human lung and up-regulated by inflammatory cytokines in lung and immune cells.
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!