scholarly journals Effect of salivary agglutination on oral streptococcal clearance by human polymorphonuclear neutrophil granulocytes

2016 ◽  
Vol 32 (3) ◽  
pp. 197-210 ◽  
Author(s):  
A. Itzek ◽  
Z. Chen ◽  
J. Merritt ◽  
J. Kreth
Keyword(s):  
Polymorphonuclear Neutrophil ◽  
Neutrophil Granulocytes ◽  
Human Polymorphonuclear Neutrophil

scholarly journals Characterization of the Priming Effect by Pituitary Canine Growth Hormone on Canine Polymorphonuclear Neutrophil Granulocyte Function

2000 ◽  
Vol 7 (2) ◽  
pp. 226-232 ◽  
Author(s):  
Thomas K. Petersen ◽  
C. Wayne Smith ◽  
Asger L. Jensen
Keyword(s):  
Growth Hormone ◽  
Priming Effect ◽  
Shape Change ◽  
Transendothelial Migration ◽  
Lower Surface ◽  
Polymorphonuclear Neutrophil ◽  
Neutrophil Granulocytes ◽  
Neutrophil Granulocyte ◽  
Microtiter Plates ◽  
Granulocyte Function

ABSTRACT In this report, we demonstrate that canine growth hormone (cGH) is capable of priming canine polymorphonuclear neutrophil granulocytes (PMN) in a manner resembling that of human PMN. The cGH influences important functions that are involved in the process of recruitment of PMN, i.e., shape change, chemotaxis, CD11b/CD18 expression, adhesion, and subsequent transendothelial migration. Also, intracellular O2 − production was evaluated. We investigated the priming effect by incubating PMN with purified pituitary cGH at various concentrations (10 to 800 μg/liter). The capacity for shape change was significantly (P < 0.05) enhanced, whereas the chemotactic response under agarose was significantly (P < 0.05) reduced. The chemotactic migration in Boyden chambers (10-μm-thick polycarbonate filter; lower surface count technique) was significantly (P < 0.05) enhanced, presumably due to cGH-induced hyperadhesiveness to the lower surface of the filters. The adhesion in albumin-coated microtiter plates and adherence to canine pulmonary fibroblasts were significantly (P < 0.05) increased, and the increased adhesion resulted in a significant (P < 0.01) increase in transendothelial migration using canine jugular vein endothelial cells. The increase in adhesion was associated with a significant increase in CD11b/CD18 expression. Furthermore, intracellular O2 − production was significantly enhanced in response to both phorbol myristate acetate (P < 0.01) and opsonized zymosan (P < 0.05). In the absence of a PMN-stimulating agent, cGH did not influence the effector functions investigated except for an increased expression of CD11b/CD18.

scholarly journals 15-Epi-LXA4and 17-epi-RvD1 restore TLR9-mediated impaired neutrophil phagocytosis and accelerate resolution of lung inflammation

2020 ◽  
Vol 117 (14) ◽  
pp. 7971-7980 ◽  
Author(s):  
Meriem Sekheri ◽  
Driss El Kebir ◽  
Natalie Edner ◽  
János G. Filep
Keyword(s):  
Lung Inflammation ◽  
Bacterial Infections ◽  
Therapeutic Potential ◽  
Polymorphonuclear Neutrophil ◽  
Neutrophil Granulocytes ◽  
Resolvin D1 ◽  
Acute Lung Inflammation ◽  
Cpg Dna ◽  
E Coli ◽  
Human Pmns

Timely resolution of bacterial infections critically depends on phagocytosis of invading pathogens by polymorphonuclear neutrophil granulocytes (PMNs), followed by PMN apoptosis and efferocytosis. Here we report that bacterial DNA (CpG DNA) and mitochondrial DNA impair phagocytosis and attenuate phagocytosis-induced apoptosis in human PMNs through Toll-like receptor 9 (TLR9)-mediated release of neutrophil elastase and proteinase 3 and subsequent down-regulation of the complement receptor C5aR. Consistently, CpG DNA delays pulmonary clearance ofEscherichia coliin mice and suppresses PMN apoptosis, efferocytosis, and generation of proresolving lipid mediators, thereby prolonging lung inflammation evoked byE. coli. Genetic deletion of TLR9 renders mice unresponsive to CpG DNA. We also show that aspirin-triggered 15-epi-lipoxin A4(15-epi-LXA4) and 17-epi-resolvin D1 (17-epi-RvD1) through the receptor ALX/FPR2 antagonize cues from CpG DNA, preserve C5aR expression, restore impaired phagocytosis, and redirect human PMNs to apoptosis. Treatment of mice with 15-epi-LXA4or 17-epi-RvD1 at the peak of inflammation accelerates clearance of bacteria, blunts PMN accumulation, and promotes PMN apoptosis and efferocytosis, thereby facilitating resolution ofE. coli-evoked lung injury. Collectively, these results uncover a TLR9-mediated endogenous mechanism that impairs PMN phagocytosis and prolongs inflammation, and demonstrate both endogenous and therapeutic potential for 15-epi-LXA4and 17-epi-RvD1 to restore impaired bacterial clearance and facilitate resolution of acute lung inflammation.

scholarly journals Lipoxin A4 induces hyperadhesiveness in human endothelial cells for neutrophils

Blood ◽  
1993 ◽  
Vol 82 (3) ◽  
pp. 948-953 ◽  
Author(s):  
R Lerner ◽  
M Heimburger ◽  
J Palmblad
Keyword(s):  
Endothelial Cells ◽  
Umbilical Vein ◽  
Interleukin 1 ◽  
Cytosolic Calcium ◽  
Leukotriene B4 ◽  
Polymorphonuclear Neutrophil ◽  
Maximal Response ◽  
Neutrophil Granulocytes ◽  
Lipoxin A4

Abstract Lipoxin A4 (LXA4), but not lipoxin B4, induced in vitro a dose- dependent, slowly emerging hyperadhesiveness in human umbilical vein endothelial cells (HUVEC), leading to a 1.9-fold increase in the binding of neutrophils (polymorphonuclear neutrophil granulocytes [PMN]). The maximal response to LXA4 occurred at 1 nmol/L and after 30 minutes of treatment of HUVEC. These response kinetics were intermediate in comparison with those of fast-acting inducers of HUVEC adhesivity (eg, thrombin, leukotriene B4 [LTB4] or platelet activating factor [PAF]), needing 5 to 15 minutes, or to the slow inducer interleukin-1 (IL-1 beta), which requires hours. The maximal LXA4 effect was slightly lower than that of LTB4 (100 nmol/L) and thrombin (1 U/mL), and less than that of PAF (100 nmol/L) or IL-1 beta (2.5 U/mL) (2.2-, 2.0-, 2.4-, or 13.6-fold increases, respectively). The LXA4 effect was inhibited by the PAF receptor antagonist WEB-2086; however, it could not be blocked by pertussis toxin. LXA4 conferred a slow, sustained increase in HUVEC cytosolic calcium ion concentrations, whereas thrombin did so rapidly and transiently. LXA4 also caused PMN to become hyperadhesive. Thus, this novel effect of LXA4 on HUVEC appears to be associated with endogenous PAF expression and slow increases of cytosolic calcium concentrations but not pertussis- sensitive G proteins.

Immunomodulator effect of phenol used as bacteriostatic agent in aqueous allergens extracts on human polymorphonuclear neutrophil cells

1996 ◽  
Vol 88 ◽  
pp. 76
Author(s):  
Maria Leonor Meisel ◽  
Luis Martins ◽  
Helena Costa ◽  
Sara Correia ◽  
Maria João Peres ◽  
...  
Keyword(s):  
Polymorphonuclear Neutrophil ◽  
Bacteriostatic Agent ◽  
Human Polymorphonuclear Neutrophil

Effects of a Hyaluronate-Carboxymethylcellulose Membrane (Seprafilm) on Human Polymorphonuclear Neutrophil Functions

2008 ◽  
Vol 149 (2) ◽  
pp. 243-249 ◽  
Author(s):  
Kohei Otake ◽  
Keiichi Uchida ◽  
Shigeyuki Yoshiyama ◽  
Mikihiro Inoue ◽  
Yoshiki Okita ◽  
...  
Keyword(s):  
Polymorphonuclear Neutrophil ◽  
Human Polymorphonuclear Neutrophil

Chemiluminescence response of the human polymorphonuclear neutrophil to lipopolysaccharides

1985 ◽  
Vol 7 (4) ◽  
pp. 283-291 ◽  
Author(s):  
Joseph Nicotra ◽  
Anthony J. Orsini ◽  
Vincent A. DeBari
Keyword(s):  
Polymorphonuclear Neutrophil ◽  
Human Polymorphonuclear Neutrophil
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