Effects of human IL-8 isoforms on bovine neutrophil function in vitro

2000 ◽  
Vol 74 (1-2) ◽  
pp. 71-85 ◽  
Author(s):  
C.L Galligan ◽  
B.L Coomber
2015 ◽  
Vol 164 (1-2) ◽  
pp. 67-73 ◽  
Author(s):  
Hussain A. Alabdullah ◽  
Lawrence K. Fox ◽  
John M. Gay ◽  
George M. Barrington ◽  
Robert H. Mealey

2018 ◽  
Vol 196 ◽  
pp. 18-21
Author(s):  
Hussain A. Alabdullah ◽  
Lawrence K. Fox ◽  
John M. Gay ◽  
George M. Barrington

1998 ◽  
Vol 39 (2) ◽  
pp. 201-213
Author(s):  
G. Trowald-Wigh ◽  
L. Håkansson ◽  
A. Johannisson ◽  
L.E. Edqvist

2008 ◽  
Vol 22 (S1) ◽  
Author(s):  
Tania Cristina Pithon‐Curi ◽  
Adriana Cristina Levada‐Pires ◽  
Thais Martins Lima ◽  
Elaine Hatanaka ◽  
Rui Curi

2020 ◽  
Vol 75 (12) ◽  
pp. 2320-2325
Author(s):  
Daisy Wilson ◽  
William Drew ◽  
Alice Jasper ◽  
Helena Crisford ◽  
Peter Nightingale ◽  
...  

Abstract Neutrophil dysfunction has been described with age, appears exaggerated in infection, with altered phosphoinositol signaling a potential mechanism. However, functional aging is heterogeneous. Frailty is a negative health status and is more common in older adults. We hypothesized that neutrophil migration may be compromised in frailty, associated with the degree of frailty experienced by the older person. We compared measures of frailty, neutrophil function, and systemic inflammation in 40 young and 77 older community-dwelling adults in the United Kingdom. Systemic neutrophils exhibited an age-associated reduction in the accuracy of migration (chemotaxis) which was further blunted with frailty. The degree of migratory inaccuracy correlated with physical (adjusted hand grip strength) and cognitive (Stroop test) markers of frailty. Regression analysis demonstrated that age, Charlson comorbidity index, and frailty index were able to predict neutrophil chemotaxis. Reduced chemotaxis of neutrophils from frail adults could be reversed using selective PI3K inhibitors. Exposure of neutrophils from young adults to plasma from chronically inflamed frail older adults could not recapitulate the migratory deficit in vitro, and there were no relationships with systemic inflammation and neutrophil dysfunction. Frailty exaggerated the neutrophil deficits seen with advanced age but aspects of the frailty-associated deficit in neutrophil function are rescuable and thus potentially form a therapeutic target to improve outcomes from infection in older adults.


Blood ◽  
1985 ◽  
Vol 66 (3) ◽  
pp. 738-741 ◽  
Author(s):  
MA Vadas ◽  
C Clarke ◽  
NA Nicola ◽  
AF Lopez

Abstract Purified human neutrophils from 48 individuals were tested for their capacity to kill antibody-coated target cells in vitro in the absence or presence of stimulating agents. The agents used to stimulate cytotoxic capacity were the monoclonal antibody (MAb) WEM-G1, colony- stimulating factor (CSF-alpha), or mononuclear cell supernatant (MNC- SN). There existed an heterogeneity among the neutrophils of different individuals in the capacity to kill target cells both in the unstimulated (“resting”) or the stimulated state. A positive correlation was found between the ability of neutrophils to kill in the “resting” state and their capacity to be stimulated by MAb WEM-G1, CSF- alpha, or MNC-SN. Furthermore, a strong positive correlation in the ability of neutrophils to be stimulated by the MAb WEM-G1 and either CSF-alpha (r = .76) or MNC-SN (r = .68), as well as between CSF-alpha and MNC-SN (r = .79) was demonstrated. No correlation was seen, however, between stimulation of neutrophil function in vitro and total blood leukocyte counts, neutrophil counts, monocyte counts, or intensity of binding of MAb WEM-G1. The observation that neutrophils respond to a similar extent to different types of stimulators, -such as cytokines (CSF-alpha and MNC-SN) and MAb, suggests that these two factors may be operating through a common mechanism and the degree of stimulation may reflect an intrinsic responsiveness of neutrophils that differs among individuals. Our results also suggest a potential clinical use of WEM-G1 in measuring neutrophil functional capacity in vitro and predicting the capacity to respond to CSF-like cytokines.


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