Related Experiment Video
Updated: Jun 7, 2026

Microfluidic Platform for Measuring Neutrophil Chemotaxis from Unprocessed Whole Blood
Published on: June 3, 2014
Enhancement of neutrophils function as a result of prior exposure to chemotactic factor
Abstract:
Exposure of human polymorphonuclear leukocytes (PMN) to chemotactic factor, as well as the migration of PMN through a 5-mum pore-size membrane, results in a PMN population with enhanced chemiluminescence, enhanced capacity for superoxide anion production, and increased Escherichia coli bactericidal activity. The enhanced PMN response resulting from exposure to chemotactic factor was observed with several chemotactic stimuli, including a mixture of casein and autologous serum, chemotactic C5 fragment, and formyl-l-methionyl-l-leucine-l-phenylalanine (f-Met-Leu-Phe). Enhanced levels of chemiluminescence were observed with both soluble stimuli (concanavalin A and phorbol myristate acetate) as well as particulate stimuli (opsonized zymosan). Once activated by chemotactic factor, PMN retained their enhanced stimulated chemiluminescence in the absence of chemotactic factor for at least 2.5 h. Enhanced activity could not be correlated with a shift in the number of immunoglobulin (Ig)G Fc receptor positive or complement receptor positive PMN. In vivo studies with guinea pigs indicated that PMN attracted to an intraperitoneal injection of casein, like those attracted through a chemotaxis membrane in vitro in response to casein, showed markedly enhanced stimulated chemiluminescence when compared with peripheral blood PMN from the same animal. Such a mechanism to stimulated PMN function may enhance the effectiveness of PMN in host defense at inflammatory foci.
Insights
Exposure to chemotactic factors enhances human polymorphonuclear leukocytes (PMN) function, boosting their chemiluminescence and bacterial killing. This improved PMN activity persists, potentially strengthening host defense at inflammatory sites.
Area of Science:
- Immunology
- Cell Biology
- Host Defense Mechanisms
Background:
- Human polymorphonuclear leukocytes (PMN) are critical immune cells involved in host defense.
- Chemotactic factors are known to attract PMN to sites of inflammation.
- The functional consequences of PMN activation by chemotaxis are not fully understood.
Purpose of the Study:
- To investigate the functional changes in PMN following exposure to chemotactic factors.
- To determine if PMN migration through membranes alters their function.
- To assess the duration of enhanced PMN activity and its potential role in host defense.
Main Methods:
- Human PMN were exposed to various chemotactic stimuli (casein, C5 fragment, f-Met-Leu-Phe).
- PMN migration through 5-mum pore-size membranes was performed.
- Chemiluminescence, superoxide anion production, and Escherichia coli bactericidal activity were measured.
- In vivo studies in guinea pigs were conducted using casein-induced peritoneal inflammation.
Main Results:
- Exposure to chemotactic factors and migration through membranes enhanced PMN chemiluminescence, superoxide production, and bactericidal activity.
- Enhanced activity was observed with diverse stimuli including soluble (concanavalin A, phorbol myristate acetate) and particulate (opsonized zymosan) agents.
- Activated PMN maintained enhanced chemiluminescence for at least 2.5 hours.
- In vivo studies confirmed enhanced PMN chemiluminescence in response to chemotaxis.
- Enhanced activity did not correlate with changes in IgG Fc or complement receptor expression.
Conclusions:
- Chemotactic factor exposure and migration significantly enhance PMN functional responses, including chemiluminescence and bactericidal capacity.
- These enhanced PMN functions are sustained and may contribute to improved host defense at inflammatory foci.
- The findings suggest a mechanism by which PMN are primed for more effective action during inflammation.
Related Concept Videos
Inflammation
Chemotaxis and Direction of Cell Migration
Differentiation of Common Myeloid Progenitor Cells
Chemotaxis in E. coli
Acute Inflammation II: Cellular Phase

