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Granulocyte colony-stimulating factor reverses septic shock-induced polymorphonuclear leukocyte dysfunction

H H Simms¹, R D'Amico

¹Department of Surgery, Brown University School of Medicine-Rhode Island Hospital, Providence 02903.

|January 1, 1994

Summary

Septic shock significantly reduces CD64 (Fc gamma RI) expression on polymorphonuclear leukocytes (PMNs). Granulocyte colony-stimulating factor can restore CD64 function, improving PMN oxidative metabolism and degranulation in patients with septic shock.

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Area of Science:

Immunology
Cell Biology

Background:

Polymorphonuclear leukocyte (PMN) function relies on Fc gamma receptor expression.
Fibronectin and laminin modulate CD32 (Fc gamma RII) and CD16 (Fc gamma RIII) but their effect on CD64 (Fc gamma RI) was unclear.

Purpose of the Study:

To define the role of CD64 (Fc gamma RI) in modulating PMN oxidative metabolism and degranulation.
To investigate the effects of fibronectin and laminin on CD64 expression and function in PMNs.

Main Methods:

PMNs from healthy volunteers and patients (controls and septic shock) were analyzed.
CD64 expression was measured after adherence to fibronectin or laminin.
Oxidative metabolism and degranulation were assessed via superoxide anion, hypochlorous acid, and N-acetyl-beta-glucosaminidase production.

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Cytokines were tested for their ability to restore CD64 activity in septic shock patients.

Main Results:

Fibronectin and laminin increased CD64 expression and activity in PMNs from healthy volunteers and control patients.
Septic shock patients showed depressed CD64 expression and activity.
Granulocyte colony-stimulating factor restored both CD64 expression and biological activity in septic shock PMNs.

Conclusions:

Septic shock impairs CD64 expression on PMNs.
Granulocyte colony-stimulating factor can restore CD64 number and function, enhancing PMN oxidative metabolism and degranulation in the context of fibronectin or laminin.
This suggests a potential therapeutic target for sepsis-related immune dysfunction.