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Alveolar Macrophage Phagocytosis and Bacteria Clearance in Mice

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Published on: March 2, 2019

Polymorphonuclear leukocyte phagocytic function increases in plasminogen knockout mice.

P K Witting¹, B Zeng, M Wong

¹Vascular Biology Group, ANZAC Research Institute, Concord, NSW 2139, Australia.

Thrombosis Research

|April 19, 2008

Summary

This summary is machine-generated.

Mice lacking plasminogen (PG-/-) show enhanced phagocytic activity in polymorphonuclear leukocytes (PMNs) mediated by Mac-1. This increased activity, crucial for fibrinogen clearance, is suppressed by plasminogen.

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Area of Science:

Immunology
Hematology
Biochemistry

Background:

Mice lacking plasminogen (PG-/-) rely on alternative fibrinolysis pathways for survival.
Polymorphonuclear leukocytes (PMNs) are crucial for PG-independent fibrin(ogen) clearance.
This study investigates enhanced phagocytic activity in PG-/- mouse PMNs.

Purpose of the Study:

To demonstrate increased Mac-1 dependent phagocytic activity in PMNs from PG-/- mice.
To compare fibrinogenolytic activity between PG-/- and wild-type (PG+/+) mice.
To elucidate the role of Mac-1 in PMN phagocytosis and fibrinogen clearance.

Main Methods:

Compared phagocytic activity of PMNs from PG-/- and PG+/+ mice using Staphylococcus aureus particles.
Assessed Mac-1 expression via flow cytometry.
Evaluated resistance to phorbol-12-myristate-13-acetate (PMA)-induced cell death.

Main Results:

PG-/- PMNs exhibited a 15-fold increase in phagocytosis compared to PG+/+ PMNs.
Mac-1 cell surface density was significantly higher in PG-/- PMNs.
Increased phagocytosis in PG-/- PMNs was inhibited by human plasminogen and anti-Mac-1 antibody.

Conclusions:

PMNs from PG-/- mice display heightened Mac-1 dependent phagocytic activity.
This enhanced activity is suppressed by plasminogen, indicating its critical role.
Increased PMN half-life and fibrinogen clearance in PG deficiency may be linked to this enhanced phagocytosis.