The role of polymorphonuclear leucocytes in the pulmonary dysfunction induced by complement activation.

Area of Science:

• Immunology
• Pulmonary Medicine
• Inflammation Research

Background:

• Polymorphonuclear leucocytes (PMNs) are crucial in inflammatory responses.
• Complement activation can lead to significant physiological changes in the lungs.

Purpose of the Study:

• To elucidate the role of PMNs in the pulmonary reactions following complement activation.
• To identify the specific mediators involved in complement-induced lung inflammation.

Main Methods:

• Infusion of complement-activated plasma (CAP), PMN supernatant, and PMN aggregates in pigs.
• Administration of indomethacin, antihistamines, and methylprednisolone to assess mediator roles.
• Monitoring of peripheral leucopenia, pulmonary vascular resistance (PVR), and arterial oxygen tension (PaO2).

Main Results:

• CAP infusion caused leucopenia, increased PVR, and decreased PaO2.
• Indomethacin mitigated CAP-induced PVR rise and PaO2 fall, indicating a role for prostanoids.
• Activated PMN supernatant increased PVR and decreased PaO2, which was counteracted by indomethacin.

Conclusions:

• Pulmonary reactions to complement activation are mediated by humoral factors from activated PMNs.
• Arachidonic acid metabolites are key players, likely triggered by PMN-released substances.
• PMNs may directly synthesize or release mediators that influence pulmonary vascular dynamics.