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An Immunological Model for Heterotopic Heart and Cardiac Muscle Cell Transplantation in Rats

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Published on: May 8, 2020

Local complement activation is associated with primary graft dysfunction after lung transplantation.

Hrishikesh S Kulkarni¹, Kristy Ramphal², Lina Ma¹

¹Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.

|August 5, 2020

Summary

Local complement activation in bronchoalveolar lavage fluid within 24 hours after lung transplantation indicates primary graft dysfunction. All three complement pathways are implicated in this local response, suggesting therapeutic targets.

Keywords:

Complement Organ transplantation Pulmonology

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Area of Science:

Immunology
Transplantation Medicine
Pulmonary Medicine

Background:

The complement system, crucial for host defense, can be detrimentally activated by ischemia/reperfusion injury (IRI).
Primary graft dysfunction (PGD) is a significant complication after lung transplantation (LTx), largely driven by IRI.
The role of local versus systemic complement activation in PGD development requires clarification.

Purpose of the Study:

To determine if local complement activation in bronchoalveolar lavage (BAL) fluid can predict PGD after LTx.
To identify which specific complement activation pathways are associated with PGD.

Main Methods:

A multicenter cohort study involving LTx recipients.
Collection of BAL and plasma specimens within 24 hours post-LTx.
Measurement of complement activation products and pathway components using ELISA.

Main Results:

Elevated levels of soluble C4d (sC4d) and soluble C5b-9 (sC5b-9) in BAL from patients with PGD.
Increased C1q, C2, C4, and C4b in BAL of PGD patients suggest classical and lectin pathway activation.
Higher Ba levels in BAL indicate alternative pathway involvement in PGD.

Conclusions:

Complement activation fragments are detectable locally in the lungs within 24 hours of LTx.
All three complement pathways (classical, lectin, alternative) show increased local activation in PGD.
These findings support the investigation of complement-targeted therapies to prevent PGD.