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Author Spotlight: Investigating the Key Factors of Obliterative Bronchiolitis After Lung Transplantation

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Published on: November 10, 2023

Host-Pathogen Interactions and Chronic Lung Allograft Dysfunction.

John Belperio¹, Scott M Palmer², S Sam Weigt¹

¹1 Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of California, Los Angeles, California; and.

Annals of the American Thoracic Society

|September 26, 2017

Summary

This summary is machine-generated.

Infections like bacterial, viral, and fungal post-lung transplant can lead to chronic lung allograft dysfunction (CLAD). These infections trigger immune responses that damage the transplanted lung, increasing mortality.

Keywords:

bacteria chronic lung allograft dysfunction fungus lung transplant virus

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Isolation and In Vitro Culture of Murine and Human Alveolar Macrophages

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Published on: April 20, 2018

Area of Science:

Immunology
Transplantation Medicine
Infectious Diseases

Background:

Lung transplantation is a vital treatment for advanced lung disease.
Post-transplant complications, particularly infections, are major causes of mortality and graft dysfunction.
Chronic lung allograft dysfunction (CLAD) is a significant concern in lung transplant recipients.

Purpose of the Study:

To explore the role of infections in the development of chronic lung allograft dysfunction (CLAD) after lung transplantation.
To understand the mechanisms by which microbial infections contribute to CLAD.
To investigate the link between specific pathogens and CLAD development.

Main Methods:

Review of existing literature on infections in lung transplant recipients.
Analysis of the association between bacterial (Staphylococcus aureus, Pseudomonas aeruginosa), viral (cytomegalovirus, community-acquired respiratory viruses), and fungal (Aspergillus) infections and CLAD.
Examination of the proposed mechanistic pathways involving chemokine induction and immune cell infiltration.

Main Results:

Bacterial, viral, and fungal infections are associated with an increased risk of developing CLAD.
Microbial interactions with allograft cells stimulate chemokine production, recruiting recipient leukocytes.
This immune cell infiltration amplifies inflammation, potentially leading to alloresponse and graft dysfunction.

Conclusions:

Infections are key contributors to the pathobiology of CLAD and associated mortality.
Altered chemokine production resulting from microbe-allograft-host immune interactions plays a role in CLAD development.
Targeting infections may be crucial for improving long-term outcomes in lung transplant recipients.