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Transcriptome of capsular contracture around breast implants mimics allograft rejection: a matched case-control study.

Plast Reconstr Surg

December 2024

Copenhagen University Hospital, Department of Plastic Surgery and Burns Treatment, Rigshospitalet, Copenhagen, Denmark.

Background: Capsular contracture is a frequent and severe complication following breast implant surgery. Although several theories on the pathophysiology exist, the exact molecular mechanisms remain unclear. This study aimed to identify the specific genes, signaling pathways, and immune cells associated with capsular contracture.

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Class I major histocompatibility complex (MHC-I) proteins play a pivotal role in adaptive immunity by displaying epitopic peptides to CD8+ T cells. The chaperones tapasin and TAPBPR promote the selection of immunogenic antigens from a large pool of intracellular peptides. Interactions of chaperoned MHC-I molecules with incoming peptides are transient in nature, and as a result, the precise antigen proofreading mechanism remains elusive.

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Common variable immunodeficiency (CVID) is the most common symptomatic and heterogeneous type of inborn errors of immunity (IEI). However, the pathogenesis process of this disease is often unknown. Epigenetic modifications may be involved in unresolved patients.

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Chronic obstructive pulmonary disease (COPD) is characterized by chronic inflammation, airway obstruction, and lung damage, often triggered by cigarette smoke. Dysregulated autophagy and inflammation are key contributors to its progression. Although double-stranded RNA-binding protein Staufen homolog 1 (STAU1), a multifunctional protein primarily involved in mRNA transport and localization, is identified as a potential biomarker, its role in COPD pathogenesis remains unclear.

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The main goal of this investigation is to find out how solute carrier family 27 member 3 (SLC27A3) is expressed in the lung tissue of mice with chronic obstructive pulmonary disease (COPD), and how it relates to lung function. A model of COPD was established by exposing organisms to cigarette smoke, followed by investigating the role of SLC27A3 in COPD through experiments conducted both in living organisms and in laboratory settings. Knockout mice lacking SLC27A3 were produced through siRNA transfection to investigate lung function and inflammatory response, using methods such as hematoxylin-eosin staining and enzyme-linked immunosorbent assay.

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