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Host Biofilm Interaction in Breast Implant Illness
Imran Khan,
Colby R. Neumann,
Christine Kelley-Patteson,
Mary E. Lester,
Aladdin H. Hassanein,
Mithun Sinha
Division of Plastic Surgery, Indiana University School of Medicine
2020-02-11
Presenter: Imran Khan
Affidavit:
The wok is original and has been conceived by me.The presenter (Imran Khan) has contributed to experimental planning and data collection.
Director Name: Mithun Sinha
Author Category: Resident Plastic Surgery
Presentation Category: Basic Science Research
Abstract Category: Breast (Aesthetic and Recon.)
Host Biofilm Interaction in Breast Implant Illness
Imran Khan1, Colby R. Neumann1, Christine Kelley-Patteson2, Mary E. Lester1,
Aladdin H. Hassanein1, Mithun Sinha1
1Division of Plastic Surgery, Indiana University
2Meridian Plastic Surgeons, Indianapolis
BACKGROUND: More than 330,000 women in US undergo breast implant augmentation. Many patients have a constellation of poorly understood symptoms believed to be related to breast implants termed Breast Implant Illness (BII). The pathophysiology of BII is unknown. Breast implants provides conducive surface for the adherence and growth of bacterial biofilms. Biofilm produced enzyme can oxidize fatty acids to form oxylipins. Oxylipins can cause inflammatory response. We hypothesize that BII is associated with the interaction of implant biofilm with native breast adipose abundant fatty acids.
METHODS: Capsulectomy and breast implants from clinically indicated procedures for patients requesting prosthetic removal were collected. Scanning electron microscopy and 16SrRNA sequencing were used for bacterial biofilm bacterial determination and speciation respectively. Oxylipins were quantitated through targeted and untargeted lipidomic analyses using LC-MS-MS. Predictive variables included age, diabetes status, co-morbidities, nature and duration of implant.
RESULTS: Thirty-seven capsule/implant specimen were removed for BII. Bacterial biofilm was detected in 21/37 specimen (56.7%). LC-MS identified increased abundance of oxylipins in capsules which had bacterial biofilms compared to control (capsules without biofilm) (p<0.05).
CONCLUSIONS: We have found that BII exhibits bacterial biofilm and increased oxylipin formation by oxidation of breast adipose. The oxylipins may lead to the activation of immune cells which promote bacterial biofilm state. This host-pathogen reaction provides insight into the pathophysiology of BII.
