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Ann Thorac Surg 2006;82:1043-1050
© 2006 The Society of Thoracic Surgeons

Original article: General thoracic

Respiratory Viral Infection in Obliterative Airway Disease After Orthotopic Tracheal Transplantation

Elbert Kuo, MD*,a, Ankit Bharat, MD*,a, Trudie Goers, MDa, Will Chapmana, Le Yan, BSc, Tyler Street, BAa, Wei Lu, MDa, Michael Walter, MDc, Alexander Patterson, MDa, Thalachallour Mohanakumar, PhDa,b,*

a Department of Surgery, Washington University, St. Louis, Missouri
b Department of Pathology and Immunology, Washington University, St. Louis, Missouri
c Department of Pulmonary and Critical Care, Washington University, St. Louis, Missouri

Accepted for publication March 31, 2006.

* Address correspondence to Dr Mohanakumar, Washington University School of Medicine, Department of Surgery, Box 8109, 660 S Euclid Ave, St. Louis, MO 63110 (Email: kumart{at}wustl.edu).

Presented at the Poster Session of the Forty-second Annual Meeting of The Society of Thoracic Surgeons, Chicago, IL, Jan 30–Feb 1, 2006.

BACKGROUND: The long-term survival after human lung transplantation is limited by bronchiolitis obliterans syndrome (BOS). Clinically, community-acquired respiratory viral infections have been correlated with an increased incidence of BOS. The goal of this study was to investigate the role of respiratory viral infections in chronic lung allograft rejection using the murine orthotopic tracheal transplantation model.

METHODS: Eighty orthotopic tracheal transplants were performed using BALB/c and C57BL/6 mice. Recipient mice were infected intranasally with Sendai virus (SdV), a murine parainfluenza type I virus. Experiments altering the infectious dose, infection time, harvest time, allogeneic response, and viral response were performed. Tracheal allograft rejection was monitored using percent fibrosis and lamina propria to cartilage ratio measurements. Interferon-{gamma} ELISPOT analysis against irradiated donor (BALB/c) splenocytes was used as immunologic indicator of alloreactivity after transplantation.

RESULTS: Sendai virus infection revealed a dose-dependent transient suppression of alloreactivity with a decrease in tracheal allograft fibrosis and frequency of alloreactive T cells at 30 days. This immunosuppression was reversed by day 60, leading to increased tracheal allograft fibrosis with a concomitant increase in the frequency of interferon-{gamma} producing alloreactive T cells. Pretransplant sensitization with donor antigens prevented the initial suppression of alloreactivity due to SdV infection. Furthermore, pretransplant immunization against SdV infection resulted in rapid clearing of the infection and reduced the immunopathology of rejection.

CONCLUSIONS: Respiratory viral infections can cause enhanced tracheal allograft rejection despite the initial phase of transient immunosuppression. Early treatment or vaccination against the respiratory infections may represent a viable intervention to reduce the risk of chronic rejection.


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