Orthotopic Tracheal Allografts Undergo Reepithelialization With Recipient-Derived Epithelium

Genden, Eric M.; Iskander, Andrew; Bromberg, Jonathan S.; Mayer, Lloyd

doi:10.1001/archotol.129.1.118

Cited by 41 publications

(36 citation statements)

References 10 publications

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“…Evidence for obliterative airways disease was present in the nonventilated allografts suggesting an association between OB and epithelial cell apoptosis. Other studies suggest that airway obliteration characteristic of the heterotopic tracheal allograft model does not occur in orthotopic allografts and that recipient epithelial cells migrating into the donor graft may actually prevent obliteration [234–236]. The role of apoptosis in this process is not known.…”

Section: Apoptosis In Airway Epithelium In Diseasementioning

confidence: 99%

Apoptosis and the Airway Epithelium

White

2011

Journal of Allergy

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The airway epithelium functions as a barrier and front line of host defense in the lung. Apoptosis or programmed cell death can be elicited in the epithelium as a response to viral infection, exposure to allergen or to environmental toxins, or to drugs. While apoptosis can be induced via activation of death receptors on the cell surface or by disruption of mitochondrial polarity, epithelial cells compared to inflammatory cells are more resistant to apoptotic stimuli. This paper focuses on the response of airway epithelium to apoptosis in the normal state, apoptosis as a potential regulator of the number and types of epithelial cells in the airway, and the contribution of epithelial cell apoptosis in important airways diseases.

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Section: Apoptosis In Airway Epithelium In Diseasementioning

confidence: 99%

Apoptosis and the Airway Epithelium

White

2011

Journal of Allergy

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“…The OTT model is distinguished from HTTs in several ways. Most notably, OTTs do not develop luminal fibrosis, and because they are contiguous with graft recipient airways, are re-epithelialized with recipienttype respiratory epithelium within 4 wk following transplantation (18,19). Additionally, dendritic cell clearance of shed epithelial cell Ags to draining lymph nodes for Ag presentation to T cells is reproduced in its native position in the neck and thorax.…”

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confidence: 99%

Simultaneous LFA-1 and CD40 Ligand Antagonism Prevents Airway Remodeling in Orthotopic Airway Transplantation: Implications for the Role of Respiratory Epithelium as a Modulator of Fibrosis

Murakawa

Kerklo

Zamora

et al. 2005

The Journal of Immunology

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Airway remodeling is a prominent feature of certain immune-mediated lung diseases such as asthma and chronic lung transplant rejection. Under conditions of airway inflammation, the respiratory epithelium may serve an important role in this remodeling process. Given the proposed role of respiratory epithelium in nonspecific injury models, we investigated the respiratory epithelium in an immune-specific orthotopic airway transplant model. MHC-mismatched tracheal transplants in mice were used to generate alloimmune-mediated airway lesions. Attenuation of this immune injury and alteration of antidonor reactivity were achieved by the administration of combined anti-LFA-1/anti-CD40L mAbs. By contrast, without immunotherapy, transplanted airways remodeled with a flattening of respiratory epithelium and significant subepithelial fibrosis. Unopposed alloimmune injury for 10 days was associated with subsequent epithelial transformation and subepithelial fibrosis that could not be reversed with immunotherapy. The relining of donor airways with recipient-derived epithelium was delayed with immunotherapy resulting in partially chimeric airways by 28 days. Partial epithelial cell chimerism was sufficient to prevent luminal fibrosis. However, epithelial chimerism was also associated with airway remodeling. Therefore, there appears to be an intimate relationship between the morphology and level of chimerism of the respiratory epithelium and the degree of airway remodeling following alloimmune injury.

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“…First, the main targets of tracheal rejection, the major histocompatibility complex (MHC) class I-expressing epithelial cells (7) lining the lumen of the tracheal allograft, can be replaced by recipient epithelium after transplantation. Although immunosuppression facilitates the process of allograft reepithelialization by impacting the quality and kinetics of the process, reepithelialization will occur in nonimmunosuppressed recipients (8,9). The second unique characteristic of tracheal grafts is that this tissue has been shown to be a rich source of dendritic cells (DCs) (10).…”

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confidence: 99%