Interstitial Pneumonitis and Lymphocytic Bronchiolitis/Bronchitis as a Direct Result of Acute Lethal Graft-Versus-Host Disease Duplicate the Histopathology of Lung Allograft Rejection1

Workman, Diane L.; Clancy, John

doi:10.1097/00007890-199405820-00013

Cited by 18 publications

(9 citation statements)

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“…38,41,48,49 Even under tightly controlled experimental conditions, several patterns of lung injury have emerged, including acute hemorrhagic alveolitis, late onset interstitial pneumonitis and lymphocytic bronchiolitis 38. In several models where the GVH reaction is induced to (1) minor H antigens, (2) class I or class II MHC antigens only or (3) both major and minor H antigens, two major abnormalities are apparent after allogeneic SCT: a dense mononuclear cell infiltrate around both pulmonary vessels ( Figure 1c) and bronchioles ( Figure 1d) and an acute pneumonitis involving the interstitium and alveolar spaces ( Figure 1e).…”

Section: The Pathogenesis Of Ipsmentioning

confidence: 99%

Acute lung injury after allogeneic stem cell transplantation: is the lung a target of acute graft-versus-host disease?

Cooke

Yanik

2004

Bone Marrow Transplant

104

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Summary:Allogeneic hematopoietic stem cell transplantation (SCT) is an important therapeutic option for a number of malignant and nonmalignant conditions but the broader application of this treatment strategy is limited by several side effects. In particular, diffuse lung injury is a major complication of SCT that responds poorly to standard therapeutic approaches and significantly contributes to transplant-related morbidity and mortality. Historically, approximately 50% of all pneumonias seen after SCT have been secondary to infection, but the judicious use of broad-spectrum antimicrobial prophylaxis in recent years has tipped the balance of pulmonary complications from infectious to noninfectious causes. This mini review will discuss the definition, risk factors and pathogeneses of noninfectious lung injury that occurs early after allogeneic SCT.

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Section: The Pathogenesis Of Ipsmentioning

confidence: 99%

Acute lung injury after allogeneic stem cell transplantation: is the lung a target of acute graft-versus-host disease?

Cooke

Yanik

2004

Bone Marrow Transplant

104

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“…Although there is a higher incidence of pulmonary toxicity in humans receiving intense conditioning regimens, these treatments, nevertheless, are beneficial in preventing relapse and promoting BM engraftment in human and rodent studies (2)(3)(4)(5)(6)(7). While the risk of developing IPS may be directly related to the degree of pre-BMT conditioning (i.e., chemotherapy, irradiation) and the severity of GVHD after BMT (i.e., allogenicity) (6,8), how allogeneic T cells alter the course of IPS generation in the early post-BMT period have not been examined previously. As the mechanisms responsible for IPS are poorly understood, the aim of this study was to determine the type and degree of lung injury in the early post-BMT period.…”

Section: Introductionmentioning

confidence: 99%

The critical early proinflammatory events associated with idiopathic pneumonia syndrome in irradiated murine allogeneic recipients are due to donor T cell infusion and potentiated by cyclophosphamide.

Panoskaltsis‐Mortari¹,

Taylor²,

Yaeger³

et al. 1997

J. Clin. Invest.

117

119

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We have hypothesized that lung damage occurring in the peri-bone marrow transplant (BMT) period is critical for the subsequent generation of idiopathic pneumonia syndrome (IPS), a major complication following human BMT. The proinflammatory events induced by a common pre-BMT conditioning regimen, cyclophosphamide (Cytoxan ® ) (Cy) and total body irradiation, were analyzed in a murine BMT model. Electron microscopy indicated that Cy exacerbated irradiation-induced epithelial cell injury as early as day 3 after BMT. Allogenicity was an important contributing factor to lung injury as measured by lung wet and dry weights and decreased specific lung compliance. The most significant pulmonary dysfunction was seen in mice receiving both allogeneic T cells and Cy conditioning. IPS was associated with an influx of T cells, macrophages, and neutrophils early post-BMT. Hydroxyproline levels were not increased, indicating that the injury was not fibrotic early post-BMT. As early as 2 h after chemoradiation, host macrophages increased in number in the lung parenchyma.

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“…The clinical presentation of this patient with cough and shortness of breath [5] is also similar to patients with bronchoalveolar lymphocytosis from other causes, such as autoimmune diseases, who also suffer from cough [16]. According to the experimental model of Workman and Clancy, the pulmonary process characterized by the sequential development of interstitial pneumonitis and lymphocytic bronchiolitis/bronchitis occurred because of the aGVHD reaction [7,8]. The perivascular lymphocytic infiltrate is nonspecific and duplicates the histology of allograft lung rejection [7,8,17], a process that-at least in theory-should be pathophysiologically similar to aGVHD.…”

Section: Discussionmentioning

confidence: 57%

“…According to the experimental model of Workman and Clancy, the pulmonary process characterized by the sequential development of interstitial pneumonitis and lymphocytic bronchiolitis/bronchitis occurred because of the aGVHD reaction [7,8]. The perivascular lymphocytic infiltrate is nonspecific and duplicates the histology of allograft lung rejection [7,8,17], a process that-at least in theory-should be pathophysiologically similar to aGVHD. Both GVHD and pulmonary allograft rejection also share the presence of lymphocytic bronchiolitis/bronchitis; this feature could not be evaluated in the biopsy due to lack of bronchial wall.…”

Section: Discussionmentioning

confidence: 99%

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Lymphocytic pneumonitis as the manifestation of acute graft‐versus‐host disease of the lung

et al. 2005

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Acute graft-versus-host disease is a common complication after allogeneic stem cell transplantation. It normally affects the skin, liver, and gut. We report a 54-year-old male who developed shortness of breath, cough, and bilateral pulmonary infiltrates in which the workup failed to demonstrate an infectious etiology 165 days post-HLA-matched allogeneic peripheral blood stem cell transplant. Eighteen days before, his tacrolimus had been tapered and it was subtherapeutic on admission. A transbronchial biopsy showed a perivascular and interstitial lymphocytic infiltrate without evident pathogens on histology or extensive workup. The clinical picture was suggestive of pulmonary acute graft-versus-host disease. No disease was present elsewhere. Accordingly, the patient was treated with steroids and tacrolimus. After 12 hr on methylprednisolone, his symptoms disappeared with eventual resolution radiologically. Acute graft-versus-host disease of the lung is a very uncommon complication after stem cell transplant, but it should be considered in patients who are at high risk for graft-versus-host disease or developing symptoms soon after discontinuing immunosuppression. Its diagnosis requires work-up to rule out an infectious etiology and a biopsy to confirm histology. Am.

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Interstitial Pneumonitis and Lymphocytic Bronchiolitis/Bronchitis as a Direct Result of Acute Lethal Graft-Versus-Host Disease Duplicate the Histopathology of Lung Allograft Rejection1

Cited by 18 publications

References 0 publications

Acute lung injury after allogeneic stem cell transplantation: is the lung a target of acute graft-versus-host disease?

Acute lung injury after allogeneic stem cell transplantation: is the lung a target of acute graft-versus-host disease?

The critical early proinflammatory events associated with idiopathic pneumonia syndrome in irradiated murine allogeneic recipients are due to donor T cell infusion and potentiated by cyclophosphamide.

Lymphocytic pneumonitis as the manifestation of acute graft‐versus‐host disease of the lung

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