Systemic and exhaled cytokine and chemokine profiles are associated with the development of bronchiolitis obliterans syndrome

Kastelijn, Elisabeth A.; Rijkers, Ger T.; Moorsel, Coline H.M. van; Zanen, Pieter; Erp, Johanna M. Kwakkel-van; Graaf, E.A. van de; Kessel, Diana A. van; Grutters, Jan C.; Bosch, Jules M.M. van den

doi:10.1016/j.healun.2010.04.013

Cited by 32 publications

(29 citation statements)

References 67 publications

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“…Kastelijn et al. found higher levels of IFN‐γ in LT than in healthy controls but found no differences comparing patients with and without CLAD . In a recent study, Saito et al.…”

Section: Discussionmentioning

confidence: 95%

BALF cytokines in different phenotypes of chronic lung allograft dysfunction in lung transplant patients

Berastegui

Gómez-Ollés

Sánchez-Vidaurre

et al. 2017

Clinical Transplantation

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The long-term success of lung transplantation (LT) is limited by chronic lung allograft dysfunction (CLAD). Different phenotypes of CLAD have been described, such as bronchiolitis obliterans syndrome (BOS) and restrictive allograft syndrome (RAS). The purpose of this study was to investigate the levels of cytokines and chemokines in bronchoalveolar lavage fluid (BALF) as markers of these CLAD phenotypes. BALF was collected from 51 recipients who underwent (bilateral and unilateral) LT. The study population was divided into three groups: stable (ST), BOS, and RAS. Levels of interleukin (IL)-4, IL-5, IL-6, IL-10, IL-13, tumor necrosis factor alpha (TNF-α), interferon-gamma (IFN-γ), and granulocyte-macrophage colony-stimulating factor (GM-CSF) were measured using the multiplex technology. BALF neutrophilia medians were higher in BOS (38%) and RAS (30%) than in ST (8%) (P=.008; P=.012). Regarding BALF cytokines, BOS and RAS patients showed higher levels of INF-γ than ST (P=.02; P=.008). Only IL-5 presented significant differences between BOS and RAS (P=.001). BALF neutrophilia is as a marker for both CLAD phenotypes, BOS and RAS, and IL-5 seems to be a potential biomarker for the RAS phenotype.

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“…Kastelijn et al. found higher levels of IFN‐γ in LT than in healthy controls but found no differences comparing patients with and without CLAD . In a recent study, Saito et al.…”

Section: Discussionmentioning

confidence: 95%

BALF cytokines in different phenotypes of chronic lung allograft dysfunction in lung transplant patients

Berastegui

Gómez-Ollés

Sánchez-Vidaurre

et al. 2017

Clinical Transplantation

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“…Immunosuppressive therapy consisted of tacrolimus, mycophenolate mofetil and prednisone [9]. Data from these patients were collected before and after lung transplantation and entered into our database every 3 months according to protocol.…”

Section: Methodsmentioning

confidence: 99%

Diabetes before and after lung transplantation in patients with cystic fibrosis and other lung diseases

et al. 2012

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“…Communicating via tumour necrosis factor (TNF)- α , interleukin (IL)-1, IL-2, IL-12, and IFN- γ [19–21], T H 1 cells play a fundamental role in acute rejection. These type 1 cytokines are upregulated early in the inflammatory process.…”

Section: Stage Zero Of Potential Organ Injury: Current Concepts Inmentioning

confidence: 99%

Inflammatory Signalling Associated with Brain Dead Organ Donation: From Brain Injury to Brain Stem Death and Posttransplant Ischaemia Reperfusion Injury

Watts

Thom

Fraser

2013

Journal of Transplantation

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Brain death is associated with dramatic and serious pathophysiologic changes that adversely affect both the quantity and quality of organs available for transplant. To fully optimise the donor pool necessitates a more complete understanding of the underlying pathophysiology of organ dysfunction associated with transplantation. These injurious processes are initially triggered by catastrophic brain injury and are further enhanced during both brain death and graft transplantation. The activated inflammatory systems then contribute to graft dysfunction in the recipient. Inflammatory mediators drive this process in concert with the innate and adaptive immune systems. Activation of deleterious immunological pathways in organ grafts occurs, priming them for further inflammation after engraftment. Finally, posttransplantation ischaemia reperfusion injury leads to further generation of inflammatory mediators and consequent activation of the recipient's immune system. Ongoing research has identified key mediators that contribute to the inflammatory milieu inherent in brain dead organ donation. This has seen the development of novel therapies that directly target the inflammatory cascade.

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Systemic and exhaled cytokine and chemokine profiles are associated with the development of bronchiolitis obliterans syndrome

Cited by 32 publications

References 67 publications

BALF cytokines in different phenotypes of chronic lung allograft dysfunction in lung transplant patients

BALF cytokines in different phenotypes of chronic lung allograft dysfunction in lung transplant patients

Diabetes before and after lung transplantation in patients with cystic fibrosis and other lung diseases

Inflammatory Signalling Associated with Brain Dead Organ Donation: From Brain Injury to Brain Stem Death and Posttransplant Ischaemia Reperfusion Injury

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