Mast cell phenotypes in the allograft after lung transplantation

Amit Banga, Yingchun Han, Xiaofeng Wang, Fred H. Hsieh

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Background: The burden of mast cell (MC) infiltration and their phenotypes, MC-tryptase (MCT) and MC-tryptase/chymase (MCTC), after lung transplantation (LT) has not been evaluated in human studies. Methods: We reviewed 20 transbronchial lung biopsy (TBLB) specimen from patients with early normal allograft (<6 months post-LT, n=5), late normal allograft (>6 months, n=5), A2 or worse acute cellular rejection (ACR, n=5), and chronic lung allograft dysfunction (CLAD, n=5). Slides were immunostained for tryptase and chymase. Total MC, MCT, MCTC and MCTCto-MCT ratio were compared between the four groups using a generalized linear mixed model. Results: Irrespective of clinicopathologic diagnosis, MC burden tends to increase with time (r2=.56, P=.009). MCTC phenotype was significantly increased in the CLAD group (8.2±4.9 cells per HPF) in comparison with the other three groups (early normal: 1.6±1.7, P=.0026; late normal: 2.5±2.3, P=.048; ACR: 2.7±3.5, P=.021). Further, the ratio of MCTC to MCT was significantly increased in CLAD group as compared to the other three groups (P<.001 for all comparisons). Conclusions: The burden of MC may increase in the allograft as function of time. Patients with CLAD have an increased relative and absolute burden of MCTC phenotype MC. Future studies are needed to confirm these findings and evaluate the potential pathologic role of MCTC in allograft dysfunction.

Original languageEnglish (US)
Pages (from-to)845-851
Number of pages7
JournalClinical Transplantation
Volume30
Issue number7
DOIs
StatePublished - Jul 1 2016

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Tryptases
Lung Transplantation
Mast Cells
Allografts
Chymases
Phenotype
Lung
varespladib methyl
Linear Models

Keywords

  • acute cellular rejection
  • chronic lung allograft dysfunction
  • innate immunity
  • transbronchial lung biopsy

ASJC Scopus subject areas

  • Transplantation

Cite this

Mast cell phenotypes in the allograft after lung transplantation. / Banga, Amit; Han, Yingchun; Wang, Xiaofeng; Hsieh, Fred H.

In: Clinical Transplantation, Vol. 30, No. 7, 01.07.2016, p. 845-851.

Research output: Contribution to journalArticle

Banga, Amit ; Han, Yingchun ; Wang, Xiaofeng ; Hsieh, Fred H. / Mast cell phenotypes in the allograft after lung transplantation. In: Clinical Transplantation. 2016 ; Vol. 30, No. 7. pp. 845-851.
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abstract = "Background: The burden of mast cell (MC) infiltration and their phenotypes, MC-tryptase (MCT) and MC-tryptase/chymase (MCTC), after lung transplantation (LT) has not been evaluated in human studies. Methods: We reviewed 20 transbronchial lung biopsy (TBLB) specimen from patients with early normal allograft (<6 months post-LT, n=5), late normal allograft (>6 months, n=5), A2 or worse acute cellular rejection (ACR, n=5), and chronic lung allograft dysfunction (CLAD, n=5). Slides were immunostained for tryptase and chymase. Total MC, MCT, MCTC and MCTCto-MCT ratio were compared between the four groups using a generalized linear mixed model. Results: Irrespective of clinicopathologic diagnosis, MC burden tends to increase with time (r2=.56, P=.009). MCTC phenotype was significantly increased in the CLAD group (8.2±4.9 cells per HPF) in comparison with the other three groups (early normal: 1.6±1.7, P=.0026; late normal: 2.5±2.3, P=.048; ACR: 2.7±3.5, P=.021). Further, the ratio of MCTC to MCT was significantly increased in CLAD group as compared to the other three groups (P<.001 for all comparisons). Conclusions: The burden of MC may increase in the allograft as function of time. Patients with CLAD have an increased relative and absolute burden of MCTC phenotype MC. Future studies are needed to confirm these findings and evaluate the potential pathologic role of MCTC in allograft dysfunction.",
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N2 - Background: The burden of mast cell (MC) infiltration and their phenotypes, MC-tryptase (MCT) and MC-tryptase/chymase (MCTC), after lung transplantation (LT) has not been evaluated in human studies. Methods: We reviewed 20 transbronchial lung biopsy (TBLB) specimen from patients with early normal allograft (<6 months post-LT, n=5), late normal allograft (>6 months, n=5), A2 or worse acute cellular rejection (ACR, n=5), and chronic lung allograft dysfunction (CLAD, n=5). Slides were immunostained for tryptase and chymase. Total MC, MCT, MCTC and MCTCto-MCT ratio were compared between the four groups using a generalized linear mixed model. Results: Irrespective of clinicopathologic diagnosis, MC burden tends to increase with time (r2=.56, P=.009). MCTC phenotype was significantly increased in the CLAD group (8.2±4.9 cells per HPF) in comparison with the other three groups (early normal: 1.6±1.7, P=.0026; late normal: 2.5±2.3, P=.048; ACR: 2.7±3.5, P=.021). Further, the ratio of MCTC to MCT was significantly increased in CLAD group as compared to the other three groups (P<.001 for all comparisons). Conclusions: The burden of MC may increase in the allograft as function of time. Patients with CLAD have an increased relative and absolute burden of MCTC phenotype MC. Future studies are needed to confirm these findings and evaluate the potential pathologic role of MCTC in allograft dysfunction.

AB - Background: The burden of mast cell (MC) infiltration and their phenotypes, MC-tryptase (MCT) and MC-tryptase/chymase (MCTC), after lung transplantation (LT) has not been evaluated in human studies. Methods: We reviewed 20 transbronchial lung biopsy (TBLB) specimen from patients with early normal allograft (<6 months post-LT, n=5), late normal allograft (>6 months, n=5), A2 or worse acute cellular rejection (ACR, n=5), and chronic lung allograft dysfunction (CLAD, n=5). Slides were immunostained for tryptase and chymase. Total MC, MCT, MCTC and MCTCto-MCT ratio were compared between the four groups using a generalized linear mixed model. Results: Irrespective of clinicopathologic diagnosis, MC burden tends to increase with time (r2=.56, P=.009). MCTC phenotype was significantly increased in the CLAD group (8.2±4.9 cells per HPF) in comparison with the other three groups (early normal: 1.6±1.7, P=.0026; late normal: 2.5±2.3, P=.048; ACR: 2.7±3.5, P=.021). Further, the ratio of MCTC to MCT was significantly increased in CLAD group as compared to the other three groups (P<.001 for all comparisons). Conclusions: The burden of MC may increase in the allograft as function of time. Patients with CLAD have an increased relative and absolute burden of MCTC phenotype MC. Future studies are needed to confirm these findings and evaluate the potential pathologic role of MCTC in allograft dysfunction.

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