Dataset Information

Lung transplant patients BALF proteomics, study of CLAD patients

ABSTRACT: In the current study, we use mass spectrometry-based proteomics to analyze bronchoalveolar lavage fluid (BALF) samples collected from a cohort of 43 patients of which 30 patients present a lung function that is stable over 36 months and 13 patients that develop CLAD within the first-year post-transplant. The mass spectrometry method used label free quantification (LFQ) of all the proteins detected as well as heavy labelled peptides for absolute quantification of mucins and related proteins.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Respiratory System Fluid/secretion, Bronchoalveolar Lavage

DISEASE(S): Lung Disease

SUBMITTER: Liisa Arike

LAB HEAD: Liisa Arike

PROVIDER: PXD044416 | Pride | 2026-06-08

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	210608_QExHF_LA_MS755_MS709_rx531_2xdil.raw	Raw
	210608_QExHF_LA_MS755_MS709_rx531_2xdil_PRM.raw	Raw
	210608_QExHF_LA_MS755_MS728_rx794_2xdil.raw	Raw
	210608_QExHF_LA_MS755_MS728_rx794_2xdil_PRM.raw	Raw
	210608_QExHF_LA_MS755_rx15_2xdil.raw	Raw

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Publications

Proteomic analysis of bronchoalveolar lavage fluid after lung transplantation associates stable allograft function with less lung damage at 12 months.

Arike Liisa L Johansson Kristina K Ermund Anna A Greer Mark M Pelaseyed Thaher T Westin Johan J Hansson Gunnar C GC Magnusson Jesper M JM

ERJ open research 20260301 2

<h4>Introduction</h4>Freedom from chronic lung allograft dysfunction (CLAD) is a key objective after lung transplantation, yet predicting its onset remains challenging. This study investigated whether early proteomic changes in bronchoalveolar lavage fluid can differentiate between patients maintaining stable graft function at 36 months and those developing CLAD within the first year. Additionally, findings were compared to proteomic data from non-transplanted individuals.<h4>Methods</h4>Broncho ...[more]

PMID: 42111374

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Project description:In this study we compared the intestinal mucus phenotype of Clca1-deficient (Clca1-/-) mice and wild-type (WT) controls. The human CLCA1 (chloride channel regulator, calcium-activated) and its murine ortholog mouse CLCA1 (formerly known as CLCA3) are secreted proteins which have been linked to human respiratory diseases such as asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD) as well as to the corresponding murine models of these diseases. Common, disease severity-related features are goblet cell hyperplasia, mucus overproduction and disturbed clearance. Neutralization of mouse CLCA1 ameliorates the symptoms in the asthmatic mouse model and restoration of the decreased mouse CLCA1 protein level in a CF mouse model ameliorates the intestinal CF lesions, pointing toward these proteins being potential therapeutic targets. The expression CLCA1 can be induced in airways but this protein is normally expressed and secreted by goblet cells of the intestinal tract in both human and mouse together with the intestinal MUC2 mucin. This makes CLCA1 a major constituent of the extracellular intestinal mucus in which the MUC2 mucin is the main structural component. To study the possible further effects of murine CLCA1 deficiency on Muc2 and on other important components of the mucus, such as Agr2, Fcgbp, Klk and Zg16, a shotgun label-free proteomics study was performed which compared their relative abundance in the mucus layer, showing a tight and significant correlation between WT and Clca1-/- mucus proteins (Pearson r = 0.931, r2 = 0.868, p < 0.0001, based on 809 valid pairs). No significant differences in known mucus protein expression were observed. However, the abundance of CLCA1 in the mucus together with the domain structure suggests a structural role and other methods to reveal the function of these domains might shed light on the overall function in mucus. Because of its abundance in the mucus and the well preserved structure thought a long evolution together with mucus we still speculate that CLCA1 was developed to protect the expressing organism, although the threat is elusive.