Airway allergy causes alveolar macrophage death, profound alveolar disorganization and surfactant dysfunction

Feo-Lucas, Lidia; Godio, Cristina; Escalera, María Minguito de la; Alvarez-Ladrón, Natalia; Villarrubia, Laura H.; Vega-Pérez, Adrián; González-Cintado, Leticia; Domínguez‐Andrés, Jorge; García-Fojeda, Belén; Montero-Fernández, Carlos; Casals, Cristina; Autilio, Chiara; Pérez‐Gil, Jesús; Crainiciuc, Georgiana; Hidalgo, Andrés; López-Bravo, Marı́a; Ardavı́n, Carlos

doi:10.3389/fimmu.2023.1125984

Cited by 4 publications

(1 citation statement)

References 46 publications

(69 reference statements)

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“…Patients with PAH tend to have proinflammatory gut dysbiosis, and HFD may help slow the disease progression, probably because metabolite butyric acid reduces hypoxia-induced AM accumulation. During hypoxiainduced PAH, AM activation is complex and partially dependent on the microenvironment; thus, in addition to directly affecting the number of AMs, butyrate has a protective effect on hypoxia-induced angiogenesis and endothelial barrier dysfunction (69,70). Besides, structural changes in the lungs are rarely reversible because PAH regression takes more time than PAH development.…”

Section: Inflammatory Injurymentioning

confidence: 99%

Alveolar macrophage modulation via the gut–lung axis in lung diseases

Chen,

Liu,

Huang

2023

Front. Immunol.

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Several studies have demonstrated great potential implications for the gut–lung axis in lung disease etiology and treatment. The gut environment can be influenced by diet, metabolites, microbiotal composition, primary diseases, and medical interventions. These changes modulate the functions of alveolar macrophages (AMs) to shape the pulmonary immune response, which greatly impacts lung health. The immune modulation of AMs is implicated in the pathogenesis of various lung diseases. However, the mechanism of the gut–lung axis in lung diseases has not yet been determined. This mini-review aimed to shed light on the critical nature of communication between the gut and AMs during the development of pulmonary infection, injury, allergy, and malignancy. A better understanding of their crosstalk may provide new insights into future therapeutic strategies targeting the gut–AM interaction.

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Section: Inflammatory Injurymentioning

confidence: 99%

Alveolar macrophage modulation via the gut–lung axis in lung diseases

Chen,

Liu,

Huang

2023

Front. Immunol.

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Extracellular matrix phenotyping by imaging mass cytometry defines distinct cellular matrix environments associated with allergic airway inflammation

Parkinson,

Ghafoor,

Dodd

et al. 2024

Preprint

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The extracellular matrix (ECM) forms the scaffold in which cells reside and interact. The composition of this scaffold guides the development of local immune responses and tissue function. With the advent of multiplexed spatial imaging methodologies, investigating the intricacies of cellular spatial organisation are more accessible than ever. However, the relationship between cellular organisation and ECM composition has been broadly overlooked. Using imaging mass cytometry, we investigated the association between cellular niches and their surrounding matrix environment during allergic airway inflammation in two commonly used mouse strains. By first classifying cells according to their canonical intracellular markers and then by developing a novel analysis pipeline to independently characterise a cells ECM environment, we integrated analysis of both intracellular and extracellular data. Applying this methodology to three distinct tissue regions we reveal disparate and restricted responses. Recruited neutrophils were dispersed within the alveolar parenchyma, alongside a loss of alveolar type I cells and an expansion of alveolar type II cells. This activated parenchyma was associated with increased proximity to hyaluronan and chondroitin sulphate. In contrast, infiltrating CD11b+ and MHCII+ cells accumulated in the adventitial cuff and aligned with an expansion of the subepithelial layer. This expanded subepithelial region was enriched for closely interacting stromal and CD11b+ immune cells which overlaid regions enriched for type-I and type-III collagen. The cell-cell and cell-matrix interactions identified here will provide a greater understanding of the mechanisms and regulation of allergic disease progression across different inbred mouse strains and provide specific pathways to target aspects of remodelling during allergic pathology.

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Innate players in Th2 and non-Th2 asthma: emerging roles for the epithelial cell, mast cell, and monocyte/macrophage network

Kotrba,

Müller,

Pausder

et al. 2024

American Journal of Physiology-Cell Physiology

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Asthma is one of the most common chronic respiratory diseases and is characterized by airway inflammation, increased mucus production and structural changes in the airways. Recently, there is increasing evidence that the disease is much more heterogeneous than expected, with several distinct asthma endotypes. Based on the specificity of T cells as the best-known driving force in airway inflammation, bronchial asthma is categorized into T helper cell (Th)2 and non-Th2 asthma. The most studied effector cells in Th2 asthma include T cells and eosinophils. In contrast to Th2 asthma, much less is known about the pathophysiology of non-Th2 asthma, which is often associated with treatment resistance. Besides T cells, the interaction of myeloid cells such as monocytes/macrophages and mast cells with the airway epithelium significantly contributes to the pathogenesis of asthma. However, the underlying molecular regulation and particularly the specific relevance of this cellular network in certain asthma endotypes remains to be understood. In this review, we summarize recent findings on the regulation of and complex interplay between epithelial cells and the "non-classical" innate effector cells, mast cells and monocytes/macrophages, in Th2 and non-Th2 asthma with the ultimate goal to provide the rationale for future research into targeted therapy regimens.

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Airway allergy causes alveolar macrophage death, profound alveolar disorganization and surfactant dysfunction

Cited by 4 publications

References 46 publications

Alveolar macrophage modulation via the gut–lung axis in lung diseases

Alveolar macrophage modulation via the gut–lung axis in lung diseases

Extracellular matrix phenotyping by imaging mass cytometry defines distinct cellular matrix environments associated with allergic airway inflammation

Innate players in Th2 and non-Th2 asthma: emerging roles for the epithelial cell, mast cell, and monocyte/macrophage network

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