Inflammatory signature in lung tissues in patients with combined pulmonary fibrosis and emphysema

Cornwell, William D.; Kim, Cynthia; Lastra, Alejandra; Dass, Chandra; Bolla, Sudhir; Wang, He; Zhao, Huaqing; Ramsey, Frederick V.; Marchetti, Nathaniel; Rogers, Thomas J.; Criner, Gerard J.

doi:10.1080/1354750x.2018.1542458

Cited by 11 publications

(11 citation statements)

References 39 publications

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“…Efforts to reveal immunological and inflammatory mechanisms of CPFE progression have included several studies of biomarkers associated with the disease. Cornwell et al [ 37 ] studied explanted lung tissue from patients who died of lethal trauma. They categorized lung tissue into emphysema only, IPF, CPFE, and healthy control groups, then compared levels of 34 inflammatory biomarkers [ 37 ].…”

Section: Pathophysiology and Biomarkersmentioning

confidence: 99%

“…Cornwell et al [ 37 ] studied explanted lung tissue from patients who died of lethal trauma. They categorized lung tissue into emphysema only, IPF, CPFE, and healthy control groups, then compared levels of 34 inflammatory biomarkers [ 37 ]. Regional comparisons of biomarkers showed no significant differences among groups (i.e., emphysema, IPF, or CPFE), except in the level of CCL22.…”

Section: Pathophysiology and Biomarkersmentioning

confidence: 99%

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Chronic Obstructive Pulmonary Disease Combined with Interstitial Lung Disease

2022

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Although chronic obstructive pulmonary disease (COPD) and interstitial lung disease (ILD) have distinct clinical features, both diseases may coexist in a patient because they share similar risk factors such as smoking, male sex, and old age. Patients with both emphysema in upper lung fields and diffuse ILD are diagnosed with combined pulmonary fibrosis and emphysema (CPFE), which causes substantial clinical deterioration. Patients with CPFE have higher mortality compared with patients who have COPD alone, but results have been inconclusive compared with patients who have idiopathic pulmonary fibrosis (IPF). Poor prognostic factors for CPFE include exacerbation, lung cancer, and pulmonary hypertension. The presence of interstitial lung abnormalities, which may be an early or mild form of ILD, is notable among patients with COPD, and is associated with poor prognosis. Various theories have been proposed regarding the pathophysiology of CPFE. Biomarker analyses have implied that this pathophysiology may be more closely associated with IPF development, rather than COPD or emphysema. Patients with CPFE should be advised to quit smoking and undergo routine lung function tests, and pulmonary rehabilitation may be helpful. Various pharmacologic agents and surgical approaches may be beneficial in patients with CPFE, but further studies are needed.

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Section: Pathophysiology and Biomarkersmentioning

confidence: 99%

Section: Pathophysiology and Biomarkersmentioning

confidence: 99%

Chronic Obstructive Pulmonary Disease Combined with Interstitial Lung Disease

2022

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“…One study assessed the tissue levels of 34 proteins and found a similar inflammatory signature in CPFE and IPF. 63 Other studies found lower levels of Krebs von den lungen-6 and CYFRA21-1 in peripheral blood of those with CPFE compared with IPF. 64,65…”

Section: Sleep Disordersmentioning

confidence: 92%

Comorbidity in idiopathic pulmonary fibrosis - what can biomarkers tell us?

Alfaro

Cordeiro

2020

Ther Adv Respir Dis

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Idiopathic pulmonary fibrosis (IPF) is characterized by progressive parenchymal scarring, leading to dyspnoea, respiratory failure and premature death. Although IPF is confined to the lungs, the importance of IPF comorbidities such as pulmonary hypertension and ischaemic heart disease, lung cancer, emphysema/chronic obstructive pulmonary disease, gastroesophageal reflux, sleep apnoea and depression has been increasingly recognized. These comorbidities may be associated with increased mortality and significant loss of quality of life, so their identification and management are vital. The development of good-quality biomarkers could lead to numerous gains in the management of these patients. Biomarkers can be used for the identification of predisposed individuals, early diagnosis, assessment of prognosis, selection of best treatment and assessment of response to treatment. However, the role of biomarkers for IPF comorbidities is still quite limited, and mostly based on evidence coming from populations without IPF. The future development of new biomarker studies could be informed by those that have been studied independently for each of these conditions. For now, clinicians should be mostly attentive to clinical manifestations of IPF comorbidities, and use validated diagnostic methods for diagnosis. As research on biomarkers of most common diseases continues, it is expected that useful biomarkers are developed for these diseases and then validated for IPF populations. The reviews of this paper are available via the supplemental material section.

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“…Inflammatory responses downregulated SFTPB, SFTPD, SCNN1A , and SCNN1B gene expression, related to surfactant production and alveolar fluid clearance in ATII cells ( 28 ). Decreased SP-D expression was detected in the lungs of emphysema patients ( 29 ), indicating the defects in ATII cell function and innate immunity. Especially the number of AM is negatively related to alveolar parenchymal tissue density ( 27 ), and impaired phagocytosis is positively associated with the severity of emphysema ( 30 ).…”

Section: Dysregulation Of Cell Signaling In Emphysema Developmentmentioning

confidence: 99%

Dysregulated Cell Signaling in Pulmonary Emphysema

2022

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Pulmonary emphysema is characterized by the destruction of alveolar septa and irreversible airflow limitation. Cigarette smoking is the primary cause of this disease development. It induces oxidative stress and disturbs lung physiology and tissue homeostasis. Alveolar type II (ATII) cells have stem cell potential and can repair the denuded epithelium after injury; however, their dysfunction is evident in emphysema. There is no effective treatment available for this disease. Challenges in this field involve the large complexity of lung pathophysiological processes and gaps in our knowledge on the mechanisms of emphysema progression. It implicates dysregulation of various signaling pathways, including aberrant inflammatory and oxidative responses, defective antioxidant defense system, surfactant dysfunction, altered proteostasis, disrupted circadian rhythms, mitochondrial damage, increased cell senescence, apoptosis, and abnormal proliferation and differentiation. Also, genetic predispositions are involved in this disease development. Here, we comprehensively review studies regarding dysregulated cell signaling, especially in ATII cells, and their contribution to alveolar wall destruction in emphysema. Relevant preclinical and clinical interventions are also described.

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Inflammatory signature in lung tissues in patients with combined pulmonary fibrosis and emphysema

Cited by 11 publications

References 39 publications

Chronic Obstructive Pulmonary Disease Combined with Interstitial Lung Disease

Chronic Obstructive Pulmonary Disease Combined with Interstitial Lung Disease

Comorbidity in idiopathic pulmonary fibrosis - what can biomarkers tell us?

Dysregulated Cell Signaling in Pulmonary Emphysema

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