Expression of tumour necrosis factor receptors by bronchoalveolar cells in hypersensitivity pneumonitis

Chen, B.; Tong, Zhaohui; Ye, Q.; Nakamura, Shinobu; Costabel, Ulrich; Guzman, Josune

doi:10.1183/09031936.05.00084704

Cited by 11 publications

(9 citation statements)

References 28 publications

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“…A variety of cytokines are produced including pro‐inflammatory and regulatory cytokines. Pro‐inflammatory cytokines such as tumour necrosis factor (TNF)‐α, IL‐1 and IL‐8 are produced by alveolar macrophages, which may explain the acute symptom of fever and neutrophilia 10–13 . Regulatory cytokines IL‐12 and IL‐18 are also produced, which can polarize lymphocytes towards a TH1‐type response.…”

Section: Immunopathogenesis Of Eaamentioning

confidence: 99%

“…Proinflammatory cytokines such as tumour necrosis factor (TNF)-α, IL-1 and IL-8 are produced by alveolar macrophages, which may explain the acute symptom of fever and neutrophilia. [10][11][12][13] Regulatory cytokines IL-12 and IL-18 are also produced, which can polarize lymphocytes towards a TH1-type response. Regulatory cytokines such as IL-10 are known to counteract many of the biological effects of interferon-γ suggesting that IL-10 plays a role in damping down the inflammatory process 14 and granuloma formation.…”

Section: Immunopathogenesis Of Eaamentioning

confidence: 99%

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Extrinsic allergic alveolitis

2006

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Extrinsic allergic alveolitis (also known as hypersensitivity pneumonitis) is caused by repeated inhalation of mainly organic antigens by sensitized subjects. This induces a hypersensitivity response in the distal bronchioles and alveoli and subjects may present clinically with a variety of symptoms. The aims of this review are to describe the current concepts of the immunological response, the diverse clinical presentation of this disease, the relevant investigations and management, and areas for future studies.

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Section: Immunopathogenesis Of Eaamentioning

confidence: 99%

Section: Immunopathogenesis Of Eaamentioning

confidence: 99%

Extrinsic allergic alveolitis

2006

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“…TNFR1 is expressed at relatively high levels on alveolar macrophages (Dai et al, 1999; Ermert et al, 2003; Gaede et al, 1999). Moreover, expression of TNFR1 has been reported to be increased in various models of inflammatory lung injury and disease, suggesting that TNFα may be a major mediator of the pathogenic response to toxicants (Bradley, 2008; Chen et al, 2005; Dai et al, 2005; Ermert et al, 2003). This is supported by findings that mice lacking TNFR1 are protected from lung injury induced by pulmonary irritants such as ozone, silica, bleomycin and radiation (Cho et al, 2001; Ortiz et al, 1999, 2001; Zhang et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Role of TNFR1 in lung injury and altered lung function induced by the model sulfur mustard vesicant, 2-chloroethyl ethyl sulfide

Sunil

Patel-Vayas

Shen

et al. 2011

Toxicology and Applied Pharmacology

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Lung toxicity induced by sulfur mustard is associated with inflammation and oxidative stress. To elucidate mechanisms mediating pulmonary damage, we used 2-chloroethyl ethyl sulfide (CEES), a model sulfur mustard vesicant. Male mice (B6129) were treated intratracheally with CEES (3 or 6 mg/kg) or control. Animals were sacrificed 3, 7 or 14 days later and bronchoalveolar lavage (BAL) fluid and lung tissue collected. Treatment of mice with CEES resulted in an increase in BAL protein, an indication of alveolar epithelial damage, within 3 days. Expression of Ym1, an oxidative stress marker also increased in the lung, along with inducible nitric oxide synthase, and at 14 days, cyclooxygenase-2 and monocyte chemotactic protein-1, inflammatory proteins implicated in tissue injury. These responses were attenuated in mice lacking the p55 receptor for TNFα (TNFR1−/−), demonstrating that signaling via TNFR1 is key to CEES-induced injury, oxidative stress, and inflammation. CEES-induced upregulation of CuZn–superoxide dismutase (SOD) and MnSOD was delayed or absent in TNFR1−/− mice, relative to WT mice, suggesting that TNFα mediates early antioxidant responses to lung toxicants. Treatment of WT mice with CEES also resulted in functional alterations in the lung including decreases in compliance and increases in elastance. Additionally, methacholine-induced alterations in total lung resistance and central airway resistance were dampened by CEES. Loss of TNFR1 resulted in blunted functional responses to CEES. These effects were most notable in the airways. These data suggest that targeting TNFα signaling may be useful in mitigating lung injury, inflammation and functional alterations induced by vesicants.

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“…Also, alveolar macrophages in HP patient are activated to express a number of molecules that may be important in generating or sustaining the inflammatory response (Yi, 2002;Chen et al, 2005). For example, in HP AMs have increased amounts of ICAM, which may enhance the antigen-presenting capability of AMs and blockade of ICAM-1 interaction with its ligand reduces fibrosis in an experimental model of HP.…”

Section: Hypersensitivity Pneumonitismentioning

confidence: 99%

Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

et al. 2007

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Pulmonary fibrosis is a general term that refers to a collection of connective tissue around alveolar structures. There are over 200 disorders where the lungs may be involved in a fibrotic response. To determine the cause of pulmonary fibrosis requires an in depth understanding of the pathogenesis of pulmonary fibrosis and breadth of knowledge of the causative agents and associated disorders that may lead to pulmonary fibrosis. A comprehensive evaluation of the patient is absolutely essential, starting with detailed history that includes an occupational and environmental history because fibrogenic exposures can occur in many settings. Equally important is a history of ingestion of pharmaceutical or nonpharmaceutical substances. A physical examination and judicious investigations are always a part of any comprehensive clinical assessment but they are not commonly helpful in elucidating the cause of most pulmonary fibrotic disorders. Although, a chest film is invariably done, a logical and strongly recommended next step is a high-resolution computed tomography (HRCT). HRCT provides a better assessment of the radiological pattern, may suggest a diagnosis as well as direct the site, and type of lung biopsy. If the history and investigations do not lead to a diagnosis then a lung biopsy is required. Prevention or removal of the inciting agent is critical to the treatment of these disorders and in some instances corticosteroids may be of help.

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Expression of tumour necrosis factor receptors by bronchoalveolar cells in hypersensitivity pneumonitis

Cited by 11 publications

References 28 publications

Extrinsic allergic alveolitis

Extrinsic allergic alveolitis

Role of TNFR1 in lung injury and altered lung function induced by the model sulfur mustard vesicant, 2-chloroethyl ethyl sulfide

Environmental, Inhaled and Ingested Causes of Pulmonary Fibrosis

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