Cell Profiles of Bronchoalveolar Lavage Fluid as Prognosticators of Idiopathic Pulmonary Fibrosis/Usual Interstitial Pneumonia among Japanese Patients

Tabuena, Rollin P.; Nagai, Sonoko; Tsutsumi, Takanobu; Handa, Tomohiro; Takeuchi, Minoru; Mikuniya, Takeshi; Shigematsu, Michio; Hamada, Kunio; Izumi, Tohru; Mishima, Michiaki

doi:10.1159/000087673

Cited by 36 publications

(33 citation statements)

References 56 publications

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“…Lymphocyte infiltration in areas of honeycombed lung in patients with UIP correlates positively with survival (114,116,141), and these lymphocytes display elevated CD4/CD8 Tcell ratios, highlighting the importance of this subpopulation in IPF. Such features are also seen in NSIP and indicate improved prognosis (76).…”

Section: Cellularity In Ipfmentioning

confidence: 99%

“…Lymphocytes likely play a more dominate role in the infiltrative lesions seen in NSIP, whereas other inflammatory cells like neutrophils are involved in the fibrotic lesions of UIP (135,152). Plasma cells infiltrating the honeycombed areas of fibrosis in surgical lung biopsies from patients with UIP also correlate with survival (114,116,141).…”

Section: Cellularity In Ipfmentioning

confidence: 99%

“…Sputum and BAL samples from patients with IPF show elevated levels of IL-8, an important neutrophil chemoattractant and proangiogenic molecule, which correlates with lung-function impairment and prognosis (14,60). Neutrophilic infiltration in the honeycombed fibrotic areas of surgical lung biopsies from patients with UIP correlates inversely with survival (114,116,141). Alveolar macrophages are elevated in BAL samples (133) and are critical in promoting neutrophil influx (63,112,137,138) through MIP-1α/CCL3 and IL-8 release (137,138).…”

Section: Cellularity In Ipfmentioning

confidence: 99%

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The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

Bringardner

Baran

Eubank

et al. 2008

Antioxidants & Redox Signaling

253

190

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The role of inflammation in idiopathic pulmonary fibrosis (IPF) is controversial. If inflammation were critical to the disease process, lung pathology would demonstrate an influx of inflammatory cells, and that the disease would respond to immunosuppression. Neither is true. The classic pathology does not display substantial inflammation, and no modulation of the immune system is effective as treatment. Recent data suggest that the pathophysiology of the disease is more a product of fibroblast dysfunction than of dysregulated inflammation. The role of inflammation in disease pathogenesis comes from pathology from atypical patients, biologic samples procured during exacerbations of the disease, and careful examination of biologic specimens from patients with stable disease. We suggest that inflammation is indeed a critical factor in IPF and propose five potential nontraditional mechanisms for the role of inflammation in the pathogenesis of IPF: the direct inflammatory hypothesis, the matrix hypothesis, the growth factor-receptor hypothesis, the plasticity hypothesis, and the vascular hypothesis. To address these, we review the literature exploring the differences in pathology, prognosis, and clinical course, as well as the role of cytokines, growth factors, and other mediators of inflammation, and last, the role of matrix and vascular supply in patients with IPF.

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Section: Cellularity In Ipfmentioning

confidence: 99%

Section: Cellularity In Ipfmentioning

confidence: 99%

Section: Cellularity In Ipfmentioning

confidence: 99%

See 1 more Smart Citation

The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

Bringardner

Baran

Eubank

et al. 2008

Antioxidants & Redox Signaling

253

190

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“…In interstitial lung diseases, the diagnosis can be rarely based on BAL findings only, but BAL often provides diagnostically relevant results [1,2,3,4]. BAL measures cellular and non-cellular constituents of the bronchoalveolar space.…”

Section: Introductionmentioning

confidence: 99%

Bronchoalveolar Lavage in Interstitial Lung Diseases: Does the Recovery Rate Affect the Results?

Schildge

Nagel²,

Grun³

2007

Respiration

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Background: Bronchoalveolar lavage (BAL) is an established diagnostic tool in interstitial lung diseases. BAL frequently yields findings of diagnostic value and at times even confirmatory diagnostic results. Objectives: The present study has been designed to investigate whether the recovery rate affects BAL results relative to the instilled volume. Methods: Six hundred and eighteen patients with the following diagnoses were included into the study: 236 with sarcoidosis, 85 with idiopathic pulmonary fibrosis, 83 with cryptogenic organizing pneumonitis, 64 with connective tissue disease affecting the lungs, 54 with respiratory bronchiolitis with interstitial lung disease, 51 with extrinsic allergic alveolitis and 45 control patients. BAL was performed during flexible bronchoscopy with an irrigation volume of 100 ml 0.9% saline solution in 5 aliquots of 20 ml each. Only patients with a recovery of at least 30 ml were evaluated. Initially, the entire patient population was analysed, followed by an analysis within the different diagnostic groups and a comparison between patients with a high (>50 ml) and low (≤50 ml) recovery rate. Results: The recovery rate varied between the diagnostic groups (p < 0.001) and was negatively correlated with age (r = –0.21, p < 0.001) and smoking history (r = –0.11, p < 0.035). There were no correlations with inspiratory vital capacity (%pred.; p = 0.26) and forced expiratory volume in 1 s (%pred.; p = 0.15), but a positive correlation with the index (forced expiratory volume in 1 s/inspiratory vital capacity) × 100 (r = 0.23, p < 0.001). The cellular and non-cellular constituents of BAL were not affected by the recovery: cells/millilitre BAL (p = 0.71), relative proportion of macrophages (p = 0.92), lymphocytes (0 = 0.33), neutrophils (p = 0.14) and eosinophils (p = 0.11), albumin concentration (p = 0.13), and proportion of albumin in total protein (p = 0.06). The same applied for the lymphocyte surface markers CD4 (p = 0.72) and CD8 (p = 0.53). In the group with a high recovery rate, patients with sarcoidosis had a lower proportion of eosinophils (p = 0.04) and patients with cryptogenic organizing pneumonitis a higher concentration of albumin (p = 0.02) and lymphocytes (p = 0.007). Otherwise, no further differences were detected. Conclusions: The recovery rate hardly affected the cellular and non-cellular constituents of BAL at a lower limit of 30% of the instilled volume.

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“…Idiopathic interstitial pneumonia comprises a group of interstitial lung diseases where the precise role of the various inflammatory cells remains poorly understood [3,4,5]. Especially in idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP), the role of inflammatory cells in the pathogenesis of fibrosis is debatable [6,7,8]. …”

Section: Introductionmentioning

confidence: 99%

Inflammatory Cell Phenotyping of the Pulmonary Interstitium in Idiopathic Interstitial Pneumonia

et al. 2006

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Background: Several studies have implicated the role of inflammation in the pathogenesis of lung damage in idiopathic interstitial pneumonias (IIPs). Investigations of inflammatory cells in IIP have show that eosinophils, neutrophils and T cells may be associated with a poorer prognosis. Objectives: The aim of our study was to map, by quantitative analysis, the number of inflammatory cells in the lung tissue of patients with non-specific interstitial pneumonia/non-specific interstitial pneumonia (NSIP/NSIP), acute interstitial pneumonia/diffuse alveolar damage (AIP/DAD) and idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP) and to correlate them with lung function tests and survival. Methods: After immunohistochemical staining, we quantified the content of inflammatory cells [macrophages, neutrophils (elastase+), plasma cells, and CD3, CD4 and CD8 T lymphocytes (TLs)] in 20 NSIP, 20 DAD and 20 UIP surgical lung biopsies. Results: The total density of inflammatory cells was significantly increased in DAD and NSIP when compared to UIP (p = 0.04). TLs were increased in DAD and NSIP when compared to UlP lungs (p < 0.05). The density of inflammatory cells in UIP showed significant differences in normal, intervening and dense fibrosis areas (p < 0.05). The most numerous cells infiltrating the mural fibrosis and honeycombing areas were plasma cells, neutrophils (elastase+), CD20+, CD3+, CD4+ and CD8+ (p < 0.05). In UIP, CD3+ TLs were directly correlated with forced expiratory volume in 1 s/forced vital capacity ratio × 100 (p = 0.05). CD68+ cells presented a significant positive correlation with the forced expiratory volume in 1 s (p = 0.04); neutrophil (elastase+) cells significantly correlated with residual volume (p = 0.02), residual volume/total lung capacity (p = 0.04) and carbon monoxide transfer factor (p = 0.03). The most important predictor of survival in UIP was CD3+ TLs (p = 0.05). Conclusion: The total density of inflammatory cells and lymphocytes presents a different distribution within the pulmonary parenchyma in AIP/DAD, NSIP/NSIP and IPF/UIP evolutionary adapted responses to injury. There is a localized distribution of inflammation in the normal, intervening and dense fibrosis areas of UIP for CD3+, associated with a lethal deterioration of the pulmonary function and poor survival. Our findings provide further evidence of the importance of inflammation in the pathophysiology of IIPs.

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Cell Profiles of Bronchoalveolar Lavage Fluid as Prognosticators of Idiopathic Pulmonary Fibrosis/Usual Interstitial Pneumonia among Japanese Patients

Cited by 36 publications

References 56 publications

The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

Bronchoalveolar Lavage in Interstitial Lung Diseases: Does the Recovery Rate Affect the Results?

Inflammatory Cell Phenotyping of the Pulmonary Interstitium in Idiopathic Interstitial Pneumonia

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