Relationship of BAL and Lung Tissue CD4+ and CD8+ T Lymphocytes, and Their Ratio in Idiopathic Pulmonary Fibrosis

Papiris, Spyros; Kollintza, Androniki; Kitsanta, Panagiota; Kapotsis, G.E.; Karatza, Marilena; Milic-Emili, J; Roussos, Charis; Daniil, Zoe

doi:10.1016/s0012-3692(15)52722-0

Cited by 44 publications

(24 citation statements)

References 29 publications

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“…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: 89%

“…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: 98%

“…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: 89%

Section: Cellularity In Ipfmentioning

confidence: 98%

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

View full text Add to dashboard Cite

show abstract

“…However, in BAL cell from TTP À/À mice, the half-lives of TNF-a and IL-1b were >2 hours after actinomycin D and carbon monoxide did not enhance the decay of LPS-induced inflammatory cytokine mRNAs (Figure 4, A and B). Because alterations in BAL reflect changes in the lung parenchyma, 36,37 these results indicate that Ttp-mediated destabilization of inflammatory cytokine mRNAs contributes to carbon monoxide's anti-inflammatory function in LPSinduced lung inflammation.…”

Section: Carbon Monoxide Enhances Degradation Of Inflammatory Cytokinmentioning

confidence: 92%

Tristetraprolin Mediates Anti-Inflammatory Effects of Carbon Monoxide on Lipopolysaccharide-Induced Acute Lung Injury

Joe

Kim

Chen

et al. 2015

The American Journal of Pathology

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“…40 Analysis of the CD4 ϩ T-cell subpopulation has shown that patients with idiopathic pulmonary fibrosis have a significantly lower CXCR3 and a higher CCR4 expression on bronchoalveolar lavage CD4 ϩ T cells. 41 Moreover, treatment of these patients with corticosteroids results in higher CXCR3 and lower CCR4 expression compared with those in untreated patients.…”

Section: Ifn-␥ Gene Transcription Via the Down-regulation Of Stat4mentioning

confidence: 99%

Overexpression of the Transcription Factor GATA-3 Enhances the Development of Pulmonary Fibrosis

Kimura

Ishii

Yoh

et al. 2006

The American Journal of Pathology

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Recent studies have demonstrated that Th2 cytokines, such as interleukin-4 and interleukin-13, enhance fibrotic processes by activating fibroblast proliferation and collagen production, whereas interferon-␥, a Th1 cytokine, inhibits these processes. Th1 and Th2 cells both differentiate from common T precursor cells, with transcription factor GATA-3 a key regulator of Th2 differentiation. In the present study, therefore, we examined the effects of GATA-3 overexpression on the development of pulmonary fibrosis in a mouse model. Wild-type C57BL/6 mice and GATA-3-overexpressing (GATA-3-tg) mice of the same background were intratracheally treated with bleomycin. The survival rate after bleomycin was significantly decreased in GATA-3-tg mice compared with wild-type mice. The degree of pulmonary fibrosis was much greater in GATA-3-tg mice than in wild-type mice 28 days after bleomycin treatment. Lung interferon-␥ concentration was significantly decreased in GATA-3-tg mice compared with wild-type mice by 7 days after either saline or bleomycin treatment. The concentration of transforming growth factor-␤, a fibrogenic cytokine, was significantly higher in GATA-3-tg mice than in wild-type mice. Exogenous administration of interferon-␥ to GATA-3-tg mice improved the degree of pulmonary fibrosis and thus increased survival. These results indicate that overexpression of GATA-3 enhances the development of pulmonary fibrosis, possibly by reducing interferon-␥ levels in the lung. (Am

show abstract

Relationship of BAL and Lung Tissue CD4+ and CD8+ T Lymphocytes, and Their Ratio in Idiopathic Pulmonary Fibrosis

Cited by 44 publications

References 29 publications

The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

Tristetraprolin Mediates Anti-Inflammatory Effects of Carbon Monoxide on Lipopolysaccharide-Induced Acute Lung Injury

Overexpression of the Transcription Factor GATA-3 Enhances the Development of Pulmonary Fibrosis

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