Increased MCP-1 and MIP-1β in bronchoalveolar lavage fluid of chronic bronchitics

Capelli, A; Stefano, Antonino Di; Gnemmi, Isabella; Balbo, Piero Emilio; Cerutti, C G; Balbi, Bruno; Lusuardi, Mirco; Cf, Donner

doi:10.1034/j.1399-3003.1999.14a27.x

Cited by 140 publications

(112 citation statements)

References 23 publications

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“…Macrophages from COPD patients are more active and secrete more inflammatory proteins, such as chemokines, metalloproteinases and cytokines. The increased amount of macrophages may depend on enhanced recruitment of monocytes from the circulation which been found in BALf from patients with chronic bronchitis [101].…”

Section: Inflammatory Cells In the Pulmonary Circulationmentioning

confidence: 98%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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In chronic lung disorders such as in asthma and chronic obstructive pulmonary disease (COPD) there is increased bronchial angiogenesis and remodelling of pulmonary vessels culminating to altered bronchial and pulmonary circulation. The involvement of residential cells such as endothelial cells, smooth muscle cells and pulmonary fibroblasts, all appear to have a crucial role in the progression of vascular inflammation and remodelling. The regulatory abnormalities, growth factors and mediators implicated in the pulmonary vascular changes of asthma and COPD subjects and potential therapeutic targets have been described in this review.

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Section: Inflammatory Cells In the Pulmonary Circulationmentioning

confidence: 98%

Pulmonary vascular changes in asthma and COPD

Harkness

Kanabar

Sharma

et al. 2014

Pulmonary Pharmacology & Therapeutics

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“…Levels of CCL4 are increased in alcoholic liver disease [9], glomerulonephritis, acute renal transplant rejection [10], human sepsis [11], and advanced atherosclerosis lesions [12]. There are no reports regarding the role of CCL4 in asthma disease but there are some observations of higher levels of this cytokine in several pulmonary conditions such as chronic bronchitis [13], pulmonary fibrosis [14], and cystic fibrosis [15].…”

mentioning

confidence: 98%

CCL4 Levels Differ between Aspirin-Tolerant and Aspirin-Intolerant Patients with Asthma

Velázquez¹,

Soid-Raggi²,

Terán³

et al. 2017

Health

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Aspirin-exacerbated respiratory disease (AERD) is an asthma phenotype characterized by nasal polyps, chronic hypertrophic eosinophilic sinusitis, asthma, and sensitivity to aspirin. Unawareness of this disease by patients and their physicians may have serious consequences because of the risk of near-fatal asthma. Its confirmative diagnosis can be established only by provocative aspirin challenge, which represents a potential risk for patient health. Purpose: Because CCL4 plays an important role in several pulmonary conditions, we tested its immunoreactivity in nasal lavages and sera from control subjects, and from aspirin-sensitive and non-aspirin-sensitive patients. Method: Immunoreactivity of CCL4 was measured in serum and nasal lavages from 30 healthy controls (HC), 23 patients with AERD, and 20 patients with aspirin-tolerant asthma (ATA). Additionally, a serum biobank contained sera from 90 HC, 83 patients with AERD, and 69 patients with ATA was employed. Results: The serum immunoreactivity of CCL4 could distinguish both types of asthma phenotypes. Conclusion: CCL4 may play an unexpected role in thephysiopathology of AERD.

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“…This was performed exactly as described previously [13,14,15]. Four bronchial mucosal biopsy specimens were taken from segmental and subsegmental airways of the right lower and upper lobes, using size-19 cupped forceps.…”

Section: Fibreoptic Bronchoscopy Collection and Processing Of Bronchmentioning

confidence: 99%

“…BAL was performed and processed as previously described [13]. Cytospin slides (Cytospin II; Shandon, London, UK), prepared with native pellet, were stained with May-Grunwald Giemsa to determine the leukocyte differential cell count.…”

Section: Processing Of Bronchoalveolar Lavagementioning

confidence: 99%

“…Biopsy specimens were gently extracted from the forceps, processed for light microscopy, as previously described, and stored frozen at -80uC until use [13]. Two 6-mm cryostat sections at an interval of 100 mm were subsequently processed for immunohistochemistry, using the following panel of antibodies: mouse anti-CD3 ( .…”

Section: Immunohistochemistry (Single-and Double-staining)mentioning

confidence: 99%

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STAT4 activation in smokers and patients with chronic obstructive pulmonary disease

Stefano¹,

Caramori²,

Capelli³

et al. 2004

Eur Respir J

Self Cite

128

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Activation of the transcription factor signal transducer and activator of transcription (STAT)-4 is critical for the differentiation of T-helper 1 cells/type-1 cytotoxic T-cells and the production of interferon (IFN)-c.Expression of STAT4, phospho-STAT4, IFN-c and T-box expressed in T-cells (Tbet) proteins in bronchial biopsies and bronchoalveolar lavage (BAL)-derived lymphocytes, obtained from 12 smokers with mild/moderate chronic obstructive pulmonary disease (COPD) (forced expiratory volume in one second (FEV1) 59¡16% predicted), 14 smokers with normal lung function (FEV1 106¡12% pred) and 12 nonsmoking subjects (FEV1 111¡14% pred), was examined by immunohistochemistry and immunocytochemistry.In bronchial biopsies of COPD patients, the number of submucosal phospho- 6103 ). In all smokers who underwent lavage, phospho-STAT4z lymphocytes correlated with airflow obstruction and the number of IFNcz lymphocytes. T-bet expression was not altered in bronchial biopsies and BAL-derived lymphocytes between the three groups.In conclusion, this study suggests that stable mild/moderate chronic obstructive pulmonary disease is associated with an active T-helper 1 cell/type-1 cytotoxic T-cell inflammatory process involving activation of signal transducer and activator of transcription 4 and interferon-gamma production.

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Increased MCP-1 and MIP-1β in bronchoalveolar lavage fluid of chronic bronchitics

Cited by 140 publications

References 23 publications

Pulmonary vascular changes in asthma and COPD

Pulmonary vascular changes in asthma and COPD

CCL4 Levels Differ between Aspirin-Tolerant and Aspirin-Intolerant Patients with Asthma

STAT4 activation in smokers and patients with chronic obstructive pulmonary disease

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