Bronchoalveolar lavage fluid cellularity and soluble intercellular adhesion molecule-1 in children with colds

Grigg, Jonathan; Riedler, Josef; Robertson, Colin F.

doi:10.1002/(sici)1099-0496(199908)28:2<109::aid-ppul6>3.0.co;2-5

Cited by 26 publications

(9 citation statements)

References 30 publications

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“…First, trivial symptoms associated with the common cold may be associated with a similar pattern of neutrophil activation. In a very small group of children with rhinovirus colds, we have previously reported the presence of BAL fluid neutrophilia, 17 which may indicate that some neutrophil transmigration may occur during most trivial colds. We speculate that children with PVW have a propensity to recruit more neutrophils in their airways, and that neutrophil products trigger bronchoconstriction via activating other inflammatory cells, such as mast cells.…”

Section: Discussionmentioning

confidence: 95%

Systemic neutrophil activation in acute preschool viral wheeze

Oommen

Patel²,

Browning³

et al. 2003

Archives of Disease in Childhood

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Background: In preschool children, attacks of wheeze are usually triggered by viral colds. The inflammatory substrate in preschool viral wheeze (PVW) is unclear, but epidemiological data suggest that most PVW is not caused by allergic inflammation. We therefore speculated that the neutrophils are an important effector cell. Systemic neutrophil activation is the first stage for the development of pulmonary neutrophilia. Markers of neutrophil activation are shedding of the adhesion molecule L-selectin from the cell surface, upregulation of Mac-1 expression, and an increase in serum soluble L-selectin. Aims: To obtain evidence for systemic neutrophil activation during PVW. Methods: Preschool children (1-5 years) admitted to hospital with acute PVW (n = 20) and normal controls (n = 18) were studied. Adhesion molecule expression on CD16 positive neutrophils was determined in both groups and expressed as molecules of equivalent fluorochrome (MEF). Serum soluble L-selectin was analysed by ELISA. Results: Compared with controls, children with PVW had reduced neutrophil L-selectin expression (median MEF (IQR): 69 (11 to 96) units versus 136 (109 to 163) units, p < 0.001) and higher serum soluble L-selectin (2.8 (2.3 to 3.1) versus 2.4 (2.2 to 2.6) µg/ml, p = 0.04). There was no significant difference in neutrophil Mac-1 expression. Conclusion: Systemic neutrophil activation is associated with acute PVW.

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Section: Discussionmentioning

confidence: 95%

Systemic neutrophil activation in acute preschool viral wheeze

Oommen

Patel²,

Browning³

et al. 2003

Archives of Disease in Childhood

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“…This is particularly pertinent to influenza and RSV, as there were very few children in whom these viruses were detected. Secondly, we used neutrophilic lower airway inflammation as a surrogate marker for active pulmonary disease, as used by other authors [34,35]. We did not, however, test for additional indirect markers of viral infection such as Toll-like receptor 3 (TLR3), interferon gamma induced protein 10 (IP-10) or virus-specific antibodies.…”

Section: Discussionmentioning

confidence: 99%

Respiratory virus detection in nasopharyngeal aspirate versus bronchoalveolar lavage is dependent on virus type in children with chronic respiratory symptoms

Wurzel

Marchant

Clark

et al. 2013

Journal of Clinical Virology

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“…Increased sICAM-1 in BAL has been described in adults with granulomatous lung diseases such as sarcoidosis, tuberculosis, hypersensitivity pneumonitis, and radiation pneumonitis (3,10,18) and in children exposed to second-hand smoke (16). Kasper et al (20) and Beck-Schimmer et al (5) have shown that a soluble form of ICAM-1 can be measured in the BAL of rats by Western blot analysis after immunoprecipitation and by ELISA, respectively.…”

Section: Discussionmentioning

confidence: 99%

Shedding of soluble ICAM-1 into the alveolar space in murine models of acute lung injury

Mendez¹,

Morris²,

Wilcoxen³

et al. 2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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is an adhesion molecule constitutively expressed in abundance on the cell surface of type I alveolar epithelial cells (AEC) in the normal lung and is a critical participant in pulmonary innate immunity. At many sites, ICAM-1 is shed from the cell surface as a soluble molecule (sICAM-1). Limited information is available regarding the presence, source, or significance of sICAM-1 in the alveolar lining fluid of normal or injured lungs. We found sICAM-1 in the bronchoalveolar lavage (BAL) fluid of normal mice (386 Ϯ 50 ng/ml). Additionally, sICAM-1 was spontaneously released by murine AEC in primary culture as type II cells spread and assumed characteristics of type I cells. Shedding of sICAM-1 increased significantly at later points in culture (5-7 days) compared with earlier time points (3-5 days). In contrast, treatment of AEC with inflammatory cytokines had limited effect on sICAM-1 shedding. BAL sICAM-1 was evaluated in in vivo models of acute lung injury. In hyperoxic lung injury, a reversible process with a major component of leak across the alveolar wall, BAL fluid sICAM-1 only increased in parallel with increased alveolar protein. However, in lung injury due to FITC, there were increased levels of sICAM-1 in BAL that were independent of changes in BAL total protein concentration. We speculate that after lung injury, changes in sICAM-1 in BAL fluid are associated with progressive injury and may be a reflection of type I cell differentiation during reepithelialization of the injured lung. alveolar epithelial cell; differentiation; aquaporin-5; cell culture; CD54INTERCELLULAR ADHESION MOLECULE-1 (ICAM-1) is an ϳ100-kDa protein belonging to the immunoglobulin superfamily that is involved in leukocyte trafficking and lymphocyte activation (37). ICAM-1 is a transmembrane protein that is the counterreceptor for the ␤ 2 -integrins CD11a/CD18 (LFA-1) and CD11b/CD18 (Mac-1), found on leukocytes. ICAM-1 expression can be induced on most structural cells, including endothelial cells, fibroblasts, and epithelial cells, by inflammatory cytokines (37). In contrast, in the normal lung, ICAM-1 is constitutively expressed in abundance on the apical surface of type I alveolar epithelial cells (AEC), but not on type II AEC in the absence of inflammatory stimulation (9,19,32). Similar to markers such as aquaporin-5 (AQP5) and RTI40 (6, 27, 41), constitutive ICAM-1 expression is a feature of type I, but not type II, AEC in the normal lung. Furthermore, when type II cells are isolated from rats, ICAM-1 expression is induced under culture conditions favoring expression of type I AEC characteristics (9). Previously, we have shown that absence or neutralization of ICAM-1 on AEC in vivo impairs function, but not recruitment, of leukocytes in the setting of pneumonia due to Klebsiella pneumoniae (19). Moreover, blockade of ICAM-1 in vitro results in decreased macrophage mobility (20), phagocytosis, and killing of K. pneumoniae (19).In addition to its expression on the cell surface of endothelial cells, ICAM-1 is shed from that surface...

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Bronchoalveolar lavage fluid cellularity and soluble intercellular adhesion molecule-1 in children with colds

Cited by 26 publications

References 30 publications

Systemic neutrophil activation in acute preschool viral wheeze

Systemic neutrophil activation in acute preschool viral wheeze

Respiratory virus detection in nasopharyngeal aspirate versus bronchoalveolar lavage is dependent on virus type in children with chronic respiratory symptoms

Shedding of soluble ICAM-1 into the alveolar space in murine models of acute lung injury

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