Upregulation of Mac-1 on polymorphonuclear leukocytes (PMNS) by IL-8 produced by RSV- infected pulmonary epithelium

N. Nakajima, E. Molina, Z. Jiang, Janak Patel

Research output: Contribution to journalArticle

Abstract

Bronchoalveolar lavage of children and animals with RSV infection of the lower respiratory tract predominantly contains PMNs. However, the mechanism of migration of PMNs towards the RSV- infected epithelium is unknown. We have shown that RSV-infected respiratory epithelium produces IL-8, a potent chemotactic cytokine that also enhances adhesion of PMNs. IL-8 increases the surface expresssion of Mac-1 (CD11b/CD18) of PMNs, which in turn is utilized for adhesion-based migration. In the present study, the effect of RSV-induced IL-8 in regulation of PMN adherence molecule Mac-1 (CD11b/CD18) was evaluated. Supematants of RSV- infected A549 cells or 0.3 ug/ml of rlL-8 were incubated with neutralizing anti-IL-8 antibody (Ab) or conrol Ab for 2 h. 5 × 105 of human PMNs obtained from a healthy donor were incubated with these suspensions for 45 min. The PMNs were then stained with FITC-conjugated anti-Mac-1 antibody and were analyzed by flow cytometry. The results are expressed as percent change in mean fluorescence when compared with sham infection (control expresssed as 0%). %Change in Mac-1 rIL-8 + control Ab 43 ± 2 rIL-8 + IL-8 Ab 9 ± 2 RSV + control Ab 50 ± 1 RSV+IL-8 Ab 14±1 On PMNs incubated with RSV supernatants or rIL-8, the expression of Mac-1 significantly increased when compared with PMNs incubated with control media (p < 0.005). On the other hand, IL-8 Ab blocked the increase in Mac-1 expression due to RSV supematants or rIL-8 These results indicated that IL-8, released from RSV-infected epithelial cells, is the predominant mediator that modulates the surface expression of Mac-1 on PMNs. IL-8, therefore, is likely to play a major role in the PMN-induced inflammation during RSV infection.

Original languageEnglish (US)
JournalJournal of Investigative Medicine
Volume44
Issue number1
StatePublished - 1996

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Interleukin-8
Neutrophils
Up-Regulation
Epithelium
Lung
Antibodies
Adhesion
Respiratory Mucosa
Flow cytometry
Fluorescein-5-isothiocyanate
Bronchoalveolar Lavage
Infection Control
Chemokines
Respiratory Tract Infections
Suspensions
Flow Cytometry
Animals
Fluorescence
Epithelial Cells
Tissue Donors

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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Upregulation of Mac-1 on polymorphonuclear leukocytes (PMNS) by IL-8 produced by RSV- infected pulmonary epithelium. / Nakajima, N.; Molina, E.; Jiang, Z.; Patel, Janak.

In: Journal of Investigative Medicine, Vol. 44, No. 1, 1996.

Research output: Contribution to journalArticle

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title = "Upregulation of Mac-1 on polymorphonuclear leukocytes (PMNS) by IL-8 produced by RSV- infected pulmonary epithelium",
abstract = "Bronchoalveolar lavage of children and animals with RSV infection of the lower respiratory tract predominantly contains PMNs. However, the mechanism of migration of PMNs towards the RSV- infected epithelium is unknown. We have shown that RSV-infected respiratory epithelium produces IL-8, a potent chemotactic cytokine that also enhances adhesion of PMNs. IL-8 increases the surface expresssion of Mac-1 (CD11b/CD18) of PMNs, which in turn is utilized for adhesion-based migration. In the present study, the effect of RSV-induced IL-8 in regulation of PMN adherence molecule Mac-1 (CD11b/CD18) was evaluated. Supematants of RSV- infected A549 cells or 0.3 ug/ml of rlL-8 were incubated with neutralizing anti-IL-8 antibody (Ab) or conrol Ab for 2 h. 5 × 105 of human PMNs obtained from a healthy donor were incubated with these suspensions for 45 min. The PMNs were then stained with FITC-conjugated anti-Mac-1 antibody and were analyzed by flow cytometry. The results are expressed as percent change in mean fluorescence when compared with sham infection (control expresssed as 0{\%}). {\%}Change in Mac-1 rIL-8 + control Ab 43 ± 2 rIL-8 + IL-8 Ab 9 ± 2 RSV + control Ab 50 ± 1 RSV+IL-8 Ab 14±1 On PMNs incubated with RSV supernatants or rIL-8, the expression of Mac-1 significantly increased when compared with PMNs incubated with control media (p < 0.005). On the other hand, IL-8 Ab blocked the increase in Mac-1 expression due to RSV supematants or rIL-8 These results indicated that IL-8, released from RSV-infected epithelial cells, is the predominant mediator that modulates the surface expression of Mac-1 on PMNs. IL-8, therefore, is likely to play a major role in the PMN-induced inflammation during RSV infection.",
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AB - Bronchoalveolar lavage of children and animals with RSV infection of the lower respiratory tract predominantly contains PMNs. However, the mechanism of migration of PMNs towards the RSV- infected epithelium is unknown. We have shown that RSV-infected respiratory epithelium produces IL-8, a potent chemotactic cytokine that also enhances adhesion of PMNs. IL-8 increases the surface expresssion of Mac-1 (CD11b/CD18) of PMNs, which in turn is utilized for adhesion-based migration. In the present study, the effect of RSV-induced IL-8 in regulation of PMN adherence molecule Mac-1 (CD11b/CD18) was evaluated. Supematants of RSV- infected A549 cells or 0.3 ug/ml of rlL-8 were incubated with neutralizing anti-IL-8 antibody (Ab) or conrol Ab for 2 h. 5 × 105 of human PMNs obtained from a healthy donor were incubated with these suspensions for 45 min. The PMNs were then stained with FITC-conjugated anti-Mac-1 antibody and were analyzed by flow cytometry. The results are expressed as percent change in mean fluorescence when compared with sham infection (control expresssed as 0%). %Change in Mac-1 rIL-8 + control Ab 43 ± 2 rIL-8 + IL-8 Ab 9 ± 2 RSV + control Ab 50 ± 1 RSV+IL-8 Ab 14±1 On PMNs incubated with RSV supernatants or rIL-8, the expression of Mac-1 significantly increased when compared with PMNs incubated with control media (p < 0.005). On the other hand, IL-8 Ab blocked the increase in Mac-1 expression due to RSV supematants or rIL-8 These results indicated that IL-8, released from RSV-infected epithelial cells, is the predominant mediator that modulates the surface expression of Mac-1 on PMNs. IL-8, therefore, is likely to play a major role in the PMN-induced inflammation during RSV infection.

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