Neutrophil Accumulation in Chronic Obstructive Lung Disease

Terpstra, G.K.; Houben, LeoA.M.J.; Oper, HarmJanHuidek

doi:10.1016/s0140-6736(88)91090-2

Cited by 1 publication

(2 citation statements)

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“…Lavage fluid was recovered and placed on ice. Ten microliters of each bronchoalveolar lavage (BAL) 3 sample was stained with Kimura, and total cell counts were made using a Neubauer chamber. Cytospins were made for each BAL sample (100 l) and stained with Diff-Quick rapid staining set (Merck, Dorset, U.K.) to allow differential cell counts to be made.…”

Section: Bronchoalveolar Lavagementioning

confidence: 99%

“…Increased levels of neutrophils in the lung have been detected in patients with inflammatory lung conditions such as acute respiratory distress syndrome (1), pneumonia (for review, see Ref. 2), and chronic obstructive pulmonary disease (3,4). Increased numbers of neutrophils may lead to tissue injury by release of histotoxic substances, including proteases and reactive oxygen species, resulting in advancement of disease.…”

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confidence: 99%

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Differential Effects of CD18, CD29, and CD49 Integrin Subunit Inhibition on Neutrophil Migration in Pulmonary Inflammation

Ridger

Wagner

Wallace

et al. 2001

The Journal of Immunology

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Neutrophil migration to lung alveoli is a characteristic of lung diseases and is thought to occur primarily via capillaries rather than postcapillary venules. The role of adhesion molecules CD18 and CD29 on this migration in a mouse model of lung inflammation has been investigated. The number of neutrophils present in bronchoalveolar lavage fluid was determined 4 h after intratracheal instillation of LPS (0.1–1 μg) or murine recombinant KC (CXC chemokine, 0.03–0.3 μg). Both stimuli produced a dose-related increase in neutrophil accumulation. Intravenous anti-mouse CD18 mAb, 2E6 (0.5 mg/mouse), significantly (p < 0.001) attenuated LPS (0.3 μg)- but not KC (0.3 μg)-induced neutrophil accumulation. The anti-mouse CD29 mAb, HMβ1-1 (0.02 mg/mouse), significantly (p < 0.05) inhibited both LPS (0.3 μg)- and KC (0.3 μg)-induced neutrophil migration. A second mAb to CD18 (GAME-46) and both F(ab′)2 and Fab of HMβ1-1 produced similar results to those above, while coadministration of mAbs did not result in greater inhibition. Electron microscopy studies showed that CD29 was involved in the movement of neutrophils from the interstitium into alveoli. The effect of mAbs to CD49 (α integrin) subunits of CD29 was also examined. mAbs to CD49e and CD49f inhibited both responses, while anti-CD49b and CD49d significantly inhibited responses to KC only. These data suggest that CD29 plays a critical role in neutrophil migration in pulmonary inflammation and that CD49b and CD49d mediate CD18-independent neutrophil accumulation.

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Section: Bronchoalveolar Lavagementioning

confidence: 99%

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confidence: 99%