The Roles of CD11/CD18 and ICAM-1 in Acute Pseudomonas aeruginosa-Induced Pneumonia in Mice

Lan Qin, William M. Quinlan, Nicholas A. Doyle, Lori Graham, James E Sligh, Fumio Takei, Arthur L. Beaudet, Claire M. Doerschuk

Research output: Contribution to journalArticle

105 Citations (Scopus)

Abstract

Neutrophil accumulation in response to Pseudomonas aeruginosa in the lungs is mediated through CD11/CD18. This study determined the roles of CD11a, CD11b, and intercellular adhesion molecule (ICAM)-1 in P. aeruginosa-induced pneumonia and compared the function of ICAM-1 using Abs or ICAM-1 mutant mice. Anesthetized BALB/c mice pretreated with either Abs against CD11a, CD11b, ICAM-1, or rat IgG received intratracheal instillation of P. aeruginosa for 4 h. In other studies, ICAM-1 mutant and wild-type mice received either anti-ICAM-1 Ab or rat IgG followed by instillation of P. aeruginosa. The data show that Abs against CD11a, CD11b, and ICAM-1 in BALB/c mice inhibited neutrophil emigration by 79, 81, and 56%, respectively. ICAM-1 mutant mice showed no inhibition of neutrophil emigration compared with wild-type mice. Pretreatment with anti-ICAM-1 Ab inhibited neutrophil emigration in wild-type (129/SvxC57) mice by 67% but had no effect in ICAM-1 mutant mice, suggesting that the Ab was acting specifically through recognition of its Ag. We conclude that CD11 a and CD11 b are required for neutrophil emigration. The observed function of ICAM-1 varies depending on the method by which it is inhibited. Abs may overestimate function by altering other cellular functions or mutant mice may develop alternative pathways of emigration.

Original languageEnglish (US)
Pages (from-to)5016-5021
Number of pages6
JournalJournal of Immunology
Volume157
Issue number11
StatePublished - Dec 1 1996
Externally publishedYes

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Intercellular Adhesion Molecule-1
Pseudomonas aeruginosa
Pneumonia
Emigration and Immigration
Neutrophils
Immunoglobulin G
129 Strain Mouse
Lung

ASJC Scopus subject areas

  • Immunology

Cite this

Qin, L., Quinlan, W. M., Doyle, N. A., Graham, L., Sligh, J. E., Takei, F., ... Doerschuk, C. M. (1996). The Roles of CD11/CD18 and ICAM-1 in Acute Pseudomonas aeruginosa-Induced Pneumonia in Mice. Journal of Immunology, 157(11), 5016-5021.

The Roles of CD11/CD18 and ICAM-1 in Acute Pseudomonas aeruginosa-Induced Pneumonia in Mice. / Qin, Lan; Quinlan, William M.; Doyle, Nicholas A.; Graham, Lori; Sligh, James E; Takei, Fumio; Beaudet, Arthur L.; Doerschuk, Claire M.

In: Journal of Immunology, Vol. 157, No. 11, 01.12.1996, p. 5016-5021.

Research output: Contribution to journalArticle

Qin, L, Quinlan, WM, Doyle, NA, Graham, L, Sligh, JE, Takei, F, Beaudet, AL & Doerschuk, CM 1996, 'The Roles of CD11/CD18 and ICAM-1 in Acute Pseudomonas aeruginosa-Induced Pneumonia in Mice', Journal of Immunology, vol. 157, no. 11, pp. 5016-5021.
Qin L, Quinlan WM, Doyle NA, Graham L, Sligh JE, Takei F et al. The Roles of CD11/CD18 and ICAM-1 in Acute Pseudomonas aeruginosa-Induced Pneumonia in Mice. Journal of Immunology. 1996 Dec 1;157(11):5016-5021.
Qin, Lan ; Quinlan, William M. ; Doyle, Nicholas A. ; Graham, Lori ; Sligh, James E ; Takei, Fumio ; Beaudet, Arthur L. ; Doerschuk, Claire M. / The Roles of CD11/CD18 and ICAM-1 in Acute Pseudomonas aeruginosa-Induced Pneumonia in Mice. In: Journal of Immunology. 1996 ; Vol. 157, No. 11. pp. 5016-5021.
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abstract = "Neutrophil accumulation in response to Pseudomonas aeruginosa in the lungs is mediated through CD11/CD18. This study determined the roles of CD11a, CD11b, and intercellular adhesion molecule (ICAM)-1 in P. aeruginosa-induced pneumonia and compared the function of ICAM-1 using Abs or ICAM-1 mutant mice. Anesthetized BALB/c mice pretreated with either Abs against CD11a, CD11b, ICAM-1, or rat IgG received intratracheal instillation of P. aeruginosa for 4 h. In other studies, ICAM-1 mutant and wild-type mice received either anti-ICAM-1 Ab or rat IgG followed by instillation of P. aeruginosa. The data show that Abs against CD11a, CD11b, and ICAM-1 in BALB/c mice inhibited neutrophil emigration by 79, 81, and 56{\%}, respectively. ICAM-1 mutant mice showed no inhibition of neutrophil emigration compared with wild-type mice. Pretreatment with anti-ICAM-1 Ab inhibited neutrophil emigration in wild-type (129/SvxC57) mice by 67{\%} but had no effect in ICAM-1 mutant mice, suggesting that the Ab was acting specifically through recognition of its Ag. We conclude that CD11 a and CD11 b are required for neutrophil emigration. The observed function of ICAM-1 varies depending on the method by which it is inhibited. Abs may overestimate function by altering other cellular functions or mutant mice may develop alternative pathways of emigration.",
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