Streptococcus pneumoniae-stimulated macrophages induce neutrophils to emigrate by a CD18-independent mechanism of adherence

William Mileski, J. Harlan, C. Rice, R. Winn

Research output: Contribution to journalArticle

43 Citations (Scopus)

Abstract

Neutrophil adherence to and emigration across endothelium are in large part dependent upon the neutrophil membrane CD11/Cd18 glycoprotein complex. Recently, however, we have demonstrated that some stimuli can elicit neutrophil emigration in the lung by a CD18-independent pathway. We examined further the mechanism involved in CD18-independent emigration in a rabbit model of inflamed peritoneum. Neutrophil emigration in the peritoneum induced by instillation of E. coli and S. pneumoniae was studied under four experimental conditions: Group 1-normal peritoneum, Group 2-peritoneum primed with protease primed with protease peptone to increase the number of macrophages, Group 3-peritoneum treated by protease peptone instillation and then depleted of the increased macrophage population, and Group 4-peritoneum with macrophages transplanted from animals enriched as in Group 2. Experiments were run in pairs with animals in each group assigned to receive either saline (control) or monoclonal antibody (MAb) 60.3 prior to bacterial instillation in the peritoneum. Neutrophil emigration in response to E. coli was > 86% inhibited by MAb 60.3 in both the normal and the macrophage-enriched peritoneum. Neutrophil emigration in response to S. pneumoniae was inhibited > 85% in the normal peritoneum and the macrophage-enriched-and-then depleted peritoneum, but was < 50% blocked in both the macrophage-enriched and the transplanted macrophage peritoneum. These data indicate that macrophages can augment PMN emigration by a non-CD18 mechanism, and may explain the increased sensitivity of organs with large resident macrophage populations, liver and lung, to injury following shock and sepsis.

Original languageEnglish (US)
Pages (from-to)259-267
Number of pages9
JournalCirculatory Shock
Volume31
Issue number3
StatePublished - 1990
Externally publishedYes

Fingerprint

Peritoneum
Streptococcus pneumoniae
Neutrophils
Macrophages
Emigration and Immigration
Peptones
Peptide Hydrolases
Monoclonal Antibodies
Escherichia coli
Lung Injury
Population Groups
Endothelium
Shock
Sepsis
Glycoproteins
Rabbits
Lung

Keywords

  • Endothelium
  • Inflammation
  • Leukocytes
  • Peritoneum
  • Rabbit

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Streptococcus pneumoniae-stimulated macrophages induce neutrophils to emigrate by a CD18-independent mechanism of adherence. / Mileski, William; Harlan, J.; Rice, C.; Winn, R.

In: Circulatory Shock, Vol. 31, No. 3, 1990, p. 259-267.

Research output: Contribution to journalArticle

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abstract = "Neutrophil adherence to and emigration across endothelium are in large part dependent upon the neutrophil membrane CD11/Cd18 glycoprotein complex. Recently, however, we have demonstrated that some stimuli can elicit neutrophil emigration in the lung by a CD18-independent pathway. We examined further the mechanism involved in CD18-independent emigration in a rabbit model of inflamed peritoneum. Neutrophil emigration in the peritoneum induced by instillation of E. coli and S. pneumoniae was studied under four experimental conditions: Group 1-normal peritoneum, Group 2-peritoneum primed with protease primed with protease peptone to increase the number of macrophages, Group 3-peritoneum treated by protease peptone instillation and then depleted of the increased macrophage population, and Group 4-peritoneum with macrophages transplanted from animals enriched as in Group 2. Experiments were run in pairs with animals in each group assigned to receive either saline (control) or monoclonal antibody (MAb) 60.3 prior to bacterial instillation in the peritoneum. Neutrophil emigration in response to E. coli was > 86{\%} inhibited by MAb 60.3 in both the normal and the macrophage-enriched peritoneum. Neutrophil emigration in response to S. pneumoniae was inhibited > 85{\%} in the normal peritoneum and the macrophage-enriched-and-then depleted peritoneum, but was < 50{\%} blocked in both the macrophage-enriched and the transplanted macrophage peritoneum. These data indicate that macrophages can augment PMN emigration by a non-CD18 mechanism, and may explain the increased sensitivity of organs with large resident macrophage populations, liver and lung, to injury following shock and sepsis.",
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