Monoclonal antibody blockade of Pneumocystis carinii GP-130 inhibits attachment to alveolar macrophages

Mehrdad Behnia, T. Weaver, R. Pasula, W. J. Martin

Research output: Contribution to journalArticlepeer-review


Purpose: Pneumocystis carinii (Pc) is a significant cause of morbidity and mortality in the immunocompromised host. Gp130, a mannose-rich glycoprotein on the surface of Pc, has been implicated in the attachment of Pc to alveolar macrophages (AM). Our study proposes to directly test this hypothesis. Methods: Murine AMs were obtained by bronchoalveolar lavage and incubated in 96-well plates for 24 hours. Pc devoid of IgG were isolated from severe combined immunodeficient (SCID) mice and were subsequently labelled with 51Cr. An in vitro attachment assay at 4 C for 4 hours was done using different concentrations of anti-gp130 IgG monoclonal antibodies (MAb). In addition, the attachment of 51Cr labelled Pc to fibronectin-coated plates was assessed in the presence and absence of anti-gp130 MAb. Results: Anti-gp130 MAb reduced the percent attachment of Pc to alveolar macrophages from 26.8±4.8 (n=17) to 10.3±2.4 (n=15) (p<0.05). Percent attachment of Pc to murine fibronectin-coated plates was reduced from 10.1±1.2 (n=3) to 5.8±0.3 (n=3) in the presence of anti-gp130 MAb (p<0.05) and was not affected in the presence of nonspecific IgG. Conclusions: Our data suggests that the surface glycoprotein gp130 is a key protein on the surface of Pc that mediates attachment of Pc to murine alveolar macrophages. Clinical Implications: Manipulation of Pc attachment to the alveolar macrophages through anti- gp130 MAb could have therapeutic potentials in controlling this infection.

Original languageEnglish (US)
Issue number4 SUPPL.
StatePublished - Oct 1 1998
Externally publishedYes

ASJC Scopus subject areas

  • Pulmonary and Respiratory Medicine
  • Critical Care and Intensive Care Medicine
  • Cardiology and Cardiovascular Medicine


Dive into the research topics of 'Monoclonal antibody blockade of Pneumocystis carinii GP-130 inhibits attachment to alveolar macrophages'. Together they form a unique fingerprint.

Cite this