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Infection and Immunity, January 2002, p. 49-54, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.49-54.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Kenneth J. Goodrum* and Jane Poulson-Dunlap

Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, Ohio 45701-2979

Received 4 June 2001/ Returned for modification 10 September 2001/ Accepted 11 October 2001

Streptococcus agalactiae (group B streptococcus [GBS]) is a leading cause of neonatal pneumonia, sepsis, and meningitis. Early-onset GBS pneumonia is characterized by marked pulmonary epithelial and endothelial cell injury. Innate proinflammatory responses to GBS infection that may contribute to the respiratory pathology include the synthesis and release of cytokines, prostaglandins, and nitric oxide (NO). The hypothesis that NO is directly induced in lung epithelial cells by invading GBS or indirectly induced by cytokines released by GBS-infected mononuclear cells was tested. A549 transformed human respiratory epithelial cells were directly cultured with GBS, cocultured with GBS-infected human mononuclear cells or purified macrophages, or exposed to conditioned culture medium from human mononuclear cells infected by GBS. The culture medium of A549 cultures was assayed for NO secretion, and the cell lysates were tested for presence of inducible nitric oxide synthase (iNOS) mRNA by reverse transcriptase PCR (RT-PCR). GBS-treated A549 cells neither secreted detectable NO nor expressed iNOS mRNA. GBS interaction with human mononuclear cells, however, stimulated release of soluble factors that readily induced iNOS mRNA expression and NO secretion by A549 cells. Inflammatory mediator-induced nitric oxide (NO) production by alveolar epithelium may exceed that of other lung cell types such as macrophages, and induction during GBS infection may play a significant role in pulmonary defense or free-radical-mediated lung injury.

* Corresponding author. Mailing address: Department of Biomedical Sciences, College of Osteopathic Medicine, Ohio University, Athens, OH 45701-2979. Phone: (740) 593-2390. Fax: (740) 597-2778. E-mail: goodrum{at}ohio.edu.

Editor: E. I. Tuomanen

Infection and Immunity, January 2002, p. 49-54, Vol. 70, No. 1
0019-9567/01/$04.00+0     DOI: 10.1128/IAI.70.1.49-54.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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