2002
DOI: 10.1128/iai.70.1.49-54.2002
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Cytokine Responses to Group B Streptococci Induce Nitric Oxide Production in Respiratory Epithelial Cells

Abstract: 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… Show more

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Cited by 16 publications
(14 citation statements)
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“…8B). Thus, our observation may complement the earlier report that A549 cells did not respond to Gram-positive group B Streptococci and their products (44,45).…”
Section: Discussionsupporting
confidence: 91%
See 1 more Smart Citation
“…8B). Thus, our observation may complement the earlier report that A549 cells did not respond to Gram-positive group B Streptococci and their products (44,45).…”
Section: Discussionsupporting
confidence: 91%
“…Likewise, this promoter was not activated by coincubation with 250 U/ml IFN-␥ and 10 g/ml LPS (data not shown). In the lungs, mononuclear phagocytes such as alveolar macrophages respond to bacteria and their products, and activate epithelial cells by producing various cytokines and chemokines (1,3,44,45). Therefore, we tested whether the coculture of A549 cells with the MM6 monocytic cell line affects hBD-2 promoter activity following LPS stimulation.…”
Section: Activation Of Hbd-2 Promoter In A549 Epithelial Cells By Lpsmentioning
confidence: 99%
“…After nonopsonic phagocytosis of GBS, macrophages produce cytokines such as tumor necrosis factor (TNF)-a [7] and nitric oxide (NO) [8,9]. GBS also stimulates NO production in respiratory epithelial cells via the paracrine effects of soluble factors released by GBS-infected mononuclear cells [10]. Despite this, GBS persists inside macrophages for long periods and induce macrophage apoptosis [11].…”
mentioning
confidence: 99%
“…Monolayers were post-fixed with 1% OsO 4 , 5 mM CaCl 2 and 0.8% K 4 [Fe(CN 6 )] in cacodylate buffer for 1 h at 22˚C, and dehydrated through a series of graded ethanol solutions and embedded in Epon. Ultra-thin sections were examined under Zeiss EM 906 transmission electron microscope (Zeiss, Oberkochen, Germany) (20).…”
Section: Transmission Electron Microscopy (Tem)mentioning
confidence: 99%
“…The serotype-specific capsular polysaccharides are essential for pathogenesis, and serotype III is prevalent among strains isolated from infants with invasive infections (5). Failure of polymorphonuclear leukocytes and pulmonary macrophages to effectively eliminate GBS from the alveolar space and the ability of bacteria to adhere to respiratory epithelial cells are essential for the development of pneumonia (6). The mechanism(s) used by GBS to cause invasive disease are not completely understood, but is clear that GBS are able to invade polarized epithelial cells (7,8).…”
Section: Introductionmentioning
confidence: 99%