Suppressed expression of ICAM-1 and LFA-1 and abrogation of leukocyte collaboration after exposure of human mononuclear leukocytes to respiratory syncytial virus in vitro. Comparison with exposure to influenza virus.

Salkind, Alan R.; Nichols, Joan E.; Roberts, Norbert J.

doi:10.1172/jci115332

Cited by 46 publications

(32 citation statements)

References 38 publications

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“…The potential for immunosuppression is indicated by the finding that exposure of human PBMC to RSV induced both IL-1 inhibitory activity and suppression of ICAM-1/LFA-1 expression. Thus, altered ICAM-1/LFA-1 expression failed to elicit the early events necessary for cellular collaboration, contributing to early suppression of the clonal expansion of RSV-specific lymphocytes (42).…”

Section: Discussionmentioning

confidence: 97%

Immune response to respiratory syncytial virus in young Brazilian children

Queiróz

Durigon

Botosso

et al. 2002

Braz J Med Biol Res

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We have evaluated the cellular and humoral immune response to primary respiratory syncytial virus (RSV) infection in young infants. Serum specimens from 65 patients £12 months of age (39 males and 26 females, 28 cases <3 months and 37 cases ³3 months; median 3 ± 3.9 months) were tested for anti-RSV IgG and IgG subclass antibodies by EIA. Flow cytometry was used to characterize cell surface markers expressed on peripheral blood mononuclear cells (PBMC) from 29 RSV-infected children. There was a low rate of seroconversion in children <3 months of age, whose acute-phase PBMC were mostly T lymphocytes (63.0 ± 9.0%). In contrast, a higher rate of seroconversion was observed in children >3 months of age, with predominance of B lymphocytes (71.0 ± 17.7%). Stimulation of PBMC with RSV (2 x 10 5 TCID 50 ) for 48 h did not induce a detectable increase in intracellular cytokines and only a few showed a detectable increase in RSVspecific secreted cytokines. These data suggest that age is an important factor affecting the infants' ability to develop an immune response to RSV.

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Section: Discussionmentioning

confidence: 97%

Immune response to respiratory syncytial virus in young Brazilian children

Queiróz

Durigon

Botosso

et al. 2002

Braz J Med Biol Res

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“…Northern Blot-Total RNA was extracted from control and infected A549 cells by the acid guanidium thiocyanate-phenol chloroform method (18). Twenty micrograms of RNA were fractionated on a 1.2% agarose-formaldehyde gel, transferred to nylon membranes, and hybridized to a radiolabeled RANTES, IRF-1, -3, and -7 cDNAs (RANTES cDNA plasmid was a generous gift of Dr A. Krensky, Stanford, CA; IRF-1, -3, and -7 cDNAs were a generous gift of Dr. Lin, Lady Davis Institute for Medical Research, Montreal, Quebec, Canada), as previously described (19).…”

Section: Methodsmentioning

confidence: 99%

Oxidant Tone Regulates RANTES Gene Expression in Airway Epithelial Cells Infected with Respiratory Syncytial Virus

Casola

Burger

Liu

et al. 2001

Journal of Biological Chemistry

118

127

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Respiratory syncytial virus (RSV) produces intense pulmonary inflammation, in part, through its ability to induce chemokine synthesis in infected airway epithelial cells. RANTES (regulated upon activation, normal T-cells expressed and secreted) is a CC chemokine which recruits and activates monocytes, lymphocytes, and eosinophils, all cell types present in the lung inflammatory infiltrate induced by RSV infection. In this study we investigated the role of reactive oxygen species in the induction of RANTES gene expression in human type II alveolar epithelial cells (A549), following RSV infection. Our results indicate that RSV infection of airway epithelial cells rapidly induces reactive oxygen species production, prior to RANTES expression, as measured by oxidation of 2,7-dichlorofluorescein. Pretreatment of airway epithelial cells with the antioxidant butylated hydroxyanisol (BHA), as well a panel of chemically unrelated antioxidants, blocks RSV-induced RANTES gene expression and protein secretion. This effect is mediated through the ability of BHA to inhibit RSV-induced interferon regulatory factor binding to the RANTES promoter interferon-stimulated responsive element, that is absolutely required for inducible RANTES promoter activation. BHA inhibits de novo interferon regulator factor (IRF)-1 and -7 gene expression and protein synthesis, and IRF-3 nuclear translocation. Together, these data indicates that a redox-sensitive pathway is involved in RSV-induced IRF activation, an event necessary for RANTES gene expression. Respiratory syncytial virus (RSV)1 is an enveloped, negativesense single-stranded RNA virus (1). Since its isolation, RSV has been identified as a leading cause of epidemic respiratory tract illness in children in the United States and worldwide. In fact, RSV is so ubiquitous that it will infect 100% of children before the age of 3. It is estimated that 40 -50% of children hospitalized with bronchiolitis and 25% of children with pneumonia are infected with RSV, resulting in 100,000 hospital admissions annually in the United States alone (1). In addition to acute morbidity, there are long-term consequences of RSV infection in infancy: RSV has been shown to predispose to the development of hyperreactive airway disease (2) and recurrent episodes of wheezing in asthmatic children are often precipitated by RSV infection. The mechanisms of RSV-induced airway disease and its long-term consequences are largely unknown, but the delicate balance between immunopathology and immunoprotection in the airway mucosa may be altered by an exuberant and unwanted local inflammatory response. Airway infiltration of monocytes and lymphocytes is typical of RSV infection (1), and activation of eosinophil and basophil leukocytes has been shown to correlate with the severity of acute RSV disease (3, 4). The composition of the cellular response at sites of tissue inflammation is controlled by gradients of chemokines, a family of small chemotactic cytokines, which direct leukocyte transendothelial migration and movement t...

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“…Total RNA was extracted from control and infected A549 cells by the acid guanidinium thiocyanatephenol-chloroform method (33). RNA (20 g) was fractionated on a 1.2% agarose-formaldehyde gel, transferred to a nylon membrane, and hybridized to a radiolabeled RANTES cDNA, as previously described (5).…”

Section: Methodsmentioning

confidence: 99%