Role of respiratory viruses in children with acute otitis media

Monobe, Hiroko; Ishibashi, Toshio; Nomura, Yujiro; Shinogami, Masanobu; Yano, Jun

doi:10.1016/s0165-5876(03)00124-1

Cited by 33 publications

(30 citation statements)

References 18 publications

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“…These findings may have important implications for immune responses in the lung following viral infections. Respiratory viral infections have been associated with an increased risk for secondary bacterial infection of the respiratory tract, including pneumonia (27) and otitis media (34). We speculate that large increases in numbers of pulmonary DC are required for effective antibacterial immune responses, exceeding the numbers of DC still present in the lung after RSV infection.…”

Section: Discussionmentioning

confidence: 88%

Local CD11c+ MHC Class II− Precursors Generate Lung Dendritic Cells during Respiratory Viral Infection, but Are Depleted in the Process

Wang

Peters

Laza-Stanca

et al. 2006

The Journal of Immunology

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Increases in numbers of lung dendritic cells (DC) observed during respiratory viral infections are assumed to be due to recruitment from bone marrow precursors. No local production has been demonstrated. In this study, we isolated defined populations of murine lung cells based on CD11c and MHC class II (MHC II) expression. After culture for 12 days with GM-CSF, we analyzed cell numbers, DC surface markers, and Ag-presenting capacity. Only CD11c+ MHC II− cells from naive mice proliferated, yielding myeloid DC, which induced Ag-specific proliferation of naive T cells. After respiratory syncytial virus (RSV) infection, numbers of pulmonary CD11c+ MHC II− precursor cells were significantly reduced and DC could not be generated. Moreover, RSV infection prevented subsequent in vivo expansion of pulmonary DC in response to influenza infection or LPS treatment. These results provide direct evidence of local generation of fully functional myeloid DC in the lung from CD11c+ MHC II− precursor cells that are depleted by RSV infection, leading to an inability to expand lung DC numbers in response to subsequent viral infection or exposure to bacterial products. This depletion of local DC precursors in respiratory viral infections may be important in explaining complex interactions between multiple and intercurrent pulmonary infections.

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Section: Discussionmentioning

confidence: 88%

Local CD11c+ MHC Class II− Precursors Generate Lung Dendritic Cells during Respiratory Viral Infection, but Are Depleted in the Process

Wang

Peters

Laza-Stanca

et al. 2006

The Journal of Immunology

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“…RSV is associated with secondary bacterial infections (3,(8)(9)(10); however, it is currently unclear how RSV alters the host response to bacterial pathogens. In vivo studies using a mouse Figure 6.…”

Section: Discussionmentioning

confidence: 99%

“…RSV infection elicits a poor adaptive immune response; therefore, infections occur repeatedly throughout life (6,7). This common paramyxovirus has also been associated with secondary bacterial infections of the lung (3,(8)(9)(10); however, as with other viralinduced secondary bacterial infections, the underlying mechanisms are not well understood.…”

Section: Abstract: Macrophages; Ifn; Signal Transduction; Transcriptimentioning

confidence: 99%

Respiratory Syncytial Virus Impairs Macrophage IFN-α/β– and IFN-γ–Stimulated Transcription by Distinct Mechanisms

Senft

Taylor

Lei

et al. 2010

Am J Respir Cell Mol Biol

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Macrophages are the primary lung phagocyte and are instrumental in maintenance of a sterile, noninflamed microenvironment. IFNs are produced in response to bacterial and viral infection, and activate the macrophage to efficiently counteract and remove pathogenic invaders. Respiratory syncytial virus (RSV) inhibits IFN-mediated signaling mechanisms in epithelial cells; however, the effects on IFN signaling in the macrophage are currently unknown. We investigated the effect of RSV infection on IFN-mediated signaling in macrophages. RSV infection inhibited IFN-b-and IFN-g-activated transcriptional mechanisms in primary alveolar macrophages and macrophage cell lines, including the transactivation of important Nod-like receptor family genes, Nod1 and class II transactivator. RSV inhibited IFN-b-and IFN-g-mediated transcriptional activation by two distinct mechanisms. RSV impaired IFN-b-mediated signal transducer and activator of transcription (STAT)-1 phosphorylation through a mechanism that involves inhibition of tyrosine kinase 2 phosphorylation. In contrast, RSV-impaired transcriptional activation after IFN-g stimulation resulted from a reduction in the nuclear STAT1 interaction with the transcriptional coactivator, CBP, and was correlated with increased phosphorylation of STAT1b, a dominantnegative STAT1 splice variant, in response to IFN-g. In support of this concept, overexpression of STAT1b was sufficient to repress the IFNg-mediated expression of class II transactivator. These results demonstrate that RSV inhibits IFN-mediated transcriptional activation in macrophages, and suggests that paramyxoviruses modulate an important regulatory mechanism that is critical in linking innate and adaptive immune mechanisms after infection. Keywords: macrophages; IFN; signal transduction; transcriptional activationRespiratory syncytial virus (RSV) is an important causative agent of severe respiratory tract infections in pediatric, immunocompromised, and elderly populations (1-5). RSV infection elicits a poor adaptive immune response; therefore, infections occur repeatedly throughout life (6, 7). This common paramyxovirus has also been associated with secondary bacterial infections of the lung (3, 8-10); however, as with other viralinduced secondary bacterial infections, the underlying mechanisms are not well understood.IFN-a and IFN-b (type I) and IFN-g (type II) are produced in the lung in response to microbial infection, and are potent activators of macrophage innate antimicrobial immunity; they also induce pathways that promote efficient antigen processing and presentation to cells of the adaptive immune system (11, 12). The requirement of IFN for the efficient clearance of pathogens is evident in IFN-b 2/2 , IFN-g 2/2 , IFN-a receptor 2/2 , and IFN-g receptor 2/2 mice, as these mice, lacking IFN signaling, display severe impairment in natural resistance to a variety of viral, bacterial, and parasitic infections (13-20). IFN-a or IFN-b ligation of the IFN-a/b receptor results in the phosphorylation and activation of the ...

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“…We reviewed 71 fulltext articles, of which 12 were included (Supplemental Fig 3). 12,18,21,30,[35][36][37][38]41,[43][44] …”

Section: Aommentioning

confidence: 99%

Bacterial Prevalence and Antimicrobial Prescribing Trends for Acute Respiratory Tract Infections

Kronman¹,

2014

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WHAT'S KNOWN ON THIS SUBJECT: Many pediatric acute respiratory tract infections (ARTI) are viral and do not require antimicrobial treatment. Recent estimates of antimicrobial overprescribing for these infections, defined based on the published bacterial disease prevalence among all ARTI, are not available. WHAT THIS STUDY ADDS:Based on the published bacterial prevalence rates for pediatric ARTI, antimicrobial agents are prescribed almost twice as often as expected to outpatients nationally, amounting to an estimated 11.4 million potentially preventable antimicrobial prescriptions annually. abstract BACKGROUND AND OBJECTIVES: Antimicrobials are frequently prescribed for acute respiratory tract infections (ARTI), although many are viral. We aimed to determine bacterial prevalence rates for 5 common childhood ARTI -acute otitis media (AOM), sinusitis, bronchitis, upper respiratory tract infection, and pharyngitis-and to compare these rates to nationally representative antimicrobial prescription rates for these ARTI. METHODS:We performed (1) a meta-analysis of English language pediatric studies published between 2000 and 2011 in Medline, Embase, and the Cochrane library to determine ARTI bacterial prevalence rates; and (2) a retrospective cohort analysis of children age ,18 years evaluated in ambulatory clinics sampled by the 2000-2010 National Ambulatory Medical Care Survey (NAMCS) to determine estimated US ARTI antimicrobial prescribing rates. RESULTS:From the meta-analysis, the AOM bacterial prevalence was 64.7% (95% confidence interval [CI], 50.5%-77.7%); Streptococcus pyogenes prevalence during pharyngitis was 20.2% (95% CI, 15.9%-25.2%). No URI or bronchitis studies met inclusion criteria, and 1 sinusitis study met inclusion criteria, identifying bacteria in 78% of subjects. Based on these condition-specific bacterial prevalence rates, the expected antimicrobial rescribing rate for ARTI overall was 27.4% (95% CI, 26.5%-28.3%). However, antimicrobial agents were prescribed in NAMCS during 56.9% (95% CI, 50.8%-63.1%) of ARTI encounters, representing an estimated 11.4 million potentially preventable antimicrobial prescriptions annually.

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Role of respiratory viruses in children with acute otitis media

Cited by 33 publications

References 18 publications

Local CD11c+ MHC Class II− Precursors Generate Lung Dendritic Cells during Respiratory Viral Infection, but Are Depleted in the Process

Local CD11c+ MHC Class II− Precursors Generate Lung Dendritic Cells during Respiratory Viral Infection, but Are Depleted in the Process

Respiratory Syncytial Virus Impairs Macrophage IFN-α/β– and IFN-γ–Stimulated Transcription by Distinct Mechanisms

Bacterial Prevalence and Antimicrobial Prescribing Trends for Acute Respiratory Tract Infections

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