Computed Tomographic Study of the Common Cold

Jm, Gwaltney; Cd, Phillips; Rd, Miller; Dk, Riker

doi:10.1056/nejm199401063300105

Cited by 596 publications

(328 citation statements)

References 12 publications

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“…It is tempting to propose that acute viral infection among patient would precipitate increased sinus changes and an exacerbation of asthma. [23][24][25] Further understanding of the relationship between sinus disease and exacerbations of asthma will need prospective studies in which the change in sinus CT at the time of an attack can be related to evidence of viral infection, allergen exposure, and inflammation. However, the problem will remain difficult to resolve without better understanding of the immunologic mechanisms that lead to persistent eosinophil-rich inflammation in the sinuses.…”

Section: Discussionmentioning

confidence: 99%

Sinus computed tomography scan and markers of inflammation in vocal cord dysfunction and asthma

Peters¹,

Hatley²,

Crater³

et al. 2003

Annals of Allergy, Asthma & Immunology

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Section: Discussionmentioning

confidence: 99%

Sinus computed tomography scan and markers of inflammation in vocal cord dysfunction and asthma

Peters¹,

Hatley²,

Crater³

et al. 2003

Annals of Allergy, Asthma & Immunology

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“…Rhinovirus infection causes concomitant inflammation of the paranasal sinuses. 12 The natural history of URTI in children has been less well defined because of reliance on parent recall or physician referral. As the rhinovirus is difficult to culture, only with the advent of sensitive and specific reverse transcriptase polymerase chain reaction techniques has the natural history been better documented.…”

Section: Symptoms and Signsmentioning

confidence: 99%

Management of upper respiratory tract infections in children

Cotton

Innes

Jaspan

et al. 2008

South African Family Practice

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Upper respiratory tract infection (URTI) occurs commonly in both children and adults and is a major cause of mild morbidity. It has a high cost to society, being responsible for absenteeism from school and work and unnecessary medical care, and is occasionally associated with serious sequelae. URTIs are usually caused by several families of virus; these are the rhinovirus, coronavirus, parainfluenza, respiratory syncytial virus (RSV), adenovirus, human metapneumovirus, influenza, enterovirus and the recently discovered bocavirus. This review will mainly focus on the rhinovirus, where significant advances have been made in understanding the epidemiology, natural history and relationship with other pathogens.

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“…R hinovirus infections are the single most prevalent cause of the common cold (1) and also have been implicated as playing a role in the exacerbation of other diseases, including asthma (2,3) and sinusitis (4,5). However, despite the high prevalence of rhinovirus infections, the biochemical mechanisms leading to the manifestation of symptoms remain unclear.…”

mentioning

confidence: 99%

Role of NF-κB in Cytokine Production Induced from Human Airway Epithelial Cells by Rhinovirus Infection

Kim

Sanders

Siekierski³

et al. 2000

The Journal of Immunology

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Infection of human epithelial cells with human rhinovirus (HRV)-16 induces rapid production of several proinflammatory cytokines, including IL-8, IL-6, and GM-CSF. We evaluated the role of NF-κB in HRV-16-induced IL-8 and IL-6 production by EMSA using oligonucleotides corresponding to the binding sites for NF-κB in the IL-6 and IL-8 gene promoters. Consistent with the rapid induction of mRNA for IL-8 and IL-6, maximal NF-κB binding to both oligonucleotides was detected at 30 min after infection. NF-κB complexes contained p65 and p50, but not c-Rel. The IL-8 oligonucleotide bound recombinant p50 with only about one-tenth the efficiency of the IL-6 oligonucleotide, even though epithelial cells produced more IL-8 protein than IL-6. Neither the potent glucocorticoid, budesonide (10−7 M), nor a NO donor inhibited NF-κB binding to either cytokine promoter or induction of mRNA for either IL-8 or IL-6. Sulfasalazine and calpain inhibitor I, inhibitors of NF-κB activation, blocked HRV-16-induced formation of NF-κB complexes with oligonucleotides from both cytokines, but did not inhibit mRNA induction for either cytokine. By contrast, sulfasalazine clearly inhibited HRV-16 induction of mRNA for GM-CSF in the same cells. Thus, HRV-16 induces epithelial expression of IL-8 and IL-6 by an NF-κB-independent pathway, whereas induction of GM-CSF is at least partially dependent upon NF-κB activation.

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Computed Tomographic Study of the Common Cold

Abstract: The common cold is associated with frequent and variable anatomical involvement of the upper airways, including occlusion and abnormalities in the sinus cavities.

Cited by 596 publications

References 12 publications

Sinus computed tomography scan and markers of inflammation in vocal cord dysfunction and asthma

Sinus computed tomography scan and markers of inflammation in vocal cord dysfunction and asthma

Management of upper respiratory tract infections in children

Role of NF-κB in Cytokine Production Induced from Human Airway Epithelial Cells by Rhinovirus Infection

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