Chemokines and Inflammation in the Nasal Passages of Infants with Respiratory Syncytial Virus Bronchiolitis

Noah, Terry L.; Ivins, Sally; Murphy, Paula C.; Kazachkova, Irina; Moats‐Staats, Billie M.; Henderson, Frederick W.

doi:10.1006/clim.2002.5248

Cited by 74 publications

(57 citation statements)

References 27 publications

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“…19,20 This is consistent with finding high levels of IL-8 in respiratory secretions of RSV-infected infants 21 or adults. 22 In the current cases, debris consisting of sloughed epithelium and macrophages with fibrin and minimal mucin was noted to fill airway lumens. Neutrophils were not seen in the interstitial infiltrates, but were present as a minority cell type in the peribronchiolar tissue, with the dominant cell type being mononuclear.…”

Section: Discussionmentioning

confidence: 53%

The histopathology of fatal untreated human respiratory syncytial virus infection

et al. 2007

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The pathology of respiratory syncytial virus (RSV) infection was evaluated 1 day after an outpatient diagnosis of RSV in a child who died in a motor vehicle accident. We then identified 11 children with bronchiolitis from the Vanderbilt University autopsy log between 1925 and 1959 who met criteria for possible RSV infection in the preintensivist era. Their tissue was re-embedded and evaluated by routine hematoxylin and eosin and PAS staining and immunostaining with RSV-specific antibodies. Tissue from three cases was immunostain-positive for RSV antigen and was examined in detail. Small bronchiole epithelium was circumferentially infected, but basal cells were spared. Both type 1 and 2 alveolar pneumocytes were also infected. Although, not possible for archival cases, tissue from the index case was evaluated by immunostaining with antibodies to define the cellular components of the inflammatory response. Inflammatory infiltrates were centered on bronchial and pulmonary arterioles and consisted of primarily CD69 þ monocytes, CD3 þ double-negative T cells, CD8 þ T cells, and neutrophils. The neutrophil distribution was predominantly between arterioles and airways, while the mononuclear cell distribution was in both airways and lung parenchyma. Most inflammatory cells were concentrated submuscular to the airway, but many cells traversed the smooth muscle into the airway epithelium and lumen. Airway obstruction was a prominent feature in all cases attributed to epithelial and inflammatory cell debris mixed with fibrin, mucus, and edema, and compounded by compression from hyperplastic lymphoid follicles. These findings inform our understanding of RSV pathogenesis and may facilitate the development of new approaches for prevention and treatment.

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Section: Discussionmentioning

confidence: 53%

The histopathology of fatal untreated human respiratory syncytial virus infection

et al. 2007

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“…In noninflamed lungs constitutive expression of RANTES/ CCL5 by airway epithelial cells might explain a continuous recruitment of effector cells from the circulation that express CCR5 the receptor for RANTES. RSV infection leads to increased levels of RANTES expression in the lungs which might explain the enhanced recruitment of CCR5 ϩ effector T cells to the lungs during an ongoing RSV infection (38,39).…”

Section: Discussionmentioning

confidence: 99%

“…4B shows an example of the RSV-specific T cell response in the context of a set of three HLA alleles that were matched between the patient T cells and the adult APC. This response was substantially higher than the response against a single virus epitope, NS1 [33][34][35][36][37][38][39][40][41] , restricted to HLA-A2. Moreover, the T cell response visualized by stimulation with RSV-infected DC showed the same kinetics as the appearance of Ki-67 ϩ /GzmB ϩ cells and CCR5 ϩ cells and represented roughly one third of the total activated T cell response in this patient.…”

Section: Rsv-specific Cd8 ϩ T Cells In Peripheral Blood Of Rsv Patientsmentioning

confidence: 99%

CD8+ T Cell Responses in Bronchoalveolar Lavage Fluid and Peripheral Blood Mononuclear Cells of Infants with Severe Primary Respiratory Syncytial Virus Infections

Heidema

Lukens

Maren

et al. 2007

The Journal of Immunology

106

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A protective role for CD8+ T cells during viral infections is generally accepted, but little is known about how CD8+ T cell responses develop during primary infections in infants, their efficacy, and how memory is established after viral clearance. We studied CD8+ T cell responses in bronchoalveolar lavage (BAL) samples and blood of infants with a severe primary respiratory syncytial virus (RSV) infection. RSV-specific CD8+ T cells with an activated effector cell phenotype: CD27+CD28+CD45RO+CCR7−CD38+HLA-DR+Granzyme B+CD127− could be identified in BAL and blood. A high proportion of these CD8+ T cells proliferated and functionally responded upon in vitro stimulation with RSV Ag. Thus, despite the very young age of the patients, a robust systemic virus-specific CD8+ T cell response was elicited against a localized respiratory infection. RSV-specific T cell numbers as well as the total number of activated effector type CD8+ T cells peaked in blood around day 9–12 after the onset of primary symptoms, i.e., at the time of recovery. The lack of a correlation between RSV-specific T cell numbers and parameters of disease severity make a prominent role in immune pathology unlikely, in contrast the T cells might be involved in the recovery process.

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“…RSV bronchiolitis showed that CCL5 was highly expressed [26], suggesting a special role for this chemokine in antiviral defence. Interestingly, a genetic variant of the key receptor for CCL5, CC chemokine receptor 5, has been associated with the severity of bronchiolitis caused by RSV [27].…”

Section: Discussionmentioning

confidence: 99%

Functional single nucleotide polymorphisms of theCCL5gene and nonemphysematous phenotype in COPD patients

Hizawa¹,

Makita²,

Nasuhara³

et al. 2008

Eur Respir J

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It was previously reported that the gain-of-function -28 guanine allele of the promoter single nucleotide polymorphism (SNP; cytosine to guanine substitution of nucleotide -28 (-28C.G)) in the CC chemokine ligand 5 gene (CCL5) was associated with susceptibility to late-onset asthma in patients who developed asthma at age o40 yrs. The clinical diagnosis of chronic obstructive pulmonary disease (COPD) includes emphysema and small airway disease, and upregulation of CCL5 has been described in the airways of patients with COPD. It was hypothesised that CCL5 has a genetic impact upon the variable expression of emphysema in patients with COPD.Patients with COPD were studied (n5267). All of the patients underwent pulmonary highresolution computed tomography (CT), and visual scoring (CT score) was performed to determine emphysema severity. Three SNPs of CCL5 were genotyped, including -403G.A, -28C.G and 375T.C.A significant difference was found in CT score according to CCL5 genotype; the -28G allele was inversely associated with CT score. When the analysis was confined to 180 patients with bronchial reversibility of ,15%, even stronger evidence for this association was noted.Functional single nucleotide polymorphisms in the CC chemokine ligand 5 gene were associated with milder emphysema. Together with previous findings, the present study may identify the CC chemokine ligand 5 gene as part of a common pathway in the pathogenesis of lateonset asthma and chronic obstructive pulmonary disease with milder emphysema.

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Chemokines and Inflammation in the Nasal Passages of Infants with Respiratory Syncytial Virus Bronchiolitis

Cited by 74 publications

References 27 publications

The histopathology of fatal untreated human respiratory syncytial virus infection

The histopathology of fatal untreated human respiratory syncytial virus infection

CD8+ T Cell Responses in Bronchoalveolar Lavage Fluid and Peripheral Blood Mononuclear Cells of Infants with Severe Primary Respiratory Syncytial Virus Infections

Functional single nucleotide polymorphisms of theCCL5gene and nonemphysematous phenotype in COPD patients

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