Leucocyte populations in respiratory syncytial virus‐induced bronchiolitis

Smith, Peter; Sz, Wang; Dowling, Kay D.; Forsyth, Kevin

doi:10.1046/j.1440-1754.2001.00618.x

Cited by 110 publications

(108 citation statements)

References 28 publications

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“…This result is consistent with the previous clinical studies on leukocyte analysis in infants with RSV-induced bronchiolitis (46,47). However, IL-5 is a potent chemokine that attracts eosinophils (48,49), and the mechanism for the lack of eosinophilia in our studies with RSV infection is unclear.…”

Section: Discussionsupporting

confidence: 92%

IL-12p40 and IL-18 Modulate Inflammatory and Immune Responses to Respiratory Syncytial Virus Infection

Wang

Bao

Rosenberger

et al. 2004

The Journal of Immunology

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Respiratory syncytial virus-induced bronchiolitis has been linked to the development of allergy and atopic asthma. IL-12 and possibly IL-18 are central mediators orchestrating Th1 and/or Th2 immune responses to infection. To determine a possible role for IL-12 in regulating the immune response to acute respiratory syncytial virus infection, IL-12p40 gene-targeted (IL-12p40−/−) and wild-type mice were intratracheally infected with respiratory syncytial virus, and lung inflammatory and immune responses were assessed. Lung inflammation and mucus production were increased in the airways of IL-12p40−/− mice as compared with those of wild-type mice, concurrent with increased levels of the Th2 effector cytokines IL-5 and IL-13. Respiratory syncytial virus clearance and levels of Th1 effector cytokine IFN-γ were not altered. Interestingly, IL-18, another mediator of IFN-γ production, was significantly increased in the lungs of IL-12p40−/− mice early during the course of infection. Abrogation of IL-18-mediated signaling in IL-12p40−/− mice further enhanced Th2 immune response and mucus production in the airways during respiratory syncytial virus infection but failed to modulate IFN-γ production or viral clearance. These findings implicate a role for IL-12 and IL-18 in modulating respiratory syncytial virus-induced airway inflammation distinct from that of viral clearance.

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Section: Discussionsupporting

confidence: 92%

IL-12p40 and IL-18 Modulate Inflammatory and Immune Responses to Respiratory Syncytial Virus Infection

Wang

Bao

Rosenberger

et al. 2004

The Journal of Immunology

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“…Analysis of the cellular composition of bronchoalveolar lavage (BAL) fluid in acutely RSVinfected infants suggests that polymorphonuclear leukocytes play an important role in the response to acute RSV infection, at least in the airway and airspace compartments. 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.…”

Section: Discussionsupporting

confidence: 86%

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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“…Inflammation in the upper and lower airways of infants with acute bronchiolitis is dominated by an intense neutrophilia, and this is accompanied by release of products, such as human neutrophil elastase and metalloproteases which are likely to be driving much of the immunopathology observed in the primary infection (6)(7)(8). This neutrophilia is driven predominantly by high levels of IL-8 produced in response to RSV.…”

Section: Discussionmentioning

confidence: 99%

Cytokine responses in primary and secondary respiratory syncytial virus infections

et al. 2016

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Background: Primary respiratory syncytial virus (RSV) infections are characterized by high levels of IL-8 and an intense neutrophilia. Little is known about the cytokine responses in secondary infections. Preschool children experiencing RSV secondary infections were recruited from the siblings of infants admitted to hospital with RSV acute bronchiolitis. Methods: Fifty-one infants with acute bronchiolitis (39 RSV positive, 12 RSV negative) and 20 age-matched control infants were recruited. In addition, seven older siblings of infants from the RSV-positive cohort and confirmed RSV infection were recruited. Samples of nasal secretions were obtained using a flocked swab, and secretions extracted using centrifugation. Cytokine bead array was used to obtain levels of interleukin (IL)-17A, IL-8, IL-6, IL-21, and tumor necrosis factor-α. results: Levels of IL-8 and IL-6 were significantly lower in the RSV-positive siblings compared with the RSV-positive infants. There were no significant differences between levels of the other cytokines in the primary and secondary infections. conclusion: The very high levels of IL-8 and IL-6 response characteristic of the primary RSV infection was not observed in secondary RSV-positive infections and this did not appear to be due to a global reduction in cytokine production.

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Leucocyte populations in respiratory syncytial virus‐induced bronchiolitis

Abstract: Neutrophils, being the dominant cellular infiltrate into the airway, are likely to contribute to the pathophysiology of bronchiolitis. Therapies targeted at limiting neutrophil influx or neutrophil-mediated damage in the airway may have a therapeutic role.

Cited by 110 publications

References 28 publications

IL-12p40 and IL-18 Modulate Inflammatory and Immune Responses to Respiratory Syncytial Virus Infection

IL-12p40 and IL-18 Modulate Inflammatory and Immune Responses to Respiratory Syncytial Virus Infection

The histopathology of fatal untreated human respiratory syncytial virus infection

Cytokine responses in primary and secondary respiratory syncytial virus infections

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