Persistence of proinflammatory response after severe respiratory syncytial virus disease in children

Bermejo-Martín, Jesús F.; Garcia-Arevalo, Maria C; Alonso, Ana; Lejarazu, Raúl Ortíz de; Pino, María; Resino, Salvador; Tenorio, Alberto; Bernardo, David; Leόn, Alberto J.; Garrote, José Antonio; Ardura, J; Domínguez‐Gil, Marta; Eiros, Jose M.; Blanco‐Quirós, Alfredo; Ma, Mai‐Juan; Kelvin, David J.; Arranz, Eduardo

doi:10.1016/j.jaci.2007.03.014

Cited by 23 publications

(27 citation statements)

References 9 publications

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“…RSV bronchiolitis is followed by a robust inflammatory response in the airways, which may persist for more than 1 month. 37 We speculate that this inflammatory response, including production of interferons, transiently protects against subsequent viral infection, resulting in fewer coinfections. 38,39 More research is needed to unravel how respiratory viruses interact at the mucosal level.…”

Section: Discussionmentioning

confidence: 94%

Respiratory Syncytial Virus and Recurrent Wheeze in Healthy Preterm Infants

et al. 2013

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Section: Discussionmentioning

confidence: 94%

Respiratory Syncytial Virus and Recurrent Wheeze in Healthy Preterm Infants

et al. 2013

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“…The authors speculated that IL-17 was contributing to both protection from more severe disease and resolution of the illness. In contrast, Bermejo-Martin et al (22) found lower levels of IL-17 in nasal secretions of infants with RSV bronchiolitis at discharge as compared to admission. The same group also found IL-17 levels in nasal samples taken 1 year after an admission with RSV bronchiolitis were elevated compared with controls (23).…”

Section: Discussionmentioning

confidence: 82%

“…IL-17-producing T cells are induced in primary infections through pathways that involve STAT3 and IL-6 (16,17). High levels of IL-6 have been found in the airways of infants with RSV bronchiolitis (18,19), and a number of studies have identified IL-17 in the airways (20)(21)(22)(23)(24) and plasma (21,24) of infants with RSV infection. Two studies have found lower levels of IL-17 in the airways of the most severely affected infants, and the authors suggested that higher IL-17 levels were associated with protection against more severe disease (21,24).…”

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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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“…Monocyte chemoattractant protein 1 (MCP-1), a chemokine of mononuclear cells and T lymphocytes, plays an important role in severe RSV infection and VED (3,31). RSV challenge of G1F/ M2-immunized mice induced dramatically increased levels of MCP-1 mRNA compared with RSV challenge of mice treated with PBS (P Ͻ 0.05), suggesting a G1F/M2-enhanced MCP-1 expression after RSV challenge.…”

Section: Humoral Immune Response Induced By Pil-27؉g1f/m2mentioning

confidence: 99%

“…It has been shown that F/M2 is effective in induction of M2 (aa 81 to 95 peptide)-and RSV-specific CTL responses as well as protective immunity in mice (16,11). G1F/M2 immunization of mice with Al(OH) 3 as an adjuvant induced a mixed Th1/Th2 response, CD8…”

mentioning

confidence: 99%

Interleukin-27 Inhibits Vaccine-Enhanced Pulmonary Disease following Respiratory Syncytial Virus Infection by Regulating Cellular Memory Responses

Zeng

Zhang

Yan

et al. 2012

J Virol

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Respiratory syncytial virus (RSV) is the most important cause of lower respiratory tract disease in infants and young children, accounting for approximately 5% of hospitalizations due to lower respiratory tract infections (15). Premature infants, immunocompromised individuals, and the elderly are the populations at the greatest risk to develop life-threatening RSV infections (10, 29). Moreover, reinfections occur frequently during life due to incomplete immunity after RSV infection. A number of clinical epidemiology studies have identified that there is a strong association between RSV bronchiolitis in infancy and the development of wheezing and asthma in later childhood (31,36,37). The World Health Organization has established a high priority for the development of an RSV vaccine. However, efforts to develop a safe and effective vaccine have been unsuccessful. In the 1960s, a formalininactivated RSV (FI-RSV) vaccine was used to immunize infants; these infants developed a more severe disease upon natural RSV infection; 80% of them but only 5% of infants that received a control vaccine required hospitalization, and two died (21). Histology performed on the lungs of the deceased revealed extensive neutrophils, mononuclear cells, and lymphocytes and increased numbers of eosinophils infiltrating the lungs (33).Although the vaccine-enhanced disease (VED) is a major concern in the development of a safe and effective RSV vaccine, its immunological mechanisms are unclear. Many pieces of evidence showed that VED was associated with an exaggerated Th2-type response. Depletion of Th2 cytokine interlukin-4 (IL-4) or IL-13 of mice immunized with FI-RSV inhibited the development of pulmonary disease after RSV challenge (18). The Th2 polarization may have been related to the absence of a Th1-promoting RSVspecific cytotoxic T lymphocyte (CTL) response after immunization with FI-RSV (29). RSV challenge of FI-RSV-immunized mice elicited a robust memory CD4 ϩ T cell response in the absence of a detectable memory CD8 ϩ T cell response, pulmonary eosinophilia, and VED (29). Immunization of BALB/c mice with a recombinant vaccinia virus (vacv) that expresses the RSV M2 protein (vacvM2) elicited an RSV-specific memory CD8 ϩ T cell response. Mice coimmunized with FI-RSV and vacvM2 after RSV challenge did not develop pulmonary eosinophilia, along with downregulation of pulmonary Th2 cytokines and upregulation of Th1 cytokines (41). Despite the beneficial role, Th1-biased or CD8 ϩ T-biased cellular memory may also be detrimental to the host. RSV challenge of mice previously immunized with vacv expressing the RSV F protein (vacvF) exhibited a memory Th1 response in the absence of a detectable memory Th2 response and developed lung inflammation characterized by mononuclear cell infiltration (5,17,28). In the mice immunized with vacvM2 or vacvF, systemic disease, including weight loss, occurs after RSV challenge, although no eosinophilia was detectable (5,17,28). These data clearly suggested that both a Th2 memory response and a Th1 or CD8 ϩ...

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Persistence of proinflammatory response after severe respiratory syncytial virus disease in children

Cited by 23 publications

References 9 publications

Respiratory Syncytial Virus and Recurrent Wheeze in Healthy Preterm Infants

Respiratory Syncytial Virus and Recurrent Wheeze in Healthy Preterm Infants

Cytokine responses in primary and secondary respiratory syncytial virus infections

Interleukin-27 Inhibits Vaccine-Enhanced Pulmonary Disease following Respiratory Syncytial Virus Infection by Regulating Cellular Memory Responses

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