C57Bl/6 mice are protected from respiratory syncytial virus (RSV) challenge and IL-5 associated pulmonary eosinophilic infiltrates following intranasal immunization with Protollin-eRSV vaccine

Cyr, Sonya; Jones, Trevor O.; Stoica-Popescu, Ioana; Burt, David S.; Ward, Brian J.

doi:10.1016/j.vaccine.2007.01.037

Cited by 24 publications

(15 citation statements)

References 13 publications

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“…Infectious dose was chosen based on references that previously characterize mucogenic strains of RSV in the mouse model [26], [29]. To compare infection of WT C57BL/6 with OPN-/-, a higher infectious dose (1×10 6 pfu/mouse) was used because previous reports indicate C57BL/6 are resistant to RSV infections [30]. After euthanasia, chest cavity was opened and the lungs were gently inflated intratracheally with 4°C 4% paraformaldehyde in PBS, removed and immersed in 4% paraformaldehyde at 4°C for an additional 6 hrs.…”

Section: Methodsmentioning

confidence: 99%

Respiratory Syncytial Virus (RSV) Infection in Elderly Mice Results in Altered Antiviral Gene Expression and Enhanced Pathology

et al. 2014

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Elderly persons are more susceptible to RSV-induced pneumonia than young people, but the molecular mechanism underlying this susceptibility is not well understood. In this study, we used an aged mouse model of RSV-induced pneumonia to examine how aging alters the lung pathology, modulates antiviral gene expressions, and the production of inflammatory cytokines in response to RSV infection. Young (2–3 months) and aged (19–21 months) mice were intranasally infected with mucogenic or non-mucogenic RSV strains, lung histology was examined, and gene expression was analyzed. Upon infection with mucogenic strains of RSV, leukocyte infiltration in the airways was elevated and prolonged in aged mice compared to young mice. Minitab factorial analysis identified several antiviral genes that are influenced by age, infection, and a combination of both factors. The expression of five antiviral genes, including pro-inflammatory cytokines IL-1β and osteopontin (OPN), was altered by both age and infection, while age was associated with the expression of 15 antiviral genes. Both kinetics and magnitude of antiviral gene expression were diminished as a result of older age. In addition to delays in cytokine signaling and pattern recognition receptor induction, we found TLR7/8 signaling to be impaired in alveolar macrophages in aged mice. In vivo, induction of IL-1β and OPN were delayed but prolonged in aged mice upon RSV infection compared to young. In conclusion, this study demonstrates inherent differences in response to RSV infection in young vs. aged mice, accompanied by delayed antiviral gene induction and cytokine signaling.

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Section: Methodsmentioning

confidence: 99%

Respiratory Syncytial Virus (RSV) Infection in Elderly Mice Results in Altered Antiviral Gene Expression and Enhanced Pathology

et al. 2014

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“…Additionally, monovalent [165] and trivalent [162] influenza A/H1N1-proteosome (no LPS) vaccines administered IN produced high antibody titers in serum as well as in nasal secretions [162,165], suggesting that IN delivery of proteosomebased vaccines may be able to produce both systemic and mucosal immunity. Furthermore, preclinical studies have shown that such a vaccine is capable of protecting mice upon challenge with the infective pathogen [163,[166][167][168].…”

Section: Proteosomesmentioning

confidence: 99%

Nanotechnology in vaccine delivery

Peek

Middaugh

Berkland

2008

Advanced Drug Delivery Reviews

481

342

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With very few adjuvants currently being used in marketed human vaccines, a critical need exists for novel immunopotentiators and delivery vehicles capable of eliciting humoral, cellular and mucosal immunity. Such crucial vaccine components could facilitate the development of novel vaccines for viral and parasitic infections, such as hepatitis, HIV, malaria, cancer, etc. In this review, we discuss clinical trial results for various vaccine adjuvants and delivery vehicles being developed that are approximately nanoscale (<1000 nm) in size. Humoral immune responses have been observed for most adjuvants and delivery platforms while only viral vectors, ISCOMs and Montanide ISA 51 and 720 have shown cytotoxic T cell responses in the clinic. MF59 and MPL have elicited Th1 responses, and virus-like particles, non-degradable nanoparticles and liposomes have also generated cellular immunity. Such vaccine components have also been evaluated for alternative routes of administration with clinical successes reported for intranasal delivery of viral vectors and proteosomes and oral delivery of a VLP vaccine.

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“…TLR2 and TLR1 or TLR2 and TLR6 complexes recognize bacterial motifs as well as a diverse range of viruses, including hepatitis C virus, herpes simplex virus, lymphocytic choriomeningitis virus, and human cytomegalovirus, and strongly promote early innate inflammatory responses after viral recognition (8,9,27,56). Genetic analysis and vaccine studies of BALB/c mice indirectly suggest that TLR2 signaling is involved in RSV recognition; however, these studies did not investigate whether TLR2 directly interacts with RSV (11,20,23). We wished to further examine the inferred relationship between RSV and TLR2, because identifying novel pathways by which RSV activates innate immunity could aid the development of safe and effective RSV vaccines.…”

mentioning

confidence: 99%

Respiratory Syncytial Virus Activates Innate Immunity through Toll-Like Receptor 2

Murawski

Bowen

Cerny

et al. 2009

J Virol

236

219

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Respiratory syncytial virus (RSV) is a common cause of infection that is associated with a range of respiratory illnesses, from common cold-like symptoms to serious lower respiratory tract illnesses such as pneumonia and bronchiolitis. RSV is the single most important cause of serious lower respiratory tract illness in children <1 year of age. Host innate and acquired immune responses activated following RSV infection have been suspected to contribute to RSV disease. Toll-like receptors (TLRs) activate innate and acquired immunity and are candidates for playing key roles in the host immune response to RSV. Leukocytes express TLRs, including TLR2, TLR6, TLR3, TLR4, and TLR7, that can interact with RSV and promote immune responses following infection. Using knockout mice, we have demonstrated that TLR2 and TLR6 signaling in leukocytes can activate innate immunity against RSV by promoting tumor necrosis factor alpha, interleukin-6, CCL2 (monocyte chemoattractant protein 1), and CCL5 (RANTES). As previously noted, TLR4 also contributes to cytokine activation (

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C57Bl/6 mice are protected from respiratory syncytial virus (RSV) challenge and IL-5 associated pulmonary eosinophilic infiltrates following intranasal immunization with Protollin-eRSV vaccine

Cited by 24 publications

References 13 publications

Respiratory Syncytial Virus (RSV) Infection in Elderly Mice Results in Altered Antiviral Gene Expression and Enhanced Pathology

Respiratory Syncytial Virus (RSV) Infection in Elderly Mice Results in Altered Antiviral Gene Expression and Enhanced Pathology

Nanotechnology in vaccine delivery

Respiratory Syncytial Virus Activates Innate Immunity through Toll-Like Receptor 2

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