Acute Respiratory Failure During Pneumonia Induced by Sendai Virus

Daal, G. J. van; Eijking, E. P.; So, K. L.; Fievez, R. B.; Sprenger, M. J. W.; Dam, Do-Won; Erdmann, W.; Lachmann, Burkhard

doi:10.1007/978-1-4615-3404-4_37

Cited by 6 publications

(4 citation statements)

References 18 publications

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“…Other animal models of direct pulmonary ALI/ARDS have also responded favorably to active exogenous surfactant. Experiments in 2 models of viral infection, one with Sendai virus in mice, 138 and another with influenza A virus, 139 show improved oxygenation and lung histology with exogenous surfactant.…”

Section: Animal Studies Of Surfactantmentioning

confidence: 99%

The Future of Exogenous Surfactant Therapy

Willson

Notter

2011

Respir Care

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Since the identification of surfactant deficiency as the putative cause of the infant respiratory distress syndrome (RDS) by Avery and Mead in 1959, our understanding of the role of pulmonary surfactant in respiratory physiology and the pathophysiology of acute lung injury (ALI) has advanced substantially. Surfactant replacement has become routine for the prevention and treatment of infant RDS and other causes of neonatal lung injury. The role of surfactant in lung injury beyond the neonatal period, however, has proven more complex. Relative surfactant deficiency, dysfunction, and inhibition all contribute to the disturbed physiology seen in ALI and acute respiratory distress syndrome (ARDS). Consequently, exogenous surfactant, while a plausible therapy, has proven to be less effective in ALI/ ARDS than in RDS, where simple deficiency is causative. This failure may relate to a number of factors, among them inadequacy of pharmaceutical surfactants, insufficient dosing or drug delivery, poor drug distribution, or simply an inability of the drug to substantially impact the underlying pathophysiology of ALI/ARDS. Both animal and human studies suggest that direct types of ALI (eg, aspiration, pneumonia) may be more responsive to surfactant therapy than indirect lung injury (eg, sepsis, pancreatitis). Animal studies are needed, however, to further clarify aspects of drug composition, timing, delivery, and dosing before additional human trials are pursued, as the results of human trials to date have been inconsistent and largely disappointing. Further study and perhaps the development of more robust pharmaceutical surfactants offer promise that exogenous surfactant will find a place in our armamentarium of treatment of ALI/ARDS in the future. Key words: surfactant; infant respiratory distress syndrome; RDS; acute lung injury; ALI; acute respiratory distress syndrome; ARDS; neonatal. [Respir Care 2011;56(9):1369 -1386.

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Section: Animal Studies Of Surfactantmentioning

confidence: 99%

The Future of Exogenous Surfactant Therapy

Willson

Notter

2011

Respir Care

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“…The surfactant dose instilled corresponds to 20 mg kg-' body weight (b.w.t.) in mice weighing 25 g. The reported surfactant doses for treatment of respiratory failure in subjects with pneumonia are generally several times higher, ranging from 50-300 mg kg-' or more (Gortner et al, 1990;Auten et al,, 1991;Eijking et al, 1991;van Daal et al, 1991;1992;Harms & Herting, 1994). However, these subjects are mechanically ventilated and receive the surfactant dose in a larger instillation volume, 2-4 ml kg-'.…”

Section: Discussionmentioning

confidence: 99%

“…Pneumonia is an important cause of acute respiratory failure and is associated with a decreased surfactant function Gunther et al, 1996). Both experimental and clinical reports have shown that instillation of exogenous surfactant in infected lungs restores gas exchange and lung function by re-expanding atelectatic lung areas van Daal et al, 1991;1992;Mikawa et al, 1993;Harms & Herting, 1994). It is expected, therefore, that use of a surfactant-antibiotic mixture has great potential in treatment of patients with severe pneumonia.…”

Section: Introductionmentioning

confidence: 99%

Pulmonary surfactant as vehicle for intratracheally instilled tobramycin in mice infected with Klebsiella pneumoniae

Veen

Mouton

Gommers

et al. 1996

British J Pharmacology

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1 The use of pulmonary surfactant has been proposed as a vehicle for antibiotic delivery to the alveolar compartment of the lung. This study investigated survival rates of mice with a respiratory Klebsiella pneumoniae infection treated intratracheally with tobramycin using a natural exogenous surfactant preparation as vehicle. 2 At day 1 after infection, animals were injected intratracheally with 20 M1 of the following solutions:(1) a mixture of surfactant (500 ug) and tobramycin (250 pg); (2) tobramycin (250 Mg) alone; (3) surfactant (500 Mg) alone; and (4) NaHCO3 buffer (control, sham-treatment

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“…These data indicated that the severe clinical disease observed following macrophage depletion in C/C′(−)-infected mice was associated with lung edema, indicative of acute respiratory distress syndromelike respiratory failure. 23…”

Section: C/c′(−) Infection In Macrophage-depleted Mice Was Associated...mentioning

confidence: 99%

Sendai virus C protein affects macrophage function, which plays a critical role in modulating disease severity during Sendai virus infection in mice

Sakuma

Morita

Tanaka

et al. 2022

Microbiology and Immunology

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Sendai virus (SeV) accessory protein C limits the generation of double-stranded RNAs, defective interfering RNAs, or both, during viral transcription and replication, thereby limiting interferon-β production. Our recent in vitro analyses on murine macrophage cell lines demonstrated that this protein also contributes to restricting macrophage function, including the production of nitric oxide (NO) and inflammatory cytokines in addition to interferon-β, in infected macrophages. This study showed that depletion of airway macrophages by clodronate-loaded liposomes led to the development of severe viral pneumonia in recombinant C gene-knockout SeV (SeVΔC)-infected mice, but did not modulate disease severity in wild-type SeVinfected mice. Furthermore, the severe disease observed in macrophage-depleted, SeVΔC-infected mice was associated with exacerbated virus replication in the lungs, leading to severe airway inflammation and pulmonary edema, indicating lung injury. These results suggested that the antimacrophage activity of SeV C protein might play a critical role in modulating lung injury and associated diseases caused by SeV.

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Acute Respiratory Failure During Pneumonia Induced by Sendai Virus

Cited by 6 publications

References 18 publications

The Future of Exogenous Surfactant Therapy

The Future of Exogenous Surfactant Therapy

Pulmonary surfactant as vehicle for intratracheally instilled tobramycin in mice infected with Klebsiella pneumoniae

Sendai virus C protein affects macrophage function, which plays a critical role in modulating disease severity during Sendai virus infection in mice

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