Comparison of protective effects of serum antibody on respiratory and systemic infection of Sendai virus in mice

Tashiro, Masato; Tobita, Kiyotake; Seto, J. T.; Rott, R.

doi:10.1007/bf01313881

Cited by 12 publications

(7 citation statements)

References 33 publications

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“…Protection against RSV and other respiratory pathogens has been accomplished by giving high-titer pooled immunoglobulin (56,325). LRI caused specifically by HPIV may be decreased (40,288,350), but little has been reported concerning the use of immunotherapy in HPIV disease. Combined immunotherapy and steroids have been demonstrated to decrease pulmonary virus titer and inflammation in a cotton rat model (291).…”

Section: Prevention and Treatmentmentioning

confidence: 99%

Parainfluenza Viruses

2003

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Human parainfluenza viruses (HPIV) were first discovered in the late 1950s. Over the last decade, considerable knowledge about their molecular structure and function has been accumulated. This has led to significant changes in both the nomenclature and taxonomic relationships of these viruses. HPIV is genetically and antigenically divided into types 1 to 4. Further major subtypes of HPIV-4 (A and B) and subgroups/genotypes of HPIV-1 and HPIV-3 have been described. HPIV-1 to HPIV-3 are major causes of lower respiratory infections in infants, young children, the immunocompromised, the chronically ill, and the elderly. Each subtype can cause somewhat unique clinical diseases in different hosts. HPIV are enveloped and of medium size (150 to 250 nm), and their RNA genome is in the negative sense. These viruses belong to the Paramyxoviridae family, one of the largest and most rapidly growing groups of viruses causing significant human and veterinary disease. HPIV are closely related to recently discovered megamyxoviruses (Hendra and Nipah viruses) and metapneumovirus

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Section: Prevention and Treatmentmentioning

confidence: 99%

Parainfluenza Viruses

2003

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“…However, the deaths are not the early pneumonic deaths but occur later and are due to the extrapulmonary spread of the virus (90,91). The effects of continuous 0.5 ppm 0 exposure on a severe influenza A/PR/34 infection were investigated.…”

Section: Impairment Ofperitoneal Macrophage Phagocytosis: the Role Ofmentioning

confidence: 99%

The Effects of Ozone on Immune Function

Jakab¹,

Spannhake²,

Canning³

et al. 1995

Environmental Health Perspectives

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A review of the literature reveals that ozone (03) exposure can either suppress or enhance immune responsiveness. These disparate effects elicited by 0 exposure depend, in large part, on the experimental design used, the immune parameters examined as well as the animal species studied.Despite the apparent contradictions, a general pattern of response to 03 exposure can be recognized. Most studies indicate that continuous 03 exposure leads to an early (days 0-3) impairment of immune responsiveness followed, with continued exposures, by a form of adaptation to 03 that results in a re-establishment of the immune response. The effects of 03 exposure on the response to antigenic stimulation also depend on the time at which 03 exposure occurred. Whereas 03 exposure prior to immunization is without effect on the response to antigen, 03 exposure subsequent to immunization suppresses the response to antigen. Although most studies have focused on immune responses in the lung, numerous investigators have provided functional and anatomical evidence to support the hypothesis that 03 exposure can have profound effects on systemic immunity. -Environ Health Perspect 1 03(Suppl 2): 77-89 (1995)

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“…Ab responses in the circulation protect against pulmonary infections and disease (1)(2)(3). Presumably, IgG Abs cross the alveolar-capillary barrier into the alveoli, where they provide resistance to infection.…”

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confidence: 99%

The Pulmonary Environment Promotes Th2 Cell Responses After Nasal-Pulmonary Immunization with Antigen Alone, but Th1 Responses Are Induced During Instances of Intense Immune Stimulation

Jones

Hodge

Fujihashi

et al. 2001

The Journal of Immunology

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The purpose of this study was to determine the nature of the CD4+ Th cell responses induced after nasal-pulmonary immunization, especially those coinciding with previously described pulmonary inflammation associated with the use of the mucosal adjuvant, cholera toxin (CT). The major T cell population in the lungs of naive mice was CD4+, and these cells were shown to be predominantly of Th2 type as in vitro polyclonal stimulation resulted in IL-4, but not IFN-γ, production. After nasal immunization with influenza Ag alone, Th2 cytokine mRNA (IL-4 and IL-5) levels were increased, whereas there was no change in Th1 cytokine (IL-2 and IFN-γ) mRNA expression. The use of the mucosal adjuvant, CT, markedly enhanced pulmonary Th2-type responses; however, there was also a Th1 component to the T cell response. Using in vitro Ag stimulation of pulmonary lymphocytes, influenza virus-specific cytokine production correlated with the mRNA cytokine results. Furthermore, there was a large increase in CD4+ Th cell numbers in lungs after nasal immunization using CT, correlating with the pulmonary inflammatory infiltrate previously described. Coincidentally, both macrophage-inflammatory protein-1α (MIP-1α) and MIP-1β mRNA expression increased in the lungs after immunization with Ag plus CT, while only MIP-1β expression increased when mice were given influenza Ag alone. Our study suggests a mechanism to foster Th1 cell recruitment into the lung, which may impact on pulmonary immune responses. Thus, while Th2 cell responses may be prevalent in modulating mucosal immunity in the lungs, Th1 cell responses contribute to pulmonary defenses during instances of intense immune stimulation.

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Comparison of protective effects of serum antibody on respiratory and systemic infection of Sendai virus in mice

Cited by 12 publications

References 33 publications

Parainfluenza Viruses

Parainfluenza Viruses

The Effects of Ozone on Immune Function

The Pulmonary Environment Promotes Th2 Cell Responses After Nasal-Pulmonary Immunization with Antigen Alone, but Th1 Responses Are Induced During Instances of Intense Immune Stimulation

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