Cytokines and the acute phase response to influenza virus in mice

Conn, Carole A.; McClellan, J. L.; Maassab, Hunein F.; Smitka, Curt W.; Majde, Jeannine A.; Kluger, Matthew J.

doi:10.1152/ajpregu.1995.268.1.r78

Cited by 82 publications

(98 citation statements)

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“…In the present study, we define central but opposite effects of COX-1 and COX-2 enzymes in the host response to this infection. Hypothermia and weight loss are well documented features of viral influenza infection in the mouse (25)(26)(27)(28)(29)(30). In the present study, we observed some differences in the early temperature response to influenza infection in the COX-1 Ϫ/Ϫ and COX-2 Ϫ/Ϫ mice.…”

Section: Discussionsupporting

confidence: 55%

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Carey¹,

Bradbury²,

Seubert³

et al. 2005

The Journal of Immunology

103

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Influenza is a significant cause of morbidity and mortality worldwide despite extensive research and vaccine availability. The cyclooxygenase (COX) pathway is important in modulating immune responses and is also a major target of nonsteroidal anti-inflammatory drugs (NSAIDs) and the newer COX-2 inhibitors. The purpose of the present study was to examine the effect of deficiency of COX-1 or COX-2 on the host response to influenza. We used an influenza A viral infection model in wild type (WT), COX-1−/−, and COX-2−/− mice. Infection induced less severe illness in COX-2−/− mice in comparison to WT and COX-1−/− mice as evidenced by body weight and body temperature changes. Mortality was significantly reduced in COX-2−/− mice. COX-1−/− mice had enhanced inflammation and earlier appearance of proinflammatory cytokines in the BAL fluid, whereas the inflammatory and cytokine responses were blunted in COX-2−/− mice. However, lung viral titers were markedly elevated in COX-2−/− mice relative to WT and COX-1−/− mice on day 4 of infection. Levels of PGE2 were reduced in COX-1−/− airways whereas cysteinyl leukotrienes were elevated in COX-2−/− airways following infection. Thus, deficiency of COX-1 and COX-2 leads to contrasting effects in the host response to influenza infection, and these differences are associated with altered production of prostaglandins and leukotrienes following infection. COX-1 deficiency is detrimental whereas COX-2 deficiency is beneficial to the host during influenza viral infection.

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Section: Discussionsupporting

confidence: 55%

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Carey¹,

Bradbury²,

Seubert³

et al. 2005

The Journal of Immunology

103

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“…Acute-phase response is defined as the dose-dependent behavioral and physiological response of host organisms to infections and is regarded as a nonspecific host defense response. 75 The acute-phase response includes fevers of different magnitudes, changes in food and water intake in mice as well as decreases in activity and body temperature, which again have been correlated to cytokine activity after influenza virus infection. 75 On recognition of viral components, PRRs initiate production of a variety of cytokines, mainly type-1 INFs (IFN-b and -a), and induce innate and adaptive immune responses.…”

Section: Cytokines As the Initial Line Of Defensementioning

confidence: 99%

“…Interleukin 6 exhibits multifunctional activities that are largely proinflammatory and their release has been correlated with the same clinical symptoms and signs related to influenza in mice. 75 Interferon g inducible protein is a chemokine that is being studied for its role in the severity of lung damage after IAV infection. BALB/c mice infected with H5N1 after administration of IP-10 presented with more fulminant and necrotizing diffuse alveolar and bronchiolar damage with lymphocyte infiltration compared to infected mice without IP-10 administration.…”

Section: Role Of Cytokines/chemokines and Their Receptorsmentioning

confidence: 99%

Influenza, Immune System, and Pregnancy

2014

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Influenza is a major health problem worldwide. Both seasonal influenza and pandemics take a major toll on the health and economy of our country. The present review focuses on the virology and complex immunology of this RNA virus in general and in relation to pregnancy. The goal is to attempt to explain the increased morbidity and mortality seen in infection during pregnancy. We discuss elements of innate and adaptive immunity as well as placental cellular responses to infection. In addition, we delineate findings in animal models as well as human disease. Increased knowledge of maternal and fetal immunologic responses to influenza is needed. However, enhanced understanding of nonimmune, pregnancy-specific factors influencing direct interaction of the virus with host cells is also important for the development of more effective prevention and treatment options in the future.

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“…During pulmonary infections cytokine production is mainly restricted to the lung and it seems that diffusion of cytokines across the bloodalveolar barrier is rather limited [87]. Consequently, the highest amounts of cytokines are detected at the lung level, and plasma cytokine levels are generally low or undetectable [11,33]. This situation contrasts with that seen during septicaemia, where endothelial and blood cells are the primary cytokine producers and systemic effects, such as shock and multiple organ failure, predominate.…”

Section: Cytokine Effects On the Respiratory Tractmentioning

confidence: 99%

Proinflammatory cytokines and viral respiratory disease in pigs

2000

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-Swine influenza virus (SIV), porcine respiratory coronavirus (PRCV) and porcine reproductive and respiratory syndrome virus (PRRSV) are enzootic viruses causing pulmonary infections in pigs. The first part of this review concentrates on known clinical and pathogenetic features of these infections. SIV is a primary respiratory pathogen; PRCV and PRRSV, on the contrary, tend to cause subclinical infections if uncomplicated but they appear to be important contributors to multifactorial respiratory diseases. The exact mechanisms whereby these viruses cause symptoms and pathology, however, remain unresolved. Classical studies of pathogenesis have revealed different lung cell tropisms and replication kinetics for each of these viruses and they suggest the involvement of different lung inflammatory responses or mediators. The proinflammatory cytokines interferon-α (IFN-α), tumour necrosis factor-α (TNF-α) and interleukin-1 (IL-1) have been shown to play key roles in several respiratory disease conditions. The biological effects of these cytokines and their involvement in human viral respiratory disease are discussed in the second part of this review. The third part summarises studies that were recently undertaken in the authors' laboratory to investigate the relationship between respiratory disease in pigs and bioactive lung lavage levels of IFN-α, TNF-α and IL-1 during single and combined infections with the above viruses. In single SIV infections, typical signs of swine "flu" were tightly correlated with an excessive and coordinate production of the 3 cytokines examined. PRCV or PRRSV infections, in contrast, were subclinical and did not induce production of all 3 cytokines. Combined infections with these 2 subclinical respiratory viruses failed to potentiate disease or cytokine production. After combined inoculation with PRCV followed by bacterial lipopolysaccharide, both clinical respiratory disease and TNF-α/IL-1 production were markedly more severe than those associated with the respective single inoculations. Taken together, these data are the first to demonstrate that proinflammatory cytokines can be important mediators of viral respiratory diseases in pigs. respiratory coronavirus, PRCV), et le virus du syndrome dysgénésique et respiratoire porcin (porcine reproductive and respiratory syndrome virus, PRRSV) sont des virus enzootiques provoquant des infections pulmonaires chez le porc. Les caractéristiques cliniques et pathogénétiques de ces infections sont données dans la première partie de cette revue. Le SIV est un agent pathogène respiratoire primaire ; les PRCV et PRRSV, en revanche, ne causent que des infections subcliniques en l'absence de complications, mais ils contribuent de manière importante aux maladies respiratoires multifactorielles. Cependant, les mécanismes précis par lesquels ces virus provoquent des symptômes et une pathologie demeurent inconnus. Les études classiques de pathogenèse ont révélé un tropisme pour les cellules pulmonaires et des cinétiques de réplication différents pour...

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Cytokines and the acute phase response to influenza virus in mice

Cited by 82 publications

References 0 publications

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Contrasting Effects of Cyclooxygenase-1 (COX-1) and COX-2 Deficiency on the Host Response to Influenza A Viral Infection

Influenza, Immune System, and Pregnancy

Proinflammatory cytokines and viral respiratory disease in pigs

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