Eicosanoids and Respiratory Viral Infection: Coordinators of Inflammation and Potential Therapeutic Targets

McCarthy, Mary K.; Weinberg, Jason B.

doi:10.1155/2012/236345

Cited by 40 publications

(38 citation statements)

References 156 publications

(172 reference statements)

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“…PGE 2 regulates immune function in many ways that are likely to affect viral pathogenesis (reviewed in 9). For example, PGE 2 promotes inflammation through vasodilatory mechanisms, leading to edema and facilitating passive leukocyte recruitment.…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 Induction during Mouse Adenovirus Type 1 Respiratory Infection Regulates Inflammatory Mediator Generation but Does Not Affect Viral Pathogenesis

et al. 2013

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Respiratory viruses cause substantial disease and are a significant healthcare burden. Virus-induced inflammation can be detrimental to the host, causing symptoms during acute infection and leading to damage that contributes to long-term residual lung disease. Prostaglandin E2 (PGE2) is a lipid mediator that is increased in response to many viral infections, and inhibition of PGE2 production during respiratory viral infection often leads to a decreased inflammatory response. We tested the hypothesis that PGE2 promotes inflammatory responses to mouse adenovirus type 1 (MAV-1) respiratory infection. Acute MAV-1 infection increased COX-2 expression and PGE2 production in wild type mice. Deficiency of the E prostanoid 2 receptor had no apparent effect on MAV-1 pathogenesis. Virus-induced induction of PGE2, IFN-γ, CXCL1, and CCL5 was reduced in mice deficient in microsomal PGE synthase-1 (mPGES-1-/- mice). However, there were no differences between mPGES-1+/+ and mPGES-1-/- mice in viral replication, recruitment of leukocytes to airways or lung inflammation. Infection of both mPGES‑1+/+ and mPGES-1-/- mice led to protection against reinfection. Thus, while PGE2 promotes the expression of a variety of cytokines in response to acute MAV-1 infection, PGE2 synthesis does not appear to be essential for generating pulmonary immunity.

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Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 Induction during Mouse Adenovirus Type 1 Respiratory Infection Regulates Inflammatory Mediator Generation but Does Not Affect Viral Pathogenesis

et al. 2013

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“…PGE 2 signals through four G protein-coupled E prostanoid (EP) receptors (McCarthy and Weinberg, 2012; Peters-Golden and Henderson, 2007). The EP1 receptor mediates PGE 2 -induced increases in intracellular Ca 2+ .…”

Section: Resultsmentioning

confidence: 99%

“…While our results suggest that PGE 2 does not play an important role in the pathogenesis of MAV-1 respiratory infection, this may not hold true for other respiratory viruses. For instance, decreased PGE 2 production as the result of COX inhibition or deficiency has been associated with decreased immunopathology and improved survival following infection of mice with RSV and influenza (reviewed in McCarthy and Weinberg, 2012), although recent work also indicates that PGE 2 may inhibit important innate and adaptive immune responses to influenza infection (Coulombe et al, 2014). To our knowledge, no existing studies directly address age-specific contributions of PGE 2 to the pathogenesis of these viruses.…”

Section: Discussionmentioning

confidence: 99%

“…PGE 2 regulates immune function in many ways that are likely to affect viral pathogenesis (reviewed in McCarthy and Weinberg, 2012). High concentrations of PGE 2 inhibit the production of the Th1 cytokines IFN-γ and IL-12 (Betz and Fox, 1991; Snijdewint et al, 1993), although lower (nanomolar) concentrations of PGE 2 have been shown to enhance Th1 function in vivo (Bloom et al, 1999; Yao et al, 2009).…”

Section: Introductionmentioning

confidence: 99%

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Prostaglandin E2 production during neonatal respiratory infection with mouse adenovirus type 1

et al. 2016

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Neonatal mice are more susceptible than adults to mouse adenovirus type 1 (MAV-1) respiratory infection. In adult mice, MAV-1 respiratory infection induces production of prostaglandin E2 (PGE2), a lipid mediator that exerts suppressive effects on a variety of host immune functions. We tested the hypothesis that exaggerated PGE2 production in neonatal mice contributes to increased susceptibility to MAV-1. PGE2 concentrations were lower in lungs of uninfected neonatal mice than in adults. PGE2 production was induced by both MAV-1 and a nonspecific stimulus to a greater degree in neonatal mice than in adults, but only in adults was PGE2 induced in a virus-specific manner. Lung viral loads were equivalent in PGE2-deficient neonatal mice and wild type controls, as was virus-induced expression of IFN-γ, IL-17A, and CCL5 in the lungs. PGE2 deficiency had minimal effect on production of virus-specific IgG or establishment of protective immunity in neonatal mice. Collectively, our data indicate that lung PGE2 production is exaggerated early in life, but this effect does not mediate increased susceptibility to MAV-1 infection.

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“…Their regulatory roles in inflammation and immune defense against viral infections are of particular interest [reviewed in [36]], especially with regard to LTB 4 , which was reported to exert appealing activity on innate defenses against pathogens. In fact, besides its association with the inflammatory process, several reports from the last decade highlight the involvement of LTB 4 in the activation of innate immune defense against viral infection.…”

Section: Ltb4 Is An Activator Of the Innate Immune Responsementioning

confidence: 99%

Leukotriene B<sub>4</sub>, an Endogenous Stimulator of the Innate Immune Response against Pathogens

2013

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Leukotriene B₄ (LTB₄) is an endogenous lipid mediator of inflammation derived from arachidonic acid by the sequential action of cytosolic phospholipase A₂ and 5-lipoxygenase. This mediator was initially recognized for its involvement in the recruitment of neutrophils. However, in the last decade, LTB₄ has been clearly demonstrated to play a significant role in the control of microbial infections through its ability to activate host innate defenses. In this review, we will focus on the modulator effects of LTB₄ on the innate defenses and discuss its therapeutic potential against viral pathogens.

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Eicosanoids and Respiratory Viral Infection: Coordinators of Inflammation and Potential Therapeutic Targets

Cited by 40 publications

References 156 publications

Prostaglandin E2 Induction during Mouse Adenovirus Type 1 Respiratory Infection Regulates Inflammatory Mediator Generation but Does Not Affect Viral Pathogenesis

Prostaglandin E2 Induction during Mouse Adenovirus Type 1 Respiratory Infection Regulates Inflammatory Mediator Generation but Does Not Affect Viral Pathogenesis

Prostaglandin E2 production during neonatal respiratory infection with mouse adenovirus type 1

Leukotriene B<sub>4</sub>, an Endogenous Stimulator of the Innate Immune Response against Pathogens

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