IL-1<b><i>β</i></b>and IL-6 Upregulation in Children with H1N1 Influenza Virus Infection

Chiaretti, Antonio; Pulitanò, Silvia; Barone, Giuseppe; Ferrara, Pietro; Romano, Valerio; Capozzi, Domenico; Riccardi, Riccardo

doi:10.1155/2013/495848

Cited by 67 publications

(60 citation statements)

References 34 publications

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“…Our results showed that IL1B and IL6 were significantly upregulated in the trachea and ileum of chickens, which is different from their expression levels in samples collected from ducks. Recent studies have shown a positive correlation between the severity of the clinical manifestations and IL6 expression levels in animals (Marais et al, 2011;Chiaretti et al, 2013). It was possible to account for different manifestation of clinical signs in the two species after infection with H9N2.…”

Section: Discussionmentioning

confidence: 98%

Different outcomes of infection of chickens and ducks with a duck-origin H9N2 influenza A virus

Wang¹,

Li²,

Diao³

et al. 2014

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Summary. -As the major aquatic and terrestrial hosts for avian influenza viruses (AIVs), ducks and chickens play a critical role in the evolution and spread of the H9N2 virus. However, the outcomes of infection of ducks and chickens with the H9N2 virus are not sufficiently documented. In this study, we compared the outcomes of infection of chickens and Peking ducks with a duck-origin H9N2 virus. The results showed that this virus caused more pronounced clinical signs and histological lesions in chickens. As for the virus shedding, chickens shed more virus in the trachea and less virus in the cloaca in levels of interferon (IFN) γ were found in the trachea of ducks compared with chickens, while comparison with ducks. As for cytokines, namely IFNs and interleukins (IL), higher higher levels of IFN-β, IFN-γ, IL-1β, and IL-6 were observed in the ileum of chickens compared with ducks. Eventually, serum hemagglutination-inhibition (HI) antibody titers were higher in chickens than in ducks. Taken together, ducks and chickens use different strategies in response to the H9N2 virus infection in tissues representing main replication sites of low-pathogenic AIVs. Given the different outcomes of the H9N2 virus infection in ducks and chickens, different measures should be taken in vaccination and treatment.Keywords: duck-origin influenza A virus; H9N2 subtype; chicken; duck * Corresponding author. E-mail: yxdiao@126.com; phone: +86 0538 8249851-8210.# These authors contributed equally to this work. Abbreviations: AIV(s) = avian influenza virus(es); CL = cloacal; HA = hemagglutinin; HI = hemagglutination-inhibition; HPAIVs = highly pathogenic avian influenza viruses; IFN = interferon; IL = interleukin; LPAIV(s) = low pathogenic avian influenza virus(es); NA = neuraminidase; OP = oropharyngeal; p.i. = post infection

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Section: Discussionmentioning

confidence: 98%

Different outcomes of infection of chickens and ducks with a duck-origin H9N2 influenza A virus

Wang¹,

Li²,

Diao³

et al. 2014

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“…Interleukin 1β has been shown to be elevated in pediatric patients with severe influenza, but so has its antagonist. 43,44 In addition, IL-1 receptor antagonist polymorphisms have been associated with severe community-acquired pneumonia in children. 45 How inflammasome activation and RLR signaling differ between children and adults is unknown and represents an important area of future investigation.…”

Section: Developmental Dependent Changes In Prr Signalingmentioning

confidence: 99%

Influenza A Virus Infection, Innate Immunity, and Childhood

et al. 2015

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Infection with influenza A virus is responsible for considerable morbidity and mortality in children worldwide. While it is apparent that adequate activation of the innate immune system is essential for pathogen clearance and host survival, an excessive inflammatory response to infection is detrimental to the young host. A review of the literature indicates that innate immune responses change throughout childhood. Whether these changes are genetically programmed or triggered by environmental cues is unknown. The objectives of this review are to summarize the role of innate immunity in influenza A virus infection in the young child and to highlight possible differences between children and adults that may make children more susceptible to severe influenza A infection. A better understanding of age-related differences in innate immune signaling will be essential to improve care for this high-risk population.Influenza A virus (IAV) is a highly contagious RNA virus that causes respiratory tract infections in humans and animals. Seasonal IAV is responsible for considerable disease worldwide, with the World Health Organization estimating 3 to 5 million severe cases of IAV each year and approximately 250 000 to 500 000 deaths. 1 Pandemics threaten to affect significantly more people. During the 1918 pandemic, it is estimated that IAV was responsible for 50 to 100 million deaths. 2 The burden of IAV infection is highest in children, the elderly, and persons with chronic medical conditions. Each year, IAV infection affects up to 40% of children younger than 5 years in the United States and 90 million

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“…These cytokines are important to induce inflammatory responses and to restrict viral replication and spread (Dienz et al, 2012). Elevated levels of pro-inflammatory cytokines are closely correlated with severity of clinical diseases, including airway inflammation and acute lung injury during influenza infection in children (Chiaretti et al, 2013). On the other hand, activation of the TBK1/IKKε/NEMO complex leads to activation of IRF3 and production type I interferon (IFN), including IFNα and IFNβ (Fitzgerald et al, 2003; Sankar et al, 2006; Zhong et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

CARMA3 Is a Host Factor Regulating the Balance of Inflammatory and Antiviral Responses against Viral Infection

et al. 2016

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Host response to RNA virus infection is sensed by RNA sensors such as RIG-I, which induce MAVS-mediated NF-κB and IRF3 activation to promote inflammatory and antiviral responses, respectively. Here, we found that CARMA3, a scaffold protein previously shown to mediate NF-κB activation induced by GPCR and EGFR, positively regulates MAVS-induced NF-κB activation. However, our data suggest that CARMA3 sequesters MAVS from forming high-molecular weight aggregates, thereby suppressing TBK1/IRF3 activation. Interestingly, following NF-κB activation upon virus infection, CARMA3 is targeted for proteasome-dependent degradation, which releases MAVS to activate IRF3. When challenged with Vesicular stomatitis virus or Influenza A virus, CARMA3-deficient mice showed reduced disease symptoms compared to those of wild type mice due to less inflammation and stronger ability to clear infected virus. Together, our studies reveal the role of CARMA3 in regulating the balance of host anti-viral and pro-inflammatory responses against RNA virus infection.

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IL-1βand IL-6 Upregulation in Children with H1N1 Influenza Virus Infection

Cited by 67 publications

References 34 publications

Different outcomes of infection of chickens and ducks with a duck-origin H9N2 influenza A virus

Different outcomes of infection of chickens and ducks with a duck-origin H9N2 influenza A virus

Influenza A Virus Infection, Innate Immunity, and Childhood

CARMA3 Is a Host Factor Regulating the Balance of Inflammatory and Antiviral Responses against Viral Infection

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