Small intestinal injury in mice infected with respiratory influenza A virus: evidence for virus induced gastroenteritis

Zhang, Shouping; Wei, Tangting; Tianv, Haiyan; Cheng, Jinlong; Xiao, Jin; Wang, Ming; Hu, Yanxin

doi:10.1007/s10529-015-1847-8

Cited by 19 publications

(14 citation statements)

References 11 publications

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“…At this time, we do not know if stromal cells and/or cells of myeloid lineage are involved in the protective effect. Zhang et al recently reported that, in addition to its profound effects on the lung, influenza infection affects mucosal epithelium in the intestinal tract 49 , consistent with our report of systemic inflammation induced by PR8 infection 16 and our results showing that administration of AT-1001 (larazotide acetate), an inhibitor of intestinal and lung leakage 28,31,32 , reduced PR8-induced mortality. Thus, it is possible that influenza-mediated intestinal leakage underlies changes in gut microbiota that are required for development of adaptive immunity 50 .…”

Section: Discussionsupporting

confidence: 92%

Novel strategies for targeting innate immune responses to influenza

et al. 2016

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We previously reported that TLR4-/- mice are refractory to mouse-adapted A/PR/8/34 (PR8) influenza-induced lethality and that therapeutic administration of the TLR4 antagonist, Eritoran, blocked PR8-induced lethality and acute lung injury (ALI) when given starting 2 days post-infection. Herein, we extend these findings: anti-TLR4- or TLR2-specific IgG therapy also conferred significant protection of wild-type (WT) mice from lethal PR8 infection. If treatment is initiated 3 h prior to PR8 infection and continued daily for 4 days, Eritoran failed to protect WT and TLR4-/- mice, implying that Eritoran must block a virus-induced, non-TLR4 signal that is required for protection. Mechanistically, we determined that (i) Eritoran blocks HMGB1-mediated, TLR4-dependent signaling in vitro and circulating HMGB1 in vivo, and an HMGB1 inhibitor protects against PR8; (ii) Eritoran inhibits pulmonary lung edema associated with ALI, (iii) IL-1β contributes significantly to PR8-induced lethality, as evidenced by partial protection by IL-1 receptor antagonist (IL-1Ra) therapy. Synergistic protection against PR8-induced lethality was achieved when Eritoran and the anti-viral drug, oseltamivir, were administered starting 4 days post-infection. Eritoran treatment does not prevent development of an adaptive immune response to subsequent PR8 challenge. Overall, our data support the potential of a host-targeted therapeutic approach to influenza infection.

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Section: Discussionsupporting

confidence: 92%

Novel strategies for targeting innate immune responses to influenza

et al. 2016

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“…As a respiratory disease, the liver injury does not typically occur during influenza A virus infection. That respiratory, gastrointestinal, and other mucosal tissues have experienced viral replication or immune damage, but do not influence non-mucosal organs, such as the liver or kidney [11][12][13]. However, some contradicting findings were obtained, such that a pandemic A ⁄ H1N1 (2009) influenza A virus, which is different from seasonal influenza, can lead to liver damage [14].…”

Section: Discussionmentioning

confidence: 99%

Influenza A virus infection induces liver injury in mice

Zhang

et al. 2019

Microbial Pathogenesis

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A B S T R A C TRespiratory infections such as SARS-CoV in humans are often accompanied by mild and self-limiting hepatitis. As a respiratory disease, influenza A virus (IAV) infection can lead to hepatitis, but the mechanism remains unclear. This study aimed to investigate the occurrence of hepatitis by establishing a model for infected mice for three different subtypes of respiratory IAVs (H1N1, H5N1, and H7N2). Histological analysis was performed, and results showed increase serum aminotransferase (ALT and AST) levels and evident liver injury on days 3 and 7, especially on day 5 post infection. Immunohistochemistry (IHC) results indicated a wide distribution of IAV's positive signals in the liver of infected mice. Real-time PCR results further revealed a similar viral titer to IHC that presented a remarkedly positive correlation with histology injury. All these data showed that the mouse model suitably contributed valuable information about the mechanism underlying the occurrence of hepatitis induced by respiratory influenza virus.

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“…Fatality of the infection is related to pneumonia, which is characterized by massive lung inflammation resulting in damage of tissue [1] . It was demonstrated that influenza A virus (H1N1, H5N1 and H7N2) infection caused not only lung injury but also intestinal structural damage, thereby leading to gastroenteritis-like symptoms [2] . Clinically, gastrointestinal symptoms including abdominal pain, nausea, vomiting, and diarrhea often occur during influenza [3] .…”

Section: Introduction mentioning

confidence: 99%

Houttuynia cordata polysaccharide alleviated intestinal injury and modulated intestinal microbiota in H1N1 virus infected mice

Chen

et al. 2019

Chinese Journal of Natural Medicines

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Houttuynia cordata polysaccharide (HCP) is extracted from Houttuynia cordata, a key traditional Chinese medicine. The study was to investigate the effects of HCP on intestinal barrier and microbiota in H1N1 virus infected mice. Mice were infected with H1N1 virus and orally administrated HCP at a dosage of 40 mgkg -1 d -1 . H1N1 infection caused pulmonary and intestinal injury and gut microbiota imbalance. HCP significantly suppressed the expression of hypoxia inducible factor-1α and decreased mucosubstances in goblet cells, but restored the level of zonula occludens-1 in intestine. HCP also reversed the composition change of intestinal microbiota caused by H1N1 infection, with significantly reduced relative abundances of Vibrio and Bacillus, the pathogenic bacterial genera. Furthermore, HCP rebalanced the gut microbiota and restored the intestinal homeostasis to some degree. The inhibition of inflammation was associated with the reduced level of Toll-like receptors and interleukin-1β in intestine, as well as the increased production of interleukin-10. Oral administration of HCP alleviated lung injury and intestinal dysfunction caused by H1N1 infection. HCP may gain systemic treatment by local acting on intestine and microbiota. This study proved the high-value application of HCP.[KEY WORDS] H1N1 influenza virus; Houttuynia cordata; Inflammation; Intestinal Barrier; Microbiota; Polysaccharide [CLC Number] R965 [Document code] A [Article ID] 2095-6975(2019)03-0187-11 Δ These authors contributed to the work equally. These authors have no conflict of interest to declare. Published by Elsevier B.V. All rights reserved

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Small intestinal injury in mice infected with respiratory influenza A virus: evidence for virus induced gastroenteritis

Abstract: Respiratory IAV infection, particularly infected by avian IAV, can cause small intestine structural damage and modify the local immune response, thereby resulting in gastroenteritis-like symptoms.

Cited by 19 publications

References 11 publications

Novel strategies for targeting innate immune responses to influenza

Novel strategies for targeting innate immune responses to influenza

Influenza A virus infection induces liver injury in mice

Houttuynia cordata polysaccharide alleviated intestinal injury and modulated intestinal microbiota in H1N1 virus infected mice

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