Orally administered live attenuated Salmonella Typhimurium protects mice against lethal infection with H1N1 influenza virus

Kamble, Nitin Machindra; Hajam, Irshad Ahmed; Lee, John Hwa

doi:10.1016/j.vetmic.2017.01.006

Cited by 10 publications

(7 citation statements)

References 30 publications

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“…GAS5 is abnormally downregulated in patients with bacterial sepsis ( Mayama et al, 2016 ). In some inflammatory diseases, GAS5 affects cell inflammatory responses by regulating TLR4 receptor ( Zhao et al, 2020 ), which is an important cell surface receptor in ST infection ( Kamble et al, 2017 ; Muneta et al, 2018 ; Lin H.H. et al, 2020 ).…”

Section: Resultsmentioning

confidence: 99%

Chlorogenic Acid Promotes Autophagy and Alleviates Salmonella Typhimurium Infection Through the lncRNAGAS5/miR-23a/PTEN Axis and the p38 MAPK Pathway

Tan

Fang

et al. 2020

Front. Cell Dev. Biol.

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Background: Salmonella typhimurium (ST) causes several intestinal diseases. Polyphenols including chlorogenic acid (CGA) inhibit pathogenesis. Objective: This study aimed to investigate the mechanisms of CGA in ST infection. Methods: The intestinal pathological changes and survival rate of ST-infected mice were measured to verify the protection of CGA on ST infection. The antibacterial effects of CGA in vitro on the invasion to intestinal epithelial cells and autophagy was evaluated. The relationships among GAS5, miR-23a, and PTEN were verified. Expression of inflammation-and autophagy-related proteins was detected. Results: CGA treatment alleviated pathological damage, improved the secretion disturbance of intestinal cytokines caused by ST infection, and reduced the mortality of mice. Intestinal GAS5 was upregulated after CGA treatment. LncRNA GAS5 competitively bound to miR-23a to upregulate PTEN and inhibit the p38 MAPK pathway. CGA regulated the p38 MAPK pathway through lncRNA GAS5/miR-23a/PTEN axis to promote autophagy in ST infection. The functional rescue experiments of miR-23a and PTEN further identified these effects. Conclusion: CGA promotes autophagy and inhibits ST infection through the GAS5/miR-23a/PTEN axis and the p38 MAPK pathway.

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Section: Resultsmentioning

confidence: 99%

Chlorogenic Acid Promotes Autophagy and Alleviates Salmonella Typhimurium Infection Through the lncRNAGAS5/miR-23a/PTEN Axis and the p38 MAPK Pathway

Tan

Fang

et al. 2020

Front. Cell Dev. Biol.

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“…As described above, bacterial pathogens given prior to influenza viruses can stimulate innate immunity that reduces the severity of influenza (56,58). Infection of mice with nonpathogenic bacteria or with a parasite that causes a chronic infection has also been shown to reduce the severity of influenza infections (34,(62)(63)(64)(65). While the mechanisms of protection may differ among coinfecting microbes, protection relies on detection of the initial infection by pattern recognition receptors.…”

Section: Discussionmentioning

confidence: 99%

Attenuation of Influenza A Virus Disease Severity by Viral Coinfection in a Mouse Model

González

Ijezie

Balemba

et al. 2018

J Virol

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Influenza viruses and rhinoviruses are responsible for a large number of acute respiratory viral infections in human populations and are detected as copathogens within hosts. Clinical and epidemiological studies suggest that coinfection by rhinovirus and influenza virus may reduce disease severity and that they may also interfere with each other's spread within a host population. To determine how coinfection by these two unrelated respiratory viruses affects pathogenesis, we established a mouse model using a minor serogroup rhinovirus (rhinovirus strain 1B [RV1B]) and mouse-adapted influenza A virus (A/Puerto Rico/8/1934 [PR8]). Infection of mice with RV1B 2 days before PR8 reduced the severity of infection by a low or medium, but not high, dose of PR8. Disease attenuation was associated with an early inflammatory response in the lungs and enhanced clearance of PR8. However, coinfection by RV1B did not reduce PR8 viral loads early in infection or inhibit replication of PR8 within respiratory epithelia or Inflammation in coinfected mice remained focal compared to diffuse inflammation and damage in the lungs of mice infected by PR8. The timing of RV1B coinfection was a critical determinant of protection, suggesting that sufficient time is needed to induce this response. Finally, disease attenuation was not unique to RV1B: dose-dependent coinfection by a murine coronavirus (mouse hepatitis virus strain 1 [MHV-1]) also reduced the severity of PR8 infection. Unlike RV1B, coinfection with MHV-1 reduced early PR8 replication, which was associated with upregulation of beta interferon (IFN-β) expression. This model is critical for understanding the mechanisms responsible for influenza disease attenuation during coinfection by unrelated respiratory viruses. Viral infections in the respiratory tract can cause severe disease and are responsible for a majority of pediatric hospitalizations. Molecular diagnostics have revealed that approximately 20% of these patients are infected by more than one unrelated viral pathogen. To understand how viral coinfection affects disease severity, we inoculated mice with a mild viral pathogen (rhinovirus or murine coronavirus), followed 2 days later by a virulent viral pathogen (influenza A virus). This model demonstrated that rhinovirus can reduce the severity of influenza A virus, which corresponded with an early but controlled inflammatory response in the lungs and early clearance of influenza A virus. We further determined the dose and timing parameters that were important for effective disease attenuation and showed that influenza disease is also reduced by coinfection with a murine coronavirus. These findings demonstrate that coinfecting viruses can alter immune responses and pathogenesis in the respiratory tract.

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“…For viral challenge experiments, mice ( n = 9, each group) were first anesthetized with sevoflurane and then challenged intranasally with 50 μl PBS (25 μl per nostril) containing a dose of 10 6 EID50 of lethal influenza virus strain A Puerto Rico/8/34 (H1N1) 4 weeks after vaccination as previously described (Kamble et al, 2017). The infected mice showed the typical effects of systemic infection caused by influenza virus.…”

Section: Methodsmentioning

confidence: 99%

An Influenza HA and M2e Based Vaccine Delivered by a Novel Attenuated Salmonella Mutant Protects Mice against Homologous H1N1 Infection

Hajam

Lee

2017

Front. Microbiol.

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Attenuated Salmonella strains constitute a promising technology for the development of a more efficient multivalent protein based vaccines. In this study, we constructed a novel attenuated strain of Salmonella for the delivery and expression of the H1N1 hemagglutinin (HA) and the conserved extracellular domain of the matrix protein 2 (M2e). We demonstrated that the constructed Salmonella strain exhibited efficient HA and M2e protein expressions and little cytotoxicity and pathogenicity in mice. Using BALB/c mice as the model, we showed that the mice vaccinated with a Salmonella strain expressing HA and M2e protein antigens, respectively, induced significant production of HA and M2e-specific serum IgG1 and IgG2a responses, and of anti-HA interferon-γ producing T cells. Furthermore, immunization with Salmonella-HA-M2e-based vaccine via different routes provided protection in 66.66% orally, 100% intramuscularly, and 100% intraperitoneally immunized mice against the homologous H1N1 virus while none of the animals survived treated with either the PBS or the Salmonella carrying empty expression vector. Ex vivo stimulated dendritic cells (DCs) with heat killed Salmonella expressing HA demonstrated that DCs play an important role in the elicitation of HA-specific humoral immune responses in mice. In summary, Salmonella-HA-M2e-based vaccine elicits efficient antigen-specific humoral and cellular immune responses, and provides significant immune protection against a highly pathogenic H1N1 influenza virus.

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Orally administered live attenuated Salmonella Typhimurium protects mice against lethal infection with H1N1 influenza virus

Cited by 10 publications

References 30 publications

Chlorogenic Acid Promotes Autophagy and Alleviates Salmonella Typhimurium Infection Through the lncRNAGAS5/miR-23a/PTEN Axis and the p38 MAPK Pathway

Chlorogenic Acid Promotes Autophagy and Alleviates Salmonella Typhimurium Infection Through the lncRNAGAS5/miR-23a/PTEN Axis and the p38 MAPK Pathway

Attenuation of Influenza A Virus Disease Severity by Viral Coinfection in a Mouse Model

An Influenza HA and M2e Based Vaccine Delivered by a Novel Attenuated Salmonella Mutant Protects Mice against Homologous H1N1 Infection

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