scholarly journals Possible Roles of Proinflammatory and Chemoattractive Cytokines Produced by Human Fetal Membrane Cells in the Pathology of Adverse Pregnancy Outcomes Associated with Influenza Virus Infection

2012 ◽  
Vol 2012 ◽  
pp. 1-32 ◽  
Author(s):  
Noboru Uchide ◽  
Kunio Ohyama ◽  
Toshio Bessho ◽  
Makoto Takeichi ◽  
Hiroo Toyoda

Pregnant women are at an increased risk of influenza-associated adverse outcomes, such as premature delivery, based on data from the latest pandemic with a novel influenza A (H1N1) virus in 2009-2010. It has been suggested that the transplacental transmission of influenza viruses is rarely detected in humans. A series of our study has demonstrated that influenza virus infection induced apoptosis in primary cultured human fetal membrane chorion cells, from which a factor with monocyte differentiation-inducing (MDI) activity was secreted. Proinflammatory cytokines, such as interleukin (IL)-6, tumor necrosis factor (TNF)-α, and interferon (IFN)-β, were identified as a member of the MDI factor. Influenza virus infection induced the mRNA expression of not only the proinflammatory cytokines but also chemoattractive cytokines, such as monocyte chemoattractant protein (MCP)-1, regulated on activation, normal T-cell expressed and secreted (RANTES), macrophage inflammatory protein (MIP)-1β, IL-8, growth-regulated oncogene (GRO)-α, GRO-β, epithelial cell-derived neutrophil-activating protein (ENA)-78, and interferon inducible protein (IP)-10 in cultured chorion cells. These cytokines are postulated to associate with human parturition. This paper, therefore, reviews (1) lessons from pandemic H1N1 2009 in pregnancy, (2) production of proinflammatory and chemoattractive cytokines by human fetal membranes and their functions in gestational tissues, and (3) possible roles of cytokines produced by human fetal membranes in the pathology of adverse pregnancy outcomes associated with influenza virus infection.

2017 ◽  
Vol 13 (11) ◽  
pp. e1006757 ◽  
Author(s):  
Elizabeth Q. Littauer ◽  
E. Stein Esser ◽  
Olivia Q. Antao ◽  
Elena V. Vassilieva ◽  
Richard W. Compans ◽  
...  

2014 ◽  
Vol 82 (11) ◽  
pp. 4834-4841 ◽  
Author(s):  
Rebecca M. Roulo ◽  
Jillian D. Fishburn ◽  
Mayowa Amosu ◽  
Ashley R. Etchison ◽  
Mary Alice Smith

ABSTRACTListeria monocytogenesis a food-borne pathogen that can result in adverse pregnancy outcomes, such as stillbirth or premature delivery. The Mongolian gerbil was recently proposed as the most appropriate small-animal model of listeriosis due to its susceptibility to the same invasion pathways as humans. The objectives of this study were to investigate invasion and adverse pregnancy outcomes in gerbils orally exposed toL. monocytogenes, to compare the dose-response data to those of other animal models, and to investigate differences in the responses of pregnant versus nonpregnant gerbils. Gerbils were orally exposed to 0 (control), 103, 105, 107, or 109CFUL. monocytogenesin whipping cream.L. monocytogeneswas recovered in a dose-dependent manner from fecal samples, adult organs, and pregnancy-associated tissues. Dams exposed to 109CFU had more invaded organs and higher concentrations ofL. monocytogenesin almost all organs than nonpregnant animals, though no differences in fecal shedding were seen between the two groups. Adverse pregnancy outcomes occurred only in the dams treated with 109CFU. A 50% infectivity dose (ID50) of 2.60 × 106CFU for fetuses was calculated by fitting the data to a logistic model. Our results suggest that the 50% lethal dose (LD50) falls within the range of 5 × 106to 5 × 108CFU. This range includes the guinea pig and nonhuman primate LD50s, but the observation thatL. monocytogenes-induced stillbirths can be seen in guinea pigs and primates exposed to lower doses than those at which stillbirths were seen in gerbils indicates that gerbils are not more sensitive toL. monocytogenesinvasion.


2008 ◽  
Vol 82 (22) ◽  
pp. 11461-11466 ◽  
Author(s):  
Karoline Droebner ◽  
Sarah Julia Reiling ◽  
Oliver Planz

ABSTRACT During H5N1 influenza virus infection, proinflammatory cytokines are markedly elevated in the lungs of infected hosts. The significance of this dysregulated cytokine response in H5N1-mediated pathogenesis remains to be determined. To investigate the influence of hypercytokinemia, or “cytokine storm,” a transgenic mouse technology was used. The classical NF-κB pathway regulates the induction of most proinflammatory cytokines. Deletion of the p50 subunit leads to a markedly reduced expression of the NF-κB-regulated cytokines and chemokines. Here we show that H5N1 influenza virus infection of this transgenic mouse model resulted in a lack of hypercytokinemia but not in altered pathogenesis.


2016 ◽  
Vol 184 (3) ◽  
pp. 163-175 ◽  
Author(s):  
Deshayne B. Fell ◽  
David L. Buckeridge ◽  
Robert W. Platt ◽  
Jay S. Kaufman ◽  
Olga Basso ◽  
...  

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