Invertebrate host responses to microsporidia infections

2018 ◽  
Vol 83 ◽  
pp. 104-113 ◽  
Author(s):  
Guoqing Pan ◽  
Jialing Bao ◽  
Zhengang Ma ◽  
Yue Song ◽  
Bing Han ◽  
...  
Keyword(s):  
Host Responses ◽  
Invertebrate Host

The Role of Toll-Like Receptors and Type I Interferons in Host Responses to Bacteria

2009 ◽  
Vol 5 (2) ◽  
pp. 143-149
Author(s):  
Marja Ojaniemi ◽  
Mari Liljeroos ◽  
Reetta Vuolteenaho
Keyword(s):  
Type I Interferons ◽  
Host Responses ◽  
Type I ◽  
Toll Like Receptors

Systems Biology Using Host Responses To Diagnose Infections

2014 ◽  
Vol 9 (12) ◽  
pp. 478-479
Author(s):  
Shannon Weiman
Keyword(s):  
Systems Biology ◽  
Host Responses

scholarly journals Influenza virus and SARS-CoV-2: pathogenesis and host responses in the respiratory tract

2021 ◽  
Author(s):  
Tim Flerlage ◽  
David F. Boyd ◽  
Victoria Meliopoulos ◽  
Paul G. Thomas ◽  
Stacey Schultz-Cherry
Keyword(s):  
Influenza Virus ◽  
Respiratory Tract ◽  
Host Responses

scholarly journals MiR-378b Modulates Chlamydia-Induced Upper Genital Tract Pathology

Pathogens ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 566
Author(s):  
Stephanie R. Lundy ◽  
Kobe Abney ◽  
Debra Ellerson ◽  
Joseph U. Igietseme ◽  
Darin Carroll ◽  
...  
Keyword(s):  
Host Responses ◽  
Chlamydia Infection ◽  
Chlamydia Trachomatis Infection ◽  
Host Immune Responses ◽  
Tubal Factor Infertility ◽  
Evolutionarily Conserved ◽  
Duration Of Infection ◽  
Tubal Factor ◽  
Pathologic Lesions ◽  
Mammalian Gene Expression

Genital Chlamydia trachomatis infection causes severe reproductive pathologies such as salpingitis and pelvic inflammatory disease that can lead to tubal factor infertility. MicroRNAs (miRNAs) are evolutionarily conserved regulators of mammalian gene expression in development, immunity and pathophysiologic processes during inflammation and infection, including Chlamydia infection. Among the miRNAs involved in regulating host responses and pathologic outcome of Chlamydia infection, we have shown that miR-378b was significantly differentially expressed during primary infection and reinfection. In this study, we tested the hypothesis that miR-378b is involved in the pathological outcome of Chlamydia infection. We developed miR-378b knockout mice (miR-378b−/−) using Crispr/Cas and infected them along with their wild-type (WT) control with Chlamydia to compare the infectivity and reproductive pathologies. The results showed that miR-378b−/− mice were unable to clear the infection compared to WT mice; also, miR-378b−/− mice exhibited a relatively higher Chlamydia burden throughout the duration of infection. However, gross pathology results showed that miR-378b−/− mice had significantly reduced uterine dilatations and pathologic lesions after two infections compared to WT mice. In addition, the pregnancy and fertility rates for infected miR-378b−/− mice showed protection from Chlamydia-induced infertility with fertility rate that was comparable to uninfected WT mice. These results are intriguing as they suggest that miR-378b is important in regulating host immune responses that control Chlamydial replication and drive the inflammation that causes complications such as infertility. The finding has important implications for biomarkers of Chlamydial complications and targets for prevention of disease.

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