scholarly journals Closer clutch inspection—quicker egg ejection: timing of host responses toward parasitic eggs

2010 ◽  
Vol 22 (1) ◽  
pp. 46-51 ◽  
Author(s):  
Milica Požgayová ◽  
Petr Procházka ◽  
Lenka Polačiková ◽  
Marcel Honza
Keyword(s):  
Author(s):  
Francisco Ruiz-Raya ◽  
Juan Diego Ibáñez-Álamo ◽  
Charline Parenteau ◽  
Olivier Chastel ◽  
Manuel Soler

Adaptations resulting from co-evolutionary interactions between avian brood parasites and their hosts have been extensively studied, yet the physiological mechanisms underlying antiparasitic host defences remain little known. Prolactin, one of the main hormones involved in the regulation of avian parental behaviour, might play a key role in the orchestration of the host responses to avian brood parasitism. Given the positive association between prolactin and parental behaviour during incubation, decreasing prolactin levels are expected to facilitate egg-rejection decisions. We tested this prediction by implanting Eurasian blackbird (Turdus merula) females with an inhibitor of prolactin secretion, bromocriptine mesylate, to experimentally decrease their plasma prolactin levels. Bromocriptine-implanted individuals ejected mimetic model eggs at higher rates, and showed shorter latency to egg ejection, than placebo-treated birds. To our knowledge, this is the first experimental evidence that behavioural host defences against avian brood parasitism are mediated by prolactin.


2009 ◽  
Vol 5 (2) ◽  
pp. 143-149
Author(s):  
Marja Ojaniemi ◽  
Mari Liljeroos ◽  
Reetta Vuolteenaho

2014 ◽  
Vol 9 (12) ◽  
pp. 478-479
Author(s):  
Shannon Weiman

Author(s):  
Tim Flerlage ◽  
David F. Boyd ◽  
Victoria Meliopoulos ◽  
Paul G. Thomas ◽  
Stacey Schultz-Cherry

Pathogens ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 566
Author(s):  
Stephanie R. Lundy ◽  
Kobe Abney ◽  
Debra Ellerson ◽  
Joseph U. Igietseme ◽  
Darin Carroll ◽  
...  

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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