Trypanosoma cruzi: the development of estrus cycle and parasitemia in female mice maintained with or without male pheromones

2001 ◽  
Vol 87 (12) ◽  
pp. 985-993 ◽  
Author(s):  
Juliane P. Schuster ◽  
Günter A. Schaub
2021 ◽  
Author(s):  
Dhanya Dhanyalayam ◽  
Kezia Lizardo ◽  
Neelam Oswal ◽  
Hariprasad Thangavel ◽  
Enriko Dolgov ◽  
...  

Coronavirus disease-2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2; CoV2) is a deadly contagious infectious disease. For those who survived COVID-19, post-COVID cardiac damage poses a major threat for the progression of cardiomyopathy and heart failure. Currently, the number of COVID-related cases and deaths is increasing in Latin America, where a major COVID comorbidity is Chagas heart disease (caused by the parasite Trypanosoma cruzi). Here, we investigated the effect of T. cruzi infection on the pathogenesis and severity of CoV2 infection and, conversely, the effect of CoV2 infection on heart pathology during coinfection. We used transgenic human angiotensin-converting enzyme 2 (huACE2) mice infected with CoV2, T. cruzi, or coinfected with both in this study. Our study shows for the first time that white adipose tissue (WAT) serves as a reservoir for CoV2 and the persistence of CoV2 in WAT alters adipose tissue morphology and adipocyte physiology. Our data demonstrate a correlation between the loss of fat cells and the pulmonary adipogenic signaling and pathology in CoV2 infection. The viral load in the lungs is inversely proportional to the viral load in WAT, which differs between male and female mice. Our findings also suggest that adiponectin-PPAR signaling may differently regulate Chagas cardiomyopathy in coinfected males and females. We conclude that adipogenic signaling may play important roles in cardio-pulmonary pathogenesis during CoV2 infection and T. cruzi coinfection. The levels of adiponectin isomers differ between male and female mice during CoV2 infection and coinfection with T. cruzi, which may differently regulate inflammation, viral load, and pathology in the lungs of both the sexes. Our findings are in line with other clinical observations that reported that males are more susceptible to COVID-19 than females and suffer greater pulmonary damage.


2012 ◽  
Vol 74 (10) ◽  
pp. 1311-1314 ◽  
Author(s):  
Saori YANO ◽  
Kentaro Q. SAKAMOTO ◽  
Yoshiaki HABARA
Keyword(s):  

2008 ◽  
Vol 53 (4) ◽  
pp. 509-517 ◽  
Author(s):  
Caroline M. Larsen ◽  
Ilona C. Kokay ◽  
David R. Grattan

2017 ◽  
Vol 46 (4) ◽  
pp. 2035-2046 ◽  
Author(s):  
Elizabeth A. McCarthy ◽  
Arman Maqsudlu ◽  
Matthew Bass ◽  
Sofia Georghiou ◽  
James A. Cherry ◽  
...  

Shock ◽  
2014 ◽  
Vol 41 (2) ◽  
pp. 145-153 ◽  
Author(s):  
Katrin M. Weixelbaumer ◽  
Susanne Drechsler ◽  
Paul Wehrenpfennig ◽  
Anna Khadem ◽  
Soheyl Bahrami ◽  
...  

2004 ◽  
Vol 81 (3) ◽  
pp. 427-434 ◽  
Author(s):  
J MONCHOBOGANI ◽  
E LANUZA ◽  
M LORENTE ◽  
F MARTINEZGARCIA

Author(s):  
Melissa E Lenert ◽  
Micaela M Chaparro ◽  
Michael D Burton

Abstract The etiology of reproductive disorders correlate with weight gain in patients, but the link between reproduction, diet, and weight has been difficult to translate in rodents. As rates of childhood obesity and reproductive disorders increase, the need to study the effects of weight and diet on adolescent females is key. Previous studies show female mice are resistant to high-fat diet (HFD)-induced weight gain, but the mechanisms are unclear. Literature also suggests that ovarian function is essential to resistance in weight gain, as an ovariectomy leads to a weight gaining phenotype similar to male mice on a HFD. However, reproductive changes that occur in adolescent mice on HFD have not been assessed. Here, we show that regulation of the estrus cycle via progesterone is critical to metabolic homeostasis in female mice on a HFD. Female mice were put on HF or control diet for twelve weeks starting at four weeks of age. Every four weeks, their estrus cycle was tracked and fasting glucose was measured. We found that after four weeks on HFD, there was no difference in weight between groups, but an increase in time spent in proestrus and estrus in mice on HFD and an increase in serum progesterone during proestrus. These results show that intact females modulate their estrus cycle in response to a HFD as a mechanism of homeostatic regulation of body weight, protecting them from metabolic abnormalities. Understanding the mechanisms behind this protection may yield therapeutic opportunities for treatment of reproductive disorders in adolescent female patients.


Animals ◽  
2020 ◽  
Vol 10 (3) ◽  
pp. 471
Author(s):  
Aneela Perveen ◽  
Jiakun Shen ◽  
Niaz Ali Kaka ◽  
Chunmei Li

Among foodborne toxicities, the T-2 toxin is the most toxic member of trichothecenes mycotoxins, which has been shown to impair the development and reproductive efficiency of animals. Pups are particularly more quickly prone to programming the effects of the maternal diet during the gestational and lactation periods. Few studies have reported the maternal toxic effect on the next generation. Dams were served the T-2 toxin at a dose of 0.005 and 0.05 mg/kg body weight/day and control group 0 mg/kg from gestation day 14 to lactation day 21. Female mice offspring were selected at the weaning age. Our observations indicate that age during the vaginal opening and di-estrus stage increased and the length of the estrus cycle, first di-estrus, and regular estrus cycling were delayed with prolonged di-estrus in the 0.05 mg/kg group compared to the 0.005 mg/kg and control group. Transcription level analysis showed that mice at a dose of 0.05 mg/kg exhibited a decrease in hypothalamic mRNA expression of Gnrh and Gnrhr, Lhb, and Fshb in the pituitary gland, with a significant decrease of Fshr and Lhr in the ovaries. Present findings report that postnatal exposure to the T-2 toxin delayed puberty age in female mice and induced oxidative stress, ovarian damage, and reduced vaginal epithelium wall majorly in the 0.05 mg/kg group, and showed fewer effects in the 0.005 mg/kg group.


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