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Epidemiological and Experimental Evidence of Sex-dependent Responses to Infection with Leishmania infantum

Award Winner

Recipient of the 10th Annual Graduate Student Symposium Award, Oral Presentations, Oak Room - First Place (2017)

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Presentation Type

Oral Presentation (Electronic Copy Not Available)

Keywords

Leishmaniasis--Sex differences; Sex factors in disease;

Abstract

Males and females experience differential prevalence, morbidity, and mortality in many infectious diseases. Some infections result in aggravated symptoms in females whereas others result in exacerbated disease in males. Infection with species of the parasitic protozoa Leishmania can lead to cutaneous, mucocutaneous, or visceral disease depending on the parasite species causing infection and the immune state of the host. We examined sex-dependent responses to infection with Leishmania infantum, which causes visceral leishmaniasis in Brazil. Macrophages isolated from male and female mice were infected with attenuated parasites and examined by light microscopy. Macrophages of male origin had a higher percent of infection and increased parasite loads compared to macrophages from females. This suggested that cellular-level differences between the sexes might influence infection. Using light microscopy and qPCR we also examined liver samples from mice infected with virulent Leishmania infantum. At various timepoints after infection male mice experienced higher parasite loads in the liver than females. These sex-based differences were observed in mice from two genetic backgrounds. Furthermore, epidemiological evidence from an endemic region of Brazil revealed a higher prevalence of symptomatic visceral leishmaniasis in males compared to females (64% versus 36%) despite similar levels of exposure to the parasite. This strong male bias was particularly pronounced post-puberty, which suggested a role for sex hormones in the dichotomous disease prevalence. Overall, our results support a model in which biological differences at the organismal and cellular level drive the increased male susceptibility to visceral leishmaniasis observed in the human population.

Start Date

4-4-2017 1:00 PM

End Date

4-4-2017 4:30 PM

Year of Award

2017 Award

Faculty Advisor

Nilda Rodriguez

Department

Department of Biology

Comments

Location: Maucker Union Oak Room

Embargo Date

4-4-2017

Electronic copy is not available through UNI ScholarWorks.

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Apr 4th, 1:00 PM Apr 4th, 4:30 PM

Epidemiological and Experimental Evidence of Sex-dependent Responses to Infection with Leishmania infantum

Males and females experience differential prevalence, morbidity, and mortality in many infectious diseases. Some infections result in aggravated symptoms in females whereas others result in exacerbated disease in males. Infection with species of the parasitic protozoa Leishmania can lead to cutaneous, mucocutaneous, or visceral disease depending on the parasite species causing infection and the immune state of the host. We examined sex-dependent responses to infection with Leishmania infantum, which causes visceral leishmaniasis in Brazil. Macrophages isolated from male and female mice were infected with attenuated parasites and examined by light microscopy. Macrophages of male origin had a higher percent of infection and increased parasite loads compared to macrophages from females. This suggested that cellular-level differences between the sexes might influence infection. Using light microscopy and qPCR we also examined liver samples from mice infected with virulent Leishmania infantum. At various timepoints after infection male mice experienced higher parasite loads in the liver than females. These sex-based differences were observed in mice from two genetic backgrounds. Furthermore, epidemiological evidence from an endemic region of Brazil revealed a higher prevalence of symptomatic visceral leishmaniasis in males compared to females (64% versus 36%) despite similar levels of exposure to the parasite. This strong male bias was particularly pronounced post-puberty, which suggested a role for sex hormones in the dichotomous disease prevalence. Overall, our results support a model in which biological differences at the organismal and cellular level drive the increased male susceptibility to visceral leishmaniasis observed in the human population.