The Relationship of Reproductive Hormones and Host Susceptibility to the Opportunistic Pathogen, Vibrio Vulnificus

Presentation Number: THR-129
Date of Presentation: March 5th, 2015

Leslie M McKee*1, James D Oliver1 and Yvette M Huet2
1Univ. of NC Charlotte, Charlotte, NC, 2Univ of NC-Charlotte, Charlotte, NC

Abstract

It is commonly found that males exhibit a higher susceptibility to infectious diseases. While the underlying mechanism for this disparity is not fully understood, one significant contributing attribute is the presence of specific sex hormones. Testosterone, the primary male sex steroid hormone, has been shown to elicit an immunosuppressive effect, depressing certain aspects of immune function; whereas estradiol, the primary female sex steroid hormone, has a protective immunological effects. Various types of sex steroids also may have a direct effect on bacterial metabolism, although the range of responses (proliferation or inhibition) appears to be bacterial-species specific. Vibrio vulnificus, a gram-negative bacterium found in the estuarine environment, is one example of a bacteria that produces an infection exhibiting a sexually dimorphic mortality rate. In this case, 85% of cases are male, with clinical symptoms ranging from gastroenteritis, to purulent wound infection, to fatal septicemia. Previous studies have suggested that the presence of estradiol protects against the endotoxic shock induced by the lipopolysaccharide (LPS) present in the outer membrane of this bacterium. We hypothesize that the presence of sex steroid hormones in serum will affect the viability of this bacterium. The present study uses serum from female rats in the various stages of the estrous cycle to determine bacterial counts of V.vulnificus at 0h, 0.5h, 2h, and 6h following bacterial inoculation as a model for a septicemic infection. Results indicate that higher endogenous estradiol levels produce an inhibitory effect on bacterial proliferation. Therefore, it appears that the presence of estrogen in higher concentrations may affect bacterial growth rates in the bloodstream, leading to a decreased burden of bacterial LPS exposure in females. This response to steroid hormones was further investigated using ratio-dependent doses of exogenous estradiol and testosterone. The bacterial response to these hormones may be one factor producing sexually dimorphic disease progression. Understanding the influence of sex steroid hormones on bacterial viability may provide further insight into sex disparities of infectious diseases.

 

Nothing to Disclose: LMM, JDO, YMH