deletions | additions       diff --git a/section_Discussion_textit_F_tularensis__.tex b/section_Discussion_textit_F_tularensis__.tex  index b2994c7..73c66c7 100644  --- a/section_Discussion_textit_F_tularensis__.tex  +++ b/section_Discussion_textit_F_tularensis__.tex 
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Temperature is known to regulate expression of \textit{F. tularensis} virulence factors \cite{18842136}. One of the advantages of insect systems in comparison with mammalian hosts is the ability to experimentally manipulate the temperature at which the host-pathogen interaction occurs. When we varied the temperature of incubation, we saw that as temperature decreased, so did \textit{F. tularensis} LVS virulence (Figure 2, Table 1). This observation raises the intriguing possibility to collect gene expression data from \textit{F. tularensis} LVS growing at different temperatures \textit{in vivo} and comparing the resulting patterns with cells grown at different temperatures \textit{in vitro}.   Host immune function is not static, but rather it varies, sometimes dramatically, across developmental stages. \color{red} \textcolor{red}{RED}  red The results presented here indicate that the OS cockroach is susceptible to infection by \textit{F. tularensis} LVS and that full virulence requires environmental (temperature) and genetic factors known to contribute to \textit{Francisella spp} pathogenesis in mammals. Increasing doses of bacteria led to decreases in the percentage of cockroaches that survived challenge and a decrease in the time to death (Figure 1). \textit{F. tularensis} virulence factors induced by growth at 37°C are known to be important for virulence in mammalian hosts (refs). We have observed that pathogenesis in the OS cockroach model is also temperature-dependent, indicating that similar virulence factors may be involved. Moreover, four mutant strains devoid of specific virulence factors required for pathogenesis in mice were severely attenuated in OS cockroaches (Table 1).