Humanity had been fascinated with space exploration and habitation. However, weak gravity force in outer space, termed as microgravity, has been known to alter normal human biology and induce health risks, such as muscle atrophy and compromised immunity. The underlying processes on how gravity is sensed by the body and how it affects immunity are still unclear. The nematode Caenorhabditis elegans, is a well-known model organism in the field of innate immunity and space research. Similar to humans, worm immune response signaling is regulating by MAPK and TGFbeta pathways. Previous microgravity experiments in C. elegans have shown an increase in
p38 MAPK
pmk-1 expression in simulated microgravity (Li, Wang, & Wang, 2018) and decreased expression of TGFbeta ligand
dbl-1 in space (Harada et al., 2016). In this study, we have utilized Enterobacter cloacae carrying tdTomato fluorescence reporter to observe gut colonization in C. elegans under simulated microgravity using a 3D clinostat. E. cloacae is a known commensal in C. elegans' gut but is invasive in immunocompromised
dbl-1 mutant worms (Berg et al., 2019). Our preliminary results have shown that simulated microgravity can induce E. cloacae gut colonization in wild type C. elegans and aggravated colonization in
pmk-1 mutants, while there is no difference observed in
dbl-1 mutants which have robust colonization in both normal earth gravity and simulated microgravity, which demonstrates potential involvement of these pathways. Our study aims to discover the underlying mechanism of gravity sensing and how it affects the immune signaling pathways. In addition, spaceflights are already scheduled to send C. elegans aboard the International Space Station (ISS) for actual space gravity experiments.