Dr. Fátima Pereira

Former Postdoc at DoME
Current: Lecturer in Molecular and Cellular Bioscience
School of Biological Sciences, Faculty of Environmental and Life Sciences
University of Southampton, Southampton, UK
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  • Competition between pathogens and commensals for host- and diet-derived nutrients in the gut
  • Impact of host-secreted small RNA molecules on the composition and function of the gut microbiome
  • Development of stable isotope-based methods to link microbial genomes to in situ functions


Nutrient partitioning in the gut

Description: Macintosh HD:Users:fatimapereira:Documents:Mee:CV:webpage:Caption1_domepage_FP.tiffOne of the key functions of the trillions of bacteria that live in the human gut, collectively known as the gut microbiota, is to protect against infection by enteropathogens. This phenomenon is termed colonization resistance and involves mechanisms such as the production of antimicrobial compounds with narrow activity against pathogens, the production of microbial associated molecular patterns (MAMPs) that incite a response by the host immune system, or the exhaustion of limited nutrient sources.

In 1983, Rolf Freter formulated the nutrient niche theory, which asserts that ecological niches in the gut are defined by available nutrients and that a species can only colonize if it is able to most efficiently use a particular limiting nutrient. Thus, if efficient utilizers from the indigenous microbiota block all possible nutrient niches, pathogens cannot colonize the intestinal environment. Perturbations of the gut microbiota triggered, for instance, by antibiotic administration, often lead to the elimination of certain species from the gut. As a consequence, nutrient niches previously occupied suddenly become available, and pathogens can establish. We seek to better understand the role of nutrient competition in colonization resistance and to identify commensal bacteria able to efficiently compete for key nutrients, keeping pathogens at bay. We are particularly interested in the pathogen Clostridioides difficile, nowadays the most common cause of enteric infections associated with antibiotic therapy in developed countries.


Role of small RNA molecules in the crosstalk between host and microbiota

In the gut, host and microbiota constantly communicate, and RNA molecules such as microRNAs (miRNAs) are important for such crosstalk. MiRNAs are small non-coding RNAs that can bind to target mRNAs, leading to translation inhibition or transcript degradation. Strikingly, the expression of several miRNAs is altered in inflammatory bowel disease (IBD) and other chronic inflammatory diseases. Furthermore, depletion of particular fecal miRNAs in mice causes shifts in microbiota composition and alters susceptibility to colitis in a microbiota-dependent fashion. Despite the clear involvement of miRNAs in IBD and gut microbiota modulation, the impact of luminal-derived miRNAs in the large intestine has not been thoroughly investigated. Combining “omic” approaches (metagenomics and transcriptomics), state-of-the-art mouse models of IBD, microbial ecology cultivation-dependent and -independent techniques, we aim to investigate in detail the impact of fecal microRNAs on the host-microbiota crosstalk. Results will advance the field of microbiome research and potentially serve as a basis to diagnose or treat IBD.



Competition between the enteric pathogen Clostridium difficile and the commensal members of the gut microbiota for mucosal sugars (Link)

Adjusting the base: (Epi)transcriptomic RNA modification in inflammation & host-microbiome crosstalk (Link)