Microbial exposure during early human development

Mishra A, Lai G, Yao L, et al. Microbial exposure during early human development primes fetal immune cells. Cell 2021; doi: 10.1016/j.cell.2021.04.039

Mishra et al attempted to examine the exposure to microbial agents in utero and their contribution towards activation of memory T lymphocyte cells (T cells) in fetal tissues. In the second trimester, there was already T cell diversity with effector memory phenotype, indicating the presence of antigenic stimuli, which drives the generation of activated T cells within fetal organs. Using 16S rRNA gene sequencing, several bacterial genera were detected in fetal gut, skin, placenta and lungs in the second trimester but in a low concentration. Several live bacterial strains including Lactobacillus, Staphylococcus, Streptococcus, Enterococcus, Bifidobacterium, Prevotella and Finegoldia could be cultured from freshly harvested fetal samples. Further scanning electron microscopy and RNA-in situ hybridisation analysis revealed discrete localisation of bacteria-like structures with mucin-like threads within fetal gut at week 14 of gestation, further suggesting that these fetal-gut associated bacteria were alive and could be propagated. On exposure with heat-killed fetal bacteria (fetal Lactobacillus or fetal Staphylococcus) primed dendritic cells, there was a significant increase in total T cell count in the fetal mesenteric lymph nodes, suggestive of the expansion of T cells postbacterial priming and there was an activated memory response towards microbes encountered in utero. This is the first study which showed that the fetal microbiota in utero could prime the fetal immune system and could provide insight into the establishment of immune competency and priming before birth.

Playing host to Clostridium difficile—it is a sweet deal

Pruss K, Sonnenburg J. C. difficile exploits a host metabolite produced during toxin-mediated disease. Nature 2021; 593(7858): 261–5. doi: 10.1038/s41586-021-03502-6

It is known that some enteric pathogens exploit host factors to grow competitively, but the way C. difficile (C. diff) does this is unclear.

Mice were colonised with …