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Bacterial coexistence driven by motility and spatial competition 期刊论文
NATURE, 2020, 578 (7796) : 588-+
作者:  Micke, P.;  Leopold, T.;  King, S. A.;  Benkler, E.;  Spiess, L. J.;  Schmoeger, L.;  Schwarz, M.;  Crespo Lopez-Urrutia, J. R.;  Schmidt, P. O.
收藏  |  浏览/下载:8/0  |  提交时间:2020/07/03

Elucidating elementary mechanisms that underlie bacterial diversity is central to ecology(1,2) and microbiome research(3). Bacteria are known to coexist by metabolic specialization(4), cooperation(5) and cyclic warfare(6-8). Many species are also motile(9), which is studied in terms of mechanism(10,11), benefit(12,13), strategy(14,15), evolution(16,17) and ecology(18,19). Indeed, bacteria often compete for nutrient patches that become available periodically or by random disturbances(2,20,21). However, the role of bacterial motility in coexistence remains unexplored experimentally. Here we show that-for mixed bacterial populations that colonize nutrient patches-either population outcompetes the other when low in relative abundance. This inversion of the competitive hierarchy is caused by active segregation and spatial exclusion within the patch: a small fast-moving population can outcompete a large fast-growing population by impeding its migration into the patch, while a small fast-growing population can outcompete a large fast-moving population by expelling it from the initial contact area. The resulting spatial segregation is lost for weak growth-migration trade-offs and a lack of virgin space, but is robust to population ratio, density and chemotactic ability, and is observed in both laboratory and wild strains. These findings show that motility differences and their trade-offs with growth are sufficient to promote diversity, and suggest previously undescribed roles for motility in niche formation and collective expulsion-containment strategies beyond individual search and survival.


In mixed bacterial populations that colonize nutrient patches, a growth-migration trade-off can lead to spatial exclusion that provides an advantage to populations that become rare, thereby stabilizing the community.


  
Feeding-dependent VIP neuron-ILC3 circuit regulates the intestinal barrier 期刊论文
NATURE, 2020, 579 (7800) : 575-+
作者:  Bhaduri, Aparna;  Andrews, Madeline G.;  Mancia Leon, Walter;  Jung, Diane;  Shin, David;  Allen, Denise;  Jung, Dana;  Schmunk, Galina;  Haeussler, Maximilian;  Salma, Jahan;  Pollen, Alex A.;  Nowakowski, Tomasz J.;  Kriegstein, Arnold R.
收藏  |  浏览/下载:37/0  |  提交时间:2020/07/03

The intestinal mucosa serves both as a conduit for the uptake of food-derived nutrients and microbiome-derived metabolites, and as a barrier that prevents tissue invasion by microorganisms and tempers inflammatory responses to the myriad contents of the lumen. How the intestine coordinates physiological and immune responses to food consumption to optimize nutrient uptake while maintaining barrier functions remains unclear. Here we show in mice how a gut neuronal signal triggered by food intake is integrated with intestinal antimicrobial and metabolic responses that are controlled by type-3 innate lymphoid cells (ILC3)(1-3). Food consumption rapidly activates a population of enteric neurons that express vasoactive intestinal peptide (VIP)(4). Projections of VIP-producing neurons (VIPergic neurons) in the lamina propria are in close proximity to clusters of ILC3 that selectively express VIP receptor type 2 (VIPR2  also known as VPAC2). Production of interleukin (IL)-22 by ILC3, which is upregulated by the presence of commensal microorganisms such as segmented filamentous bacteria(5-7), is inhibited upon engagement of VIPR2. As a consequence, levels of antimicrobial peptide derived from epithelial cells are reduced but the expression of lipid-binding proteins and transporters is increased(8). During food consumption, the activation of VIPergic neurons thus enhances the growth of segmented filamentous bacteria associated with the epithelium, and increases lipid absorption. Our results reveal a feeding- and circadian-regulated dynamic neuroimmune circuit in the intestine that promotes a trade-off between innate immune protection mediated by IL-22 and the efficiency of nutrient absorption. Modulation of this pathway may therefore be effective for enhancing resistance to enteropathogens(2,3,9) and for the treatment of metabolic diseases.


Feeding controls a neuroimmune circuit comprising VIP-producing neurons and type-3 innate lymphoid cells that helps to regulate the efficiency of nutrient uptake and IL-22-mediated immune protection in the intestine.