Faculty Opinions recommendation of Intestinal epithelial tuft cells initiate type 2 mucosal immunity to helminth parasites.

2016 ◽  
Author(s):  
Noah Shroyer ◽  
Catherine Bradley
Keyword(s):  
Mucosal Immunity ◽  
Helminth Parasites ◽  
Intestinal Epithelial ◽  
Tuft Cells

scholarly journals Intestinal epithelial tuft cells initiate type 2 mucosal immunity to helminth parasites

Nature ◽  
2016 ◽  
Vol 529 (7585) ◽  
pp. 226-230 ◽  
Author(s):  
François Gerbe ◽  
Emmanuelle Sidot ◽  
Danielle J. Smyth ◽  
Makoto Ohmoto ◽  
Ichiro Matsumoto ◽  
...  
Keyword(s):  
Mucosal Immunity ◽  
Helminth Parasites ◽  
Intestinal Epithelial ◽  
Tuft Cells

scholarly journals Activation of intestinal tuft cell-expressed Sucnr1 triggers type 2 immunity in the mouse small intestine

2018 ◽  
Vol 115 (21) ◽  
pp. 5552-5557 ◽  
Author(s):  
Weiwei Lei ◽  
Wenwen Ren ◽  
Makoto Ohmoto ◽  
Joseph F. Urban ◽  
Ichiro Matsumoto ◽  
...  
Keyword(s):  
Goblet Cell ◽  
Mucosal Immunity ◽  
Cell Activation ◽  
Nippostrongylus Brasiliensis ◽  
Infectious Agents ◽  
Cell Hyperplasia ◽  
Type 2 Immunity ◽  
Tuft Cell ◽  
Tuft Cells

The hallmark features of type 2 mucosal immunity include intestinal tuft and goblet cell expansion initiated by tuft cell activation. How infectious agents that induce type 2 mucosal immunity are detected by tuft cells is unknown. Published microarray analysis suggested that succinate receptor 1 (Sucnr1) is specifically expressed in tuft cells. Thus, we hypothesized that the succinate–Sucnr1 axis may be utilized by tuft cells to detect certain infectious agents. Here we confirmed that Sucnr1 is specifically expressed in intestinal tuft cells but not in other types of intestinal epithelial cells, and demonstrated that dietary succinate induces tuft and goblet cell hyperplasia via Sucnr1 and the tuft cell-expressed chemosensory signaling elements gustducin and Trpm5. Conventional mice with a genetic Sucnr1 deficiency (Sucnr1−/−) showed diminished immune responses to treatment with polyethylene glycol and streptomycin, which are known to enhance microbiota-derived succinate, but responded normally to inoculation with the parasitic worm Nippostrongylus brasiliensis that also produces succinate. Thus, Sucnr1 is required for microbiota-induced but not for a generalized worm-induced type 2 immunity.

scholarly journals Case of Poliomyelitis Caused by Significantly Diverged Derivative of the Poliovirus Type 3 Vaccine Sabin Strain Circulating in the Orphanage

Viruses ◽  
2020 ◽  
Vol 12 (9) ◽  
pp. 970
Author(s):  
Ekaterina A. Korotkova ◽  
Maria A. Prostova ◽  
Anatoly P. Gmyl ◽  
Liubov I. Kozlovskaya ◽  
Tatiana P. Eremeeva ◽  
...  
Keyword(s):  
Genome Sequencing ◽  
Mucosal Immunity ◽  
Neutralizing Antibodies ◽  
Oral Poliovirus Vaccine ◽  
Paralytic Poliomyelitis ◽  
Epidemiological Investigation ◽  
Poliovirus Type ◽  
Complete Rejection ◽  
Type 3

Significantly divergent polioviruses (VDPV) derived from the oral poliovirus vaccine (OPV) from Sabin strains, like wild polioviruses, are capable of prolonged transmission and neuropathology. This is mainly shown for VDPV type 2. Here we describe a molecular-epidemiological investigation of a case of VDPV type 3 circulation leading to paralytic poliomyelitis in a child in an orphanage, where OPV has not been used. Samples of feces and blood serum from the patient and 52 contacts from the same orphanage were collected twice and investigated. The complete genome sequencing was performed for five polioviruses isolated from the patient and three contact children. The level of divergence of the genomes of the isolates corresponded to approximately 9–10 months of evolution. The presence of 61 common substitutions in all isolates indicated a common intermediate progenitor. The possibility of VDPV3 transmission from the excretor to susceptible recipients (unvaccinated against polio or vaccinated with inactivated poliovirus vaccine, IPV) with subsequent circulation in a closed children’s group was demonstrated. The study of the blood sera of orphanage residents at least twice vaccinated with IPV revealed the absence of neutralizing antibodies against at least two poliovirus serotypes in almost 20% of children. Therefore, a complete rejection of OPV vaccination can lead to a critical decrease in collective immunity level. The development of new poliovirus vaccines that create mucosal immunity for the adequate replacement of OPV from Sabin strains is necessary.

scholarly journals Celiac Anti-Type 2 Transglutaminase Antibodies Induce Phosphoproteome Modification in Intestinal Epithelial Caco-2 Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (12) ◽  
pp. e84403 ◽  
Author(s):  
Gaetana Paolella ◽  
Ivana Caputo ◽  
Anna Marabotti ◽  
Marilena Lepretti ◽  
Anna Maria Salzano ◽  
...  
Keyword(s):  
Intestinal Epithelial

scholarly journals Prox1-positive cells monitor and sustain the murine intestinal epithelial cholinergic niche

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Moritz Middelhoff ◽  
Henrik Nienhüser ◽  
Giovanni Valenti ◽  
H. Carlo Maurer ◽  
Yoku Hayakawa ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Function ◽  
Feedback Inhibition ◽  
Cell Number ◽  
Intestinal Stem Cell ◽  
Compensatory Mechanism ◽  
Intestinal Epithelial ◽  
Immune Functions ◽  
Cholinergic Blockade ◽  
Tuft Cells

AbstractThe enteric neurotransmitter acetylcholine governs important intestinal epithelial secretory and immune functions through its actions on epithelial muscarinic Gq-coupled receptors such as M3R. Its role in the regulation of intestinal stem cell function and differentiation, however, has not been clarified. Here, we find that nonselective muscarinic receptor antagonism in mice as well as epithelial-specific ablation of M3R induces a selective expansion of DCLK1-positive tuft cells, suggesting a model of feedback inhibition. Cholinergic blockade reduces Lgr5-positive intestinal stem cell tracing and cell number. In contrast, Prox1-positive endocrine cells appear as primary sensors of cholinergic blockade inducing the expansion of tuft cells, which adopt an enteroendocrine phenotype and contribute to increased mucosal levels of acetylcholine. This compensatory mechanism is lost with acute irradiation injury, resulting in a paucity of tuft cells and acetylcholine production. Thus, enteroendocrine tuft cells appear essential to maintain epithelial homeostasis following modifications of the cholinergic intestinal niche.

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