Soil bacteria are some of the key players affecting plant productivity. Soil today is exposed to emerging contaminants like metal engineered nanoparticles. The objective of this study was to evaluate the toxicological effects of silver and zinc oxide nanoparticles on bacteria classified as plant growth-promoting bacteria. Three types of bacteria-nitrogen fixers, phosphate solubilizers, and biofilm formers-were exposed to engineered nanoparticles. Initially, the effect of silver and zinc oxide nanoparticles was determined on pure cultures of the bacteria. These nanoparticles were then applied to soil to assess changes in composition of bacterial communities. Impacts of the nanoparticles were analyzed using Illumina MiSeq sequencing of 16S rRNA genes. In the soil used, relative abundances of the dominant and agriculturally significant phyla, namely, Proteobacteria, Actinobacteria, and Firmicutes, were altered in the presence of silver nanoparticles. Silver nanoparticles changed the abundance of the three phyla by 25 to 45%. Zinc oxide nanoparticles showed negligible effects at the phylum level. Thus, silver nanoparticles may impact bacterial communities in soil, and this in turn may influence processes carried out by soil bacteria.

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Clusters of neuron cell bodies, termed nuclei, residing in the brainstem are the origin of cranial nerves which transmit action potentials controlling organ function. Neurons residing in the brainstem dorsal motor nucleus (DMN) project in the vagus nerve to communicate with the pancreas, liver, gastrointestinal tract and other organs. Cholinergic signaling in the vagus nerve‐mediated inflammatory reflex also controls immune system responses by inhibiting the production of cytokines in the spleen, although the function of DMN neurons in regulating pancreatic inflammation is not known. Here, we demonstrate that selective activation of cholinergic neurons in the DMN attenuates pancreatitis severity. Pancreatitis was induced with two intraperitoneal injections of the cholecystokinin analogue caerulein (50 mcg/kg), given one hour apart. A fiber‐optic cannula was inserted under stereotactic guidance into the DMN in transgenic mice expressing light‐responsive ion channel, channelrhodopsin, in cholinergic neurons under the choline acetyltransferase promoter. Animals were subjected to either optogenetic stimulation (473nm, 20 Hz, 25% duty cycle, 8‐12 mW total power) or sham stimulation (no light) for five minutes. Optogenetic stimulation but not sham stimulation of the cholinergic neurons in the DMN significantly attenuates serum amylase (4043mU/mL ± 264.4 vs. 2940mU/mL ± 170.9, p=0.0074; n=9‐11 mice/group) and pancreatic IL‐6 levels (1907pg/mg ± 879.3 vs. 1046pg/mg± 288.1, p=0.0330; n=9‐11 mice/group). The decreased severity of pancreatitis in optogenetically stimulated mice is further demonstrated by a significant improvement in pancreatic histologic severity score (6.86 ± 1.67 vs. 5.35 ± 1.44, p = 0.0462; n = 9‐11). Pharmacological blockade and surgical ablation of the vagus nerve signaling inhibit protective effects of DMN cholinergic neurons activation. Pre‐treatment with mecamylamine, a nicotinic receptor antagonist, attenuates the reduction in serum amylase following light stimulation (Sham stimulation vs. DMN vs DMN + Mecamylamine: 5047 ± 315.4 vs. 3769 ± 241.5 vs. 5620 ± 385.9, p = 0037; n = 10 mice/group). Additionally, mice with subdiaphragmatic vagotomy has no difference in serum amylase levels following optogenetic stimulation (2761mU/mL ± 787.3 vs. 2517mU/mL, p= 0.300; n=3), whereas sham surgery controls show a significant reduction in serum amylase levels (3224mU/mL ± 593.1 vs. 2087 mU/mL ± 951.2, p=0.0303; n=6 mice/group). These studies identify DMN as an important locus that regulates the severity of acute pancreatitis in vagus‐nerve‐dependent fashion, and provide new insights into the identity and central origin of the efferent vagus nerve fibers regulating acute pancreatitis.