Severe community-acquired pneumonia caused by Chlamydia psittaci genotype E/B strain circulating among geese in Lishui city, Zhejiang province, China.

Between November 2021 and January 2022, four patients of community-acquired pneumonia were admitted to the hospitals in Lishui city, Zhejiang province, China. Their main clinical manifestations were fever and dry cough as well as radiographic infiltrate, but the empiric antimicrobial therapy or traditional Chinese medicine was not effective for their illness. Clinical specimens from the patients as well as environmental and poultry specimens were collected for the determination of the causative pathogen. The ompA gene and seven housekeeping genes of Chlamydia psittaci were successfully amplified from all the patients, and the sequences of each gene were identical to one another, suggesting that they were infected by the same strain of C. psittaci. A novel strain of C. psittaci (LS strain) was isolated from the bronchoalveolar lavage fluid of patient 2 and its whole genome was obtained. Phylogenetic analyses based on the whole-genome sequences showed that the isolate is most closely related to the strain (WS/RT/E30) identified as genotype E/B. In addition, The ompA gene and four housekeeping genes of C. psittaci were also amplified from two of four faeces samples of geese at the home of patient 2, and the sequences from geese were 100% identical to those from the patients. Accordingly, these cases could be attributed to a circulating C. psittaci strain of genotype E/B in the local geese. Therefore, there is an urgent need to strengthen the regional surveillance on C. psittaci among poultry and humans for prevention and control of the outbreak of psittacosis in the city.

The stimulating effect of ghrelin on gastric motility and firing activity of gastric-distension-sensitive hippocampal neurons and its underlying regulation by the hypothalamus.

Ghrelin is an acylated peptide originally identified in the rat stomach as the endogenous ligand for growth hormone secretagogue receptor (GHSR) that promotes gastric motility. Our aims were to explore the effects of ghrelin on gastric-distension-sensitive neurons in the hippocampus and the potential for ghrelin to regulate gastric motility through the arcuate nucleus (Arc). Single-unit discharges in the hippocampus were recorded extracellularly, and gastric motility in conscious rats was monitored. The expression of GHSR-1a in the hippocampus was determined by PCR, Western blot and fluo-immunohistochemistry staining. Retrograde tracing and fluo-immunohistochemistry staining were used to determine ghrelin neuron projection. Ghrelin-Fluoro-Gold double-labelled neurons and GHSR-1a expression were observed in the Arc and hippocampus, respectively. There were gastric-distension-sensitive neurons in the hippocampus that could be excited by ghrelin or by electrical stimulation of the Arc. The excitatory effects could be blocked completely or partly by pretreatment with the ghrelin receptor antagonist [d-Lys-3]-GHRP-6. Gastric motility was significantly promoted by the administration of ghrelin into the hippocampus in a dose-dependent manner that could be completely abolished by [d-Lys-3]-GHRP-6. Electrical stimulation of the Arc could promote gastric motility as well. Nevertheless, these effects could be mitigated by pretreatment with [d-Lys-3]-GHRP-6. Electrical lesioning of the hippocampus diminished the excitatory effects on gastric motility that were induced by electrical stimulation the Arc. Our findings suggest that ghrelin plays an important role in promoting gastric motility via the hippocampus. The Arc may be involved in regulation of the influence of the hippocampus on gastric motility.

Effects of ghrelin on gastric distention sensitive neurons in the arcuate nucleus of hypothalamus and gastric motility in diabetic rats.

This study was performed to observe the effects of ghrelin on the activity of gastric distention (GD) sensitive neurons in the arcuate nucleus of hypothalamus (Arc) and on gastric motility in vivo in streptozocin (STZ) induced diabetes mellitus (DM) rats. Electrophysiological results showed that ghrelin could excite GD-excitatory (GD-E) neurons and inhibit GD-inhibitory (GD-I) neurons in the Arc. However, fewer GD-E neurons were excited by ghrelin and the excitatory effect of ghrelin on GD-E neurons was much weaker in DM rats. Gastric motility research in vivo showed that microinjection of ghrelin into the Arc could significantly promote gastric motility and it showed a dose-dependent manner. The effect of ghrelin promoting gastric motility in DM rats was weaker than that in normal rats. The effects induced by ghrelin could be blocked by growth hormone secretagogue receptor (GHSR) antagonist [d-Lys-3]-GHRP-6 or BIM28163. RIA and real-time PCR data showed that the levels of ghrelin in the plasma, stomach and ghrelin mRNA in the Arc increased at first but decreased later and the expression of GHSR-1a mRNA in the Arc maintained a low level in DM rats. The present findings indicate that ghrelin could regulate the activity of GD sensitive neurons and gastric motility via ghrelin receptors in the Arc. The reduced effects of promoting gastric motility induced by ghrelin could be connected with the decreased expression of ghrelin receptors in the Arc in diabetes. Our data provide new experimental evidence for the role of ghrelin in gastric motility disorder in diabetes.

Involvement of the hippocampus and neuronal nitric oxide synthase [correction of synapse] in the gastric electrical stimulation therapy for obesity.

BACKGROUND: Gastric electrical stimulation (GES) has been introduced for treating obesity. However, possible central mechanisms remain to be revealed. Hippocampus has been shown to be involved in the regulation of gastrointestinal functions. Changes in hypothalamic neuronal nitric oxide synthase (nNOS) have been observed in genetically obese rodents. The aim of this study was to investigate the involvement of nNOS with GES in the rodent hippocampus. METHODS: The effect of GES on gastric distension (GD) neurons was investigated using four different sets of parameters (GES-A, pulse train of standard parameters; GES-B, reduced on time; GES-C, increased pulse width, and GES-D: reduced pulse frequency), and the expression of nNOS in hippocampus was observed by fluoimmunohistochemistry staining. RESULTS: CA1 region neurons (90.8%) responded to GD, 50.6% of which showed excitation (GD-E neurons) and 49.4% showed inhibition (GD-I neurons). Most of GD-responsive neurons (63.3%) were excited with GES. The response to GES was associated with stimulation strength, pulse width and frequency. GD-E neurons (62.5%, 76.9%, 100%, and 62.3%) and GD-I (63.6%, 47.1%, 85.7% and 50.0%) showed excitatory responses to GES-A, GES-B, GES-C, and GES-D, respectively (P < 0.05, GES-C vs. others). nNOS immunoreactive (nNOS-IR) positive neurons were observed in hippocampus CA1, CA2-3 regions and the dentate gyrus. The expression of nNOS-IR positive neurons was significantly decreased in CA1 and CA2-3 region (P < 0.05) after GES (para-C) for 2 h. CONCLUSIONS: Excitation of GD-responsive neurons and reduced expression of nNOS in the hippocampus are indicative of the central effect of GES.

[Effect of motilin receptor agonist-erythromycin on the glucose responsive neurons in hypothalamus of rats].

AIM: In order to explore the mechanism of central motilin-induced feeding behavior, the effects of erythromycin, a motilin receptor agonist, on glucose responsive neurons in hypothalamus were observed. METHODS: Extracellular recordings were made from single neurons in region of lateral hypothalamic area (LHA) and ventromedial hypothalamic nucleus (VMH) in anesthetized rats. On the basis of their responsiveness to intracarotid injection of 0.58 mol/L glucose solution 0.2 ml, glucose-sensitive neurons (GSNs) in LHA and glucoreceptor neurons (GRNs) in VMH were recognized. Effects of intracerebroventricularly (i. c. v.) administration of 4 microg erythromycin on neural activities of glucose responsive neurons and non-glucose responsive neurons were examined. The mixture of EM and GM-109 1 microl were used to GSNs and GRNs which were sensitive to i. c. v. administration of EM. RESULTS: In LHA, EM increased activity of GSNs significantly (P < 0.05 vs non-glucose-sensitive neurons group). Whereas in VMH, EM significantly decreased the activities of GRNs (P < 0.01 vs non-glucoreceptor neurons group). The mixture of EM and GM-109 had no effect on GSNs and GRNs. CONCLUSION: EM, a motilin receptor agonist, can stimulate GSNs in LHA and suppress GRNs in VMH and this may contribute to central motilin's effect on feeding behavior.