[Study on protective effect of water extract from Sabia parviflora on liver injury in mice induced by acetaminophen].

The aim of this study was to observe the protective effect of water extract from Sabia parviflora on mice with acute liver injury induced by acetaminophen, and investigate its possible mechanism. Fifty-eight Kunming mice were divided into 6 groups, 8 in the normal group, 10 in the model group, 10 in the biphenyl diester group, and 10 each in the low, medium and high dose groups. After adaptive feeding for one week, the mice in normal group were intragastrically administered with an equal volume of 0.5% sodium carboxymethylcellulose sodium(CMC-Na), and the mice in other groups were intragastrically administered with corresponding drugs at 20 mL·kg~(-1) once a day. Then acetaminophen(200 mg·kg~(-1)) was administered after the above drug administration except the normal group. The behavior and signs of the experimental animals were observed every day and the samples were taken for experiments on the next day of the final administration. The liver mass and mass index were calculated. The blood was collected from the abdominal aorta and centrifuged to obtain the serum for detecting aspartate aminotransferase(AST) activity and alanine aminotransferase(ALT) activity. The liver tissue homogenate was used to detect superoxide dismutase(SOD) activity, glutathione(glutathione, r-glutamyl cysteingl+glycine, GSH) activity and malondialdehyde(MDA) content. Liver tissue was analyzed for histological analysis. The results showed that S. parviflora could alleviate the lipid peroxidation damage in the liver caused by acetaminophen, reduce the ALT and AST activities in serum, increase the levels of SOD and GSH in liver tissue, decrease the content of MDA in liver tissue, and inhibit the apoptosis. S. parviflora could also improve the live histopathological profile, protect liver cells and restore liver function. Among them, the high dose had the most significant effect and showed dose-effect relationship. This study indicated that S. parviflora had a significant protective effect on acetaminophen-induced liver injury in mice, and its mechanism may be related to its anti-oxidation effect and inhi-bitory effect on apoptosis.

Selective and stable elimination of endosymbionts from multiple-infected whitefly Bemisia tabaci by feeding on a cotton plant cultured in antibiotic solutions.

The maternally heritable endosymbiont provides many ecosystem functions. Antibiotic elimination of a specific symbiont and establishment of experimental host lines lacking certain symbionts enable the roles of a given symbiont to be explored. The whitefly Bemisia tabaci (Gennadius) in China harbors obligate symbiont Portiera infecting each individual, as well as facultative symbionts, such as Hamiltonella, Rickettsia and Cardinium, with co-infections occurring relatively frequently. So far no studies have evaluated the selectivity and efficacy of a specific symbiont elimination using antibiotics in whiteflies co-infected with different symbionts. Furthermore, no success has been achieved in establishing certain symbiont-free B. tabaci lines. In this study, we treated Hamiltonella-infected B. tabaci line, Hamiltonella-Rickettsia-co-infected line and Hamiltonella-Cardinium co-infected line by feeding B. tabaci adults with cotton plants cultured in water containing rifampicin, ampicillin or a mixture of them, aiming to selectively curing symbiont infections and establishing stable symbiont-free lines. We found ampicillin selectively eliminated Cardinium without affecting Portiera, Hamiltonella and Rickettsia, although they coexisted in the same host body. Meanwhile, all of the symbionts considered in our study can be removed by rifampicin. The reduction of facultative symbionts occurred at a much quicker pace than obligate symbiont Portiera during rifampicin treatment. Also, we measured the stability of symbiont elimination in whitefly successive generations and established Rickettsia-infected and Cardinium-infected lines which are absent in natural populations. Our results provide new protocols for selective elimination of symbionts co-existing in a host and establishment of different symbiont-infected host lines.

Infection by the parasitic helminth Trichinella spiralis activates a Tas2r-mediated signaling pathway in intestinal tuft cells.

The parasitic helminth Trichinella spiralis, which poses a serious health risk to animals and humans, can be found worldwide. Recent findings indicate that a rare type of gut epithelial cell, tuft cells, can detect the helminth, triggering type 2 immune responses. However, the underlying molecular mechanisms remain to be fully understood. Here we show that both excretory-secretory products (E-S) and extract of T. spiralis can stimulate the release of the cytokine interleukin 25 (IL-25) from the mouse small intestinal villi and evoke calcium responses from tuft cells in the intestinal organoids, which can be blocked by a bitter-taste receptor inhibitor, allyl isothiocyanate. Heterologously expressed mouse Tas2r bitter-taste receptors, the expression of which is augmented during tuft-cell hyperplasia, can respond to the E-S and extract as well as to the bitter compound salicin whereas salicin in turn can induce IL-25 release from tuft cells. Furthermore, abolishment of the G-protein γ13 subunit, application of the inhibitors for G-protein αo/i, Gßγ subunits, and phospholipase Cß2 dramatically reduces the IL-25 release. Finally, tuft cells are found to utilize the inositol triphosphate receptor type 2 (Ip3r2) to regulate cytosolic calcium and thus Trpm5 activity, while potentiation of Trpm5 by a sweet-tasting compound, stevioside, enhances tuft cell IL-25 release and hyperplasia in vivo. Taken together, T. spiralis infection activates a signaling pathway in intestinal tuft cells similar to that of taste-bud cells, but with some key differences, to initiate type 2 immunity.

Effects of Taste Signaling Protein Abolishment on Gut Inflammation in an Inflammatory Bowel Disease Mouse Model.

Inflammatory bowel disease (IBD) is one of the immune-related gastrointestinal disorders, including ulcerative colitis and Crohn's disease, that affects the life quality of millions of people worldwide. IBD symptoms include abdominal pain, diarrhea, and rectal bleeding, which may result from the interactions among gut microbiota, food components, intestinal epithelial cells, and immune cells. It is of particular importance to assess how each key gene expressed in intestinal epithelial and immune cells affects inflammation in the colon. G protein-coupled taste receptors, including G protein subunit α-gustducin and other signaling proteins, have been found in the intestines. Here, we use α-gustducin as a representative and describe a dextran sulfate sodium (DSS)-induced IBD model to evaluate the effect of gustatory gene mutations on gut mucosal immunity and inflammation. This method combines gene knockout technology with the chemically induced IBD model, and thus can be applied to assess the outcome of gustatory gene nullification as well as other genes that may exuberate or dampen the DSS-induced immune response in the colon. Mutant mice are administered with DSS for a certain period during which their body weight, stool, and rectal bleeding are monitored and recorded. At different timepoints during administration, some mice are euthanized, then the sizes and weights of their spleens and colons are measured and gut tissues are collected and processed for histological and gene expression analyses. The data show that the α-gustducin knockout results in excessive weight loss, diarrhea, intestinal bleeding, tissue damage, and inflammation vs. wild-type mice. Since the severity of induced inflammation is affected by mouse strains, housing environment, and diet, optimization of DSS concentration and administration duration in a pilot experiment is particularly important. By adjusting these factors, this method can be applied to assess both anti- and pro-inflammatory effects.

Wolbachia-Host Interactions: Host Mating Patterns Affect Wolbachia Density Dynamics.

Wolbachia are maternally inherited intracellular bacteria that infect a wide range of arthropods and cause an array of effects on host reproduction, fitness and mating behavior. Although our understanding of the Wolbachia-associated effects on hosts is rapidly expanding, our knowledge of the host factors that mediate Wolbachia dynamics is rudimentary. Here, we explore the interactions between Wolbachia and its host, the two-spotted spider mite Tetranychus urticae Koch. Our results indicate that Wolbachia induces strong cytoplasmic incompatibility (CI), increases host fecundity, but has no effects on the longevity of females and the mating competitiveness of males in T. urticae. Most importantly, host mating pattern was found to affect Wolbachia density dynamics during host aging. Mating of an uninfected mite of either sex with an infected mite attenuates the Wolbachia density in the infected mite. According to the results of Wolbachia localization, this finding may be associated with the tropism of Wolbachia for the reproductive tissue in adult spider mites. Our findings describe a new interaction between Wolbachia and their hosts.

Host-symbiont interactions in spider mite Tetranychus truncates doubly infected with Wolbachia and Cardinium.

Inherited bacteria Wolbachia, and more recently Cardinium, have received a great deal of attention for their ability to manipulate the reproduction and fitness of their host species. Wolbachia and Cardinium have been found to co-infect the same host species. In this study, both Wolbachia and Cardinium were found to manipulate host reproduction through cytoplasmic incompatibility and to affect the male-biased sex-ratio in the doubly infected spider mite Tetranychus truncates Ehara. We also investigated effects of double infection with Wolbachia and Cardinium on host fecundity and longevity. Results indicated that Wolbachia and Cardinium increased the fecundity of doubly infected females, although no infection effect on host longevity was observed. Our most important finding was that the mating of uninfected mites facilitated the proliferation of Wolbachia and Cardinium in double-infected mites. We discuss the results observed with respect to the spread of bacterial infection in natural populations and the evolution of the endosymbiont-T. truncates symbiosis.

Multiple infections with Cardinium and two strains of Wolbachia in the spider mite Tetranychus phaselus Ehara: revealing new forces driving the spread of Wolbachia.

Cytoplasmic incompatibility (CI) has been proposed as a major mechanism by which certain strains of Wolbachia to invade and persist in host populations. However, mechanisms that underlie the invasion and persistence of non-CI strains are less well understood. Here, we established a spider mite Tetranychus phaselus population multiply infected by Cardinium as well as two distinct lineages of Wolbachia, designated wCon and wOri, to study the forces driving the spread of the non-CI strain of Wolbachia wOri. Interestingly, we found that wOri provided a longevity advantage to its female hosts under ideal conditions, making wOri stay longer in this population, and then being transmitted to more offspring. Furthermore, the lifespan of uninfected females was reduced when mated with multiple-infected males. As a result, the uninfected population is attenuated by the multiple-infected males. Thus, we infer that the host age effects of multiple infection may represent sufficient forces driving the spread of wOri through the host population.

Expression of cytoplasmic incompatibility and host fitness effects in field populations of Sogatella furcifera infected with Cardinium.

'Candidatus Cardinium' is a maternally inherited intracellular bacterium that infects a wide range of arthropods and causes diverse reproductive alterations of its arthropod hosts, including cytoplasmic incompatibility (CI), parthenogenesis and feminization. CI is the most common effect and is expressed as a reduction in the number of offspring in crosses between infected males and uninfected females (or females infected with a different bacterial strain). The white-backed planthopper Sogatella furcifera (Horváth) is a major rice pest in Asia and is a vector of the Southern rice black-streaked dwarf virus (SRBSDV). In this study, we found severe CI expression induced by Cardinium in Yunnan and Guangxi populations of S. furcifera by performing four crosses of Cardinium-infected (C) and uninfected (U) planthoppers: female U x male U, female U x male C, Female C x Male U, Female C x Male C. Investigations of the fitness costs and benefits of Cardinium infection in these populations showed that it had no effect on the fecundity of females, but could shorten the developmental time of nymphs.