scholarly journals Characterization of the Horizontal and Vertical Sexual Transmission ofChlamydiaGenital Infections in a New Mouse Model

2019 ◽  
Vol 87 (7) ◽  
Author(s):  
Sukumar Pal ◽  
Delia F. Tifrea ◽  
Luis M. de la Maza
Keyword(s):  
Mouse Model ◽  
Vertical Transmission ◽  
Sexual Transmission ◽  
Vaginal Swab ◽  
Male Mice ◽  
Infected Male ◽  
Newborn Mice ◽  
Content Type ◽  
Female Mice ◽  
Swab Specimen

ABSTRACTChlamydia trachomatisis the most common sexually transmitted bacterial pathogen worldwide, and there is a need to control this epidemic. So far there is no established animal model in which both the horizontal and the vertical transmission ofChlamydiacan be studied. To implement a horizontal sexual transmission model, male mice were inoculated in the meatus urethra withChlamydia muridarumand they were caged with naive female mice. Urine and vaginal swab specimens were collected for culture. To study vertical transmission, newborns were euthanized and specimens were cultured. As controls, females were mated with sham-infected male mice. AllC. muridarum-inoculated male mice had positive urine cultures. As determined by serology, all females caged withC. muridarum-inoculated males became infected, and 93% of them had positive vaginal swab specimen cultures. More females mated withC. muridarum-infected male mice (35%) than females mated with sham-infected male mice (0%) were infertile (P < 0.05). Also,C. muridarum-infected females delivered significantly fewer pups (3.8 ± 3.2/mouse) than control females (6.3 ± 1.6/mouse) (P < 0.05). Of the newborn mice, 32% wereC. muridarumpositive either in the lungs or in the intestines. Female mice housed with sham-infected males had no positive vaginal swab specimen cultures orC. muridarum-positive pups. This new mouse model of horizontal and vertical sexual transmission ofChlamydiaclosely parallelsC. trachomatissexual transmission in humans and may be a good model system to better understand the pathogenesis of these infections.

scholarly journals Localized Suppression of Inflammation at Sites of Helicobacter pylori Colonization

2011 ◽  
Vol 79 (10) ◽  
pp. 4186-4192 ◽  
Author(s):  
Alison L. Every ◽  
Garrett Z. Ng ◽  
Caroline D. Skene ◽  
Stacey N. Harbour ◽  
Anna K. Walduck ◽  
...  
Keyword(s):  
Helicobacter Pylori ◽  
Potential Model ◽  
Gastric Ph ◽  
Male Mice ◽  
Wild Type ◽  
Content Type ◽  
Female Mice ◽  
Gastric Corpus ◽  
Acid Secreting ◽  
H Pylori

ABSTRACTWhile gastric adenocarcinoma is the most serious consequence ofHelicobacter pyloriinfection, not all infected persons develop this pathology. Individuals most at risk of this cancer are those in whom the bacteria colonize the acid-secreting region of the stomach and subsequently develop severe inflammation in the gastric corpus. It has been reported anecdotally that male mice become infected with greater numbers ofH. pyloribacteria than female mice. While investigating this phenomenon, we found that increasedH. pyloriinfection densities in male mice were not related to antibody production, and this phenomenon was not normalized by gonadectomy. However, the gastric pH in male 129/Sv mice was significantly elevated compared with that in female mice. Differences in colonization were evident within 1 day postinfection and significantly arose due to colonization of the gastric corpus region in male mice. This provided a potential model for comparing the effect of corpus colonization on the development of gastritis. This was explored using two models ofH. pylori-induced inflammation, namely, 2-month infections ofMuc1−/−mice and 6-month infections of wild-type 129/Sv mice. WhileH. pyloriinfection of female mice induced a severe, corpus-predominant atrophic gastritis, to our surprise, male mice developed minimal inflammation despite being colonized with significantly moreH. pyloribacteria than female controls. Thus, colonization of the gastric corpus in male mice was associated with a loss of inflammation in that region. The suppression of inflammation concomitant with infection of the gastric corpus in male mice demonstrates a powerful localized suppression of inflammation induced at sites ofH. pyloricolonization.

scholarly journals Effects of litter size and subsequent gold-thioglucose-induced obesity on adipose tissue weight, distribution and cellularity in male and female mice: an age study

1988 ◽  
Vol 59 (3) ◽  
pp. 519-533 ◽  
Author(s):  
Jennifer L. Roberts ◽  
Frances M. Whittington ◽  
Michael Enser
Keyword(s):  
Litter Size ◽  
Tissue Growth ◽  
Male Mice ◽  
Newborn Mice ◽  
Small Litter ◽  
Male And Female ◽  
Cell Numbers ◽  
Female Mice ◽  
Gold Thioglucose ◽  
Large Litter

1. Over- or undernutrition of newborn mice was caused by suckling in litters consisting initially of four or eighteen pups. After weaning mice were fed ad lib. At 13 weeks of age some mice from large litters received gold thioglucose (GTG: 600 mg/kg intraperitoneally) to induce hyperphagia, and mice were killed at 13, 19·5, 26, 39 and 52 weeks.2. Total carcass lipid and the size and number of adipocytes in the inguinal subcutaneous, genital, perirenal and mesenteric depots were determined.3. Mice, both male and female, raised in small litters were heavier and had more carcass fat at all ages than mice raised in large litters. After GTG-treatment mice from large litters were heavier and fatter than mice raised in small litters.4. Fat distribution between the depots was related to carcass lipid content and not to treatment. The order of depot development was subcutaneous, parametrial, perirenal and mesenteric in females and epididymal, subcutaneous, perirenal and mesenteric in males. At 13 weeks the depots in males were more developed than those in females.5. Litter size had no effect on adipocyte volume in female mice at 13 weeks but by 52 weeks small-litter mice had larger cells in all depots and more cells in the parametrial and perirenal depots.6. Male mice from small litters had bigger cells at 13 weeks in all depots compared with males from large litters but by 52 weeks no significant differences remained. Greater numbers of cells were present only in the perirenal and mesenteric depots of small-litter males at some ages.7. Depots of GTG-treated large-litter female mice had larger cells than those of small-litter females, while a similar number of cells was found by 52 weeks in all but the perirenal depot, which had significantly more cells.8. GTG treatment of male mice from large litters also caused bigger cells than in small-litter mice, and an increased depot cell number at earlier ages in all but the epididymal depot. By 52 weeks cell numbers were similar in depots from small-litter and GTG-treated large-litter mice, except for the epididymal depot from the latter which had fewer cells.9. Increases in cell numbers with age in different depots occurred independently of existing cell mean volume and even of tissue growth, suggesting the presence of an in-built chronology, at least in older mice.10. We suppose that the differences in response to the level of preweaning nutrition in males and females result from a greater effect on the hypothalamic appetite centre in the latter. Whereas the cellular changes in large-litter males occur in the late-developing depots and are reversed naturally with time, those in the large-litter females are more extensive and require induction of hyperphagia for reversal.

scholarly journals The induction of obesity in rodents by means of monosodium glutamate

1976 ◽  
Vol 35 (1) ◽  
pp. 25-39 ◽  
Author(s):  
J. Bunyan ◽  
Elspeth A. Murrell ◽  
P. P. Shah
Keyword(s):  
Body Weight ◽  
Lipid Content ◽  
Monosodium Glutamate ◽  
Female Rats ◽  
Male Mice ◽  
Fat Pad ◽  
Newborn Mice ◽  
Female Mice ◽  
Gold Thioglucose ◽  
Male And Female Rats

1. Monosodium glutamate (MSG) was administered by various methods to mice and rats of various ages and the incidence of obesity was later measured.2. Newborn mice were injected subcutaneously with 3 mg MSG/g body-weight at 1, 2, 3, 6, 7 and 8 d of age; 16% died before weaning. Of the survivors, 90% or more became markedly obese. Mean carcass lipid content was increased by about 120% in both sexes at 20–30 weeks of age. In male mice, MSG treatment increased body-weight and epididymal fat pad weight, and greatly decreased adrenaline-stimulated lipolysis in isolated fat cells. Body-weight of females was not increased significantly. Food intake was not increased in either sex from weeks 13 to 15. Blood glucose level was not generally increased by MSG but some of the male mice had abnormally high values.3. Obesity was not detected in the offspring of female mice that had received 100 g MSG/kg diet, either from 3 weeks before mating until weaning, or from the 14th day of pregnancy until weaning.4. Intraperitoneal injection of 10 mg MSG/g body-weight (in two doses) at weaning increased carcass lipid content in female mice by 34% by 23 weeks of age, but female rats were not affected.5. The addition of 20 g MSG/l to the drinking-water from weaning onwards did not increase carcass lipid content in female rats or mice.6. The addition of 20 g MSG/kg diet from weaning onwards did not alter body-weight or carcass lipid content in male and female rats by 14 weeks of age.7. The obesity induced in mice by MSG was not associated with hyperphagia, unlike genetic obesity and obesity induced by gold thioglucose (GTG).8. All types of mouse studied, obese and lean, had essentially the same linear relationship between carcass water content and carcass lipid content.9. Although MSG-obese mice could not readily be differentiated from normal mice by the increase in body-weight, which was only about 10% compared to 50–120% for genetic and GTG-induced obesity, the proposed schedule of injections in the newborn was almost 100% reliable in inducing a high extent of adiposity.

scholarly journals Sex-Specific Difference in Adipose Tissue and Blood Pressure in a New Mouse Model Expressing Human Soluble Prorenin Receptor in Adipocytes

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 56-56
Author(s):  
Kellea Nichols ◽  
Audrey Poupeau ◽  
Eva Gatineau ◽  
Gertrude Arthur ◽  
Ming Gong ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Mouse Model ◽  
Fat Mass ◽  
Lean Mass ◽  
Soluble Form ◽  
Male Mice ◽  
Female Mice ◽  
Prorenin Receptor ◽  
Body Weights

Abstract Objectives Sex differences exist in obesity associated with cardiovascular disease; however, underlying mechanisms are not completely understood. Previous studies from our laboratory demonstrated that the prorenin receptor (PRR) and its soluble form (sPRR) contribute to adipogenesis and blood pressure control. The present study aimed to determine whether adipose-sPRR stimulated obesity is associated with hypertension and whether it is sex-dependent. Methods Transgenic mice on the C57BL/6 J background were generated expressing the human form of the soluble prorenin receptor (HsPRR) in a Cre-inducible manner. Male mice expressing Cre recombinase under the control of the adiponectin promotor were bred to heterozygote HsPRR/+ female mice to generate mice over-secreting sPRR (adi-HsPRR) and control littermate mice (CTL). The secretion of sPRR in the media doubled in primary adipocytes of adi-HsPRR mice compared to control mice (sPRR. CTL: 3729 ± 805 pg/ml; adi-HsPRR: 6170 ± 1237 pg/ml, P &lt; 0.05) validating the mouse model. Male (CTL = 4; adi-HsPRR = 8) and female mice (CTL = 10; adi-HsPRR = 10) were fed a low-fat (LF) diet or a high-fat diet (HF) for 20 weeks. Body weight was assessed weekly and EchoMRI was examined monthly. Results After 20 weeks on LF diet, adi-HsPRR male mice gained significantly more weight than CTL male mice (CTL: 25.1 ± 0.8 g; adi-HsPRR: 29.0 ± 0.8 g P &lt; 0.05), whereas no significant differences in body weights were observed in female mice. The body composition revealed a significant increase of fat mass, specifically in the epidydimal fat (CTL: 0.35 ± 0.04 g; adi-HsPRR: 0.61 ± 0.07 g, P &lt; 0.05), and lean mass of HsPRR male mice compared to CTL male mice. In contrast, female mice exhibited similar body weights (CTL: 20.6 ± 0.3 g; adi-HsPRR: 20.4 ± 0.4 g) and there was no differences of fat mass or lean mass between CTL and adi-HsPRR female mice. The sex-specific mechanism of sPRR on adipogenesis and blood pressure (by radiotelemetry) with LF and HF diet is currently under investigation. Conclusions Overall, sPRR stimulated body weight gain and fat mass expansion in male mice but not in female mice suggesting that female mice are protected from sPRR induced-hypertrophic effect. Funding Sources R01_HL142969–01 Yiannikouris, PI 07/15/2018–06/30/2022 NIH/NHLBI Title: The role of soluble prorenin receptor in hypertension associated with obesity Role: Ph.D Graduate Student.

scholarly journals Estrogen modulation of baroreflex function in conscious mice

2003 ◽  
Vol 284 (4) ◽  
pp. R983-R989 ◽  
Author(s):  
Jaya Pamidimukkala ◽  
Julia A. Taylor ◽  
Wade V. Welshons ◽  
Dennis B. Lubahn ◽  
Meredith Hay
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Mouse Model ◽  
Sodium Nitroprusside ◽  
Autonomic Function ◽  
Ang Ii ◽  
Male Mice ◽  
Female Mice ◽  
Reflex Bradycardia ◽  
Baroreflex Function

It has been suggested that estrogen modulates baroreflex regulation of autonomic function. The present study evaluated the effects of estrogen on baroreflex regulation of heart rate in response to changes in blood pressure with phenylephrine (PE), ANG II, and sodium nitroprusside (SNP) in a conscious mouse model. Males and ovariectomized females with (OvxE+) and without (OvxE−) estradiol replacement chronically implanted with arterial and venous catheters were used in these studies. The slope of the baroreflex bradycardic responses to PE was significantly facilitated in OvxE+ females (−7.65 ± 1.37) compared with OvxE− females (−4.5 ± 0.4). Likewise, the slope of the baroreflex bradycardic responses to ANG II was significantly facilitated in OvxE+ females (−7.97 ± 1.06) compared with OvxE− females (−4.8 ± 1.6). Reflex tachycardic responses to SNP were comparable in all the groups. Finally, in male mice, the slope of ANG II-induced baroreflex bradycardia (−5.17 ± 0.95) was significantly less than that induced by PE (−8.50 ± 0.92), but this ANG II-mediated attenuation of reflex bradycardia was not observed in the female mice. These data support the hypothesis that estrogen facilitates baroreflex function in female mice and suggest that ANG II-mediated acute blunting of baroreflex regulation of heart rate may be sex dependent.

scholarly journals Evaluation of Sex Differences in Murine Diabetic Ketoacidosis and Neutropenic Models of Invasive Mucormycosis

2021 ◽  
Author(s):  
Teclegiorgis Gebremariam ◽  
Sondus Alkhazraji ◽  
Abdullah Alqarihi ◽  
Nathan P. Wiederhold ◽  
Laura K. Najvar ◽  
...  
Keyword(s):  
Mouse Model ◽  
Mucor Circinelloides ◽  
Male Mice ◽  
Rhizopus Delemar ◽  
Female Mice ◽  
Pulmonary Mucormycosis ◽  
Susceptibility To Infection ◽  
Cytokine Levels ◽  
Untreated Female ◽  
The Difference

There is increased concern that the quality, generalizability, and reproducibility of biomedical research can be influenced by the sex of animals used. We studied the differences between male and female mice in response to invasive pulmonary mucormycosis including susceptibility to infection, host immune reaction, and responses to antifungal therapy. We used diabetic ketoacidotic (DKA) or neutropenic mice infected with either Rhizopus delemar or Mucor circinelloides. The only difference detected was that when DKA mice were infected with M. circinelloides, female mice were more resistant to infection than male mice (median survival time of 5 vs. 2 days for female and male mice, respectively). However, a 100% lethality was detected among infected animals of both sexes. Treatment with either liposomal amphotericin B (L-AMB) or posaconazole (POSA) protected mice from infection and eliminated the difference seen between infected but untreated female and male mice. Treatment with L-AMB consistently outperformed POSA in prolonging survival and reducing tissue fungal burden of DKA and neutropenic mice infected with R. delemar or M. circinelloides, in both mouse sexes. Although little difference was detected in cytokine levels among both sexes, mucormycosis infection in the DKA mouse model induced more inflammatory cytokines/chemokines involved in neutrophil (CXCL1) and macrophage (CXCL2) recruitment vs. uninfected mice. As expected, this inflammatory response was reduced in the neutropenic mouse model. Our studies show that there are few differences between female and male DKA or neutropenic mice infected with mucormycosis with no effect on the outcome of treatment or host immune response.

scholarly journals Sexual transmission of murine papillomavirus (MmuPV1) in Mus musculus

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Megan E Spurgeon ◽  
Paul F Lambert
Keyword(s):  
Mus Musculus ◽  
Reproductive Tract ◽  
Sexual Transmission ◽  
Human Papillomaviruses ◽  
Laboratory Animals ◽  
Study Endpoint ◽  
Male Mice ◽  
Sexually Transmitted ◽  
Female Mice ◽  
Model Animal

Human papillomaviruses (HPVs) are the most common sexually transmitted infectious agents. Because of the species specificity of HPVs, study of their natural transmission in laboratory animals is not possible. The papillomavirus, MmuPV1, which infects laboratory mice (Mus musculus), can cause infections in the female cervicovaginal epithelium of immunocompetent mice that progress to cancer. Here, we provide evidence that MmuPV1 is sexually transmitted in unmanipulated, immunocompetent male and female mice. Female 'donor' mice experimentally infected with MmuPV1 in their lower reproductive tract were housed with unmanipulated male mice. The male mice were then transferred to cages holding 'recipient' female mice. One third of the female recipient mice acquired cervicovaginal infections. Prolonged infections were verified by histopathology and in situ hybridization analyses of both male and recipient female mice at the study endpoint. These findings indicate that MmuPV1 is a new model animal papillomavirus with which to study sexually transmission of papillomaviruses.

scholarly journals Androgen aggravates liver fibrosis by activation of NLRP3 inflammasome in CCl4-induced liver injury mouse model

2020 ◽  
Vol 318 (5) ◽  
pp. E817-E829 ◽  
Author(s):  
Xingyu Ma ◽  
Yang Zhou ◽  
Bingke Qiao ◽  
Songhong Jiang ◽  
Qian Shen ◽  
...  
Keyword(s):  
Liver Injury ◽  
Inflammatory Response ◽  
Mouse Model ◽  
Nlrp3 Inflammasome ◽  
Acute Injury ◽  
Receptor Protein ◽  
Inflammasome Activation ◽  
Male Mice ◽  
Female Mice ◽  
Key Factor

Studies have shown that there are differences between the sexes regarding to the occurrence and development of liver diseases, which may be associated with sex hormones. However, the mechanisms behind it are largely unknown. In this study, we first investigated the differences of liver injury between male and female mice, using the CCl4-induced liver injury mouse model. It showed that the liver damage of male mice was much more severe than that of female mice. Both the acute injury and fibrosis of the liver were reduced when androgens were depleted by castration of male mice. The vulnerability of male liver was associated with testis endocrine and excessive activation of inflammatory response in the liver. Castrated male mice with testosterone supplementation showed aggravated liver inflammatory response and fibrosis. The activity of NOD-like receptor protein 3 (NLRP3) inflammasome was increased when testosterone supplementation was provided. However, the enhanced inflammatory response and fibrosis due to testosterone supplementation were negated by inhibiting the activation of NLRP3 using the specific small molecule inhibitor MCC950. It suggests that testosterone is a key factor that influences liver injury by regulating the NLRP3 inflammasome activation-mediated inflammatory response.

scholarly journals Evaluation of Sex Differences in Murine Diabetic Ketoacidosis and Neutropenic Models of Invasive Mucormycosis

2021 ◽  
Vol 7 (4) ◽  
pp. 313
Author(s):  
Teclegiorgis Gebremariam ◽  
Sondus Alkhazraji ◽  
Abdullah Alqarihi ◽  
Nathan P. Wiederhold ◽  
Laura K. Najvar ◽  
...  
Keyword(s):  
Mouse Model ◽  
Mucor Circinelloides ◽  
Male Mice ◽  
Rhizopus Delemar ◽  
Female Mice ◽  
Pulmonary Mucormycosis ◽  
Susceptibility To Infection ◽  
Cytokine Levels ◽  
Untreated Female ◽  
The Difference

There is increased concern that the quality, generalizability and reproducibility of biomedical research can be influenced by the sex of animals used. We studied the differences between male and female mice in response to invasive pulmonary mucormycosis including susceptibility to infection, host immune reaction and responses to antifungal therapy. We used diabetic ketoacidotic (DKA) or neutropenic mice infected with either Rhizopus delemar or Mucor circinelloides. The only difference detected was that when DKA mice were infected with M. circinelloides, female mice were more resistant to infection than male mice (median survival time of 5 vs. 2 days for female and male mice, respectively). However, a 100% lethality was detected among infected animals of both sexes. Treatment with either liposomal amphotericin B (L-AMB) or posaconazole (POSA) protected mice from infection and eliminated the difference seen between infected but untreated female and male mice. Treatment with L-AMB consistently outperformed POSA in prolonging survival and reducing tissue fungal burden of DKA and neutropenic mice infected with R. delemar or M. circinelloides, in both mouse sexes. While little difference was detected in cytokine levels among both sexes, mucormycosis infection in the DKA mouse model induced more inflammatory cytokines/chemokines involved in neutrophil (CXCL1) and macrophage (CXCL2) recruitment vs. uninfected mice. As expected, this inflammatory response was reduced in the neutropenic mouse model. Our studies show that there are few differences between female and male DKA or neutropenic mice infected with mucormycosis with no effect on the outcome of treatment or host immune response.

Gender-dependent physiological implications of combined PAI-1 and TIMP-1 gene deficiency characterized in a mouse model

2007 ◽  
Vol 293 (4) ◽  
pp. R1630-R1639 ◽  
Author(s):  
Jakob Harslund ◽  
Ole Lerberg Nielsen ◽  
Nils Brünner ◽  
Hanne Offenberg
Keyword(s):  
Gene Expression ◽  
Body Weight ◽  
Mouse Model ◽  
Physiological Parameters ◽  
Male Mice ◽  
Female Mice ◽  
Leukocyte Counts ◽  
Blood Leukocyte ◽  
Pai 1

The endogenous proteinase inhibitors plasminogen activator inhibitor type 1 (PAI-1) and tissue inhibitor of metalloproteinase type 1 (TIMP-1) are two distinct proteins with separate molecular pathways. However, a close relationship between PAI-1 and TIMP-1 has been proposed indicating some degree of functional overlap due to their involvement in ECM turnover, tissue remodeling, and cellular migration and signaling. To study the housekeeping physiological implications of PAI-1 and TIMP-1, we generated a combined PAI-1 and TIMP-1 gene-deficient mouse model. We present the results on generating this specific mouse model with particular emphasis on phenotypical characteristics, blood leukocyte counts, histology, and gene expression studies of PAI-1 and TIMP-1 in various organs. We observed a significant deviation in segregation of offspring only in male mice ( P < 0.01) predominantly caused by PAI-1 deficiency. In addition, the body weight in 3- and 20-wk-old male and 20-wk-old female mice was significantly different between genotypes ( P ≤ 0.0008). Furthermore, blood leukocyte counts were significantly different between genotypes in 20-wk-old male mice ( P ≤ 0.0002), whereas no significant differences were observed between genotypes in 20-wk-old female mice ( P ≥ 0.13). Quantifying the relative expression of PAI-1 and TIMP-1 revealed upregulation of PAI-1 ( P < 0.001) in male mice only. Our data highlight the complex roles of PAI-1 and TIMP-1 on physiological parameters such as segregation of offspring (embryonic development and survival), body weight (metabolism), blood leukocyte counts (immunity), and gene expression (regulatory redundancy). We conclude that PAI-1 and TIMP-1 seem to possess gender-dependent regulatory properties on various housekeeping physiological parameters and stress the potential implications in pathological conditions.

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