Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The immune response after vaginal application of antigens was investigated in six sexually mature female rhesus monkeys. Two model antigens, i.e., lipopolysaccharide (LPS) OF Salmonella typhosa and abortive type T-4 coliphages were applied with or without adjuvant. A plastic sponge used as the antigen carrier was introduced into the upper vagina and placed against the ectocervix. For primary immunization, each monkey received 18 vaginal antigen applications and 10 applications for each booster course. For comparison, three other female rhesus monkeys were immunized systemically. Alum or LPS was used as adjuvant. Blood was obtained two times and cervical mucus three times weekly from each monkey. Antibodies were only barely detectable in cervical mucus after the primary vaginal immunization. However, booster treatments resulted in definite antibody responses. Specific antibodies were also detected in the circulating blood after vaginal booster immunization. The antibody level in cervical secretion in three of four cases was higher than that in circulatin blood. Systemic immunization resulted in high levels of circulating antibodies, but less than 10% appeared in cervical secretions. A characteristic decrease in antibody levels in cervical mucus was usually observed at midcycle after local immunization as well as after systemic immunization. More than 90% of T-4 coliphages applied vaginally were absorbed within 48 hours. Although alum appeared to retard the absorption of antigens, it seemed to enhance the local response. More than 90% of the antibodies to the T-4 coliphages could be removed from the serum and cervial mucus by treatment with anti-immunoglobuin G antiserum. The lymphocyte response to antigens was studied by measuring the 3H-thymidine uptake by peripheral blood lymphocytes in culture. A positive response was observed in three of three systemically immunized and in only two of six locally immunized aminals. In general, the immune response was significantly weaker after local vaginal immunization than after systemic immunization.
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PMID:Immune response after vaginal application of antigens in the rhesus monkey. 11 25

Neonatal female NMRI mice were given injections of olive oil (controls) or daily doses of corticosterone (10 micrograms), 17 beta-estradiol (10 micrograms), or diethylstilbestrol (DES) (0.01, 0.1, 1, or 5 micrograms) for the first 5 days after birth. The 5-micrograms dose of DES resulted in a persistently reduced in vitro mitogen response to concanavalin A or bacterial lipopolysaccharide of spleen lymphocytes from 6-, 10-, and 18-week-old or 17-month-old females. DES injections from day 6 through day 10 did not influence the later mitogen response. Treatment of ovariectomized 10-week-old females with 5 micrograms DES for 5 days resulted in a tendency to a reduced mitogen response (not statistically significant) 24 hours after the last DES injection. Four weeks later, the mitogen response was the same in experimental and control females. Different possible mechanisms for the persistent effect on the mitogen response are discussed. Neonatal DES treatment not only resulted in persistent changes in the cervicovaginal epithelium and in the hypothalamic-pituitary gland control system but also in the spleen lymphocyte mitogen response. The altered mitogen response should be a stimulus for a detailed analysis of the immune system in women exposed to DES during fetal life, some of whom develop later in life clear cell adenocarcinoma of the uterine cervix and vagina.
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PMID:Long-term effects of neonatal estrogen treatment on mitogen responsiveness of mouse spleen lymphocytes. 28 31

Most human pyelonephritis Escherichia coli isolates express both mannose (MS)- and globoside (Gal-Gal)-binding pili. An ascending E. coli urinary tract infection model was established in the 16-wk-old female BALB/c mouse to compare the pathogenic significance of MS and Gal-Gal pili and their efficacy as vaccines for the prevention of pyelonephritis. The distribution and density of pilus receptor compounds in urogenital tissues and as soluble compounds in urine were determined with antibodies to the synthetic receptor analogues, alpha D-Gal(1----4) beta D-Gal and alpha D-Man(1----2) alpha D-Man. Both carbohydrates were detected in vagina, bladder, ureter, and renal pelvis epithelium and in collecting duct and tubular cells. A pilus receptor compound also was detected in urine. It competitively inhibited the binding capacity of MS pili and was found to be physically, chemically, and immunologically related to Tamm-Horsfall uromucoid. Infectivity and invasiveness were quantitatively and histologically characterized for four E. coli strains: J96, a human pyelonephritis strain that expresses both MS and Gal-Gal pili; two recombinant strains prepared from J96 chromosomal DNA encoding MS pili or Gal-Gal pili; and the nonpiliated K12 recipient. Intravesicular administration of J96 (10(6) colony-forming units [CFU]) resulted in renal colonization and invasion in each of nine mice. The Gal-Gal clone (10(6) CFU) colonized the kidneys in each of 10 mice but did not invade. In contrast, the MS clone (10(6) CFU) did not colonize renal epithelium or invade. This effect was superceded when larger doses (greater than or equal to 10(10) CFU) of the MS clone were administered in volumes that cause acute vesicoureteric reflux. The efficacy was determined of vaccines composed of pure MS or Gal-Gal pili or the lipopolysaccharide containing O somatic antigen of the challenge strain, J96. The Gal-Gal pilus vaccine blocked renal colonization in 19 of 22 mice and renal invasion in 10 of 11 mice. Gal-Gal pili may be useful immunogens for the prevention of pyelonephritis in anatomically normal urinary tracts.
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PMID:Molecular basis of Escherichia coli colonization of the upper urinary tract in BALB/c mice. Gal-Gal pili immunization prevents Escherichia coli pyelonephritis in the BALB/c mouse model of human pyelonephritis. 285 30

Female BALB/c mice were immunized intranasally with the mouse pneumonitis biovar of Chlamydia trachomatis and subsequently challenged in the ovarian bursa (C. trachomatis immunized, C. trachomatis challenged). Two groups of mice served as controls. One group was sham immunized intranasally with mock-infected HeLa 229 cell extracts and was challenged in the ovarian bursa with C. trachomatis MoPn (sham immunized, C. trachomatis challenged). The second control group was sham immunized and not challenged (sham immunized, nonchallenged). Before challenge, the C. trachomatis-immunized, C. trachomatis-challenged animals mounted a significant humoral response as shown by high immunoglobulin G (IgG), IgM, and IgA levels and high levels of neutralizing antibodies in serum and moderate IgG and IgA titers in vaginal secretions. Reactivity by Western blot (immunoblot) to the lipopolysaccharide, 30-, 40- (major outer membrane protein), and 60-kDa cysteine-rich proteins and 75- and 100-kDa chlamydial components could be demonstrated. However, reactivity to the 60-kDa heat shock protein was only observed 22 days after challenge. In addition, this group of animals mounted a significant immune response to chlamydial antigens, as shown by a lymphocyte proliferation assay, compared with the sham-immunized nonchallenged mice. After intrabursal challenge, there was no C. trachomatis shedding from the vagina in the C. trachomatis-immunized, C. trachomatis-challenged animals, while 63% of the sham-immunized, C. trachomatis-challenged mice had a positive C. trachomatis culture. In addition, histological sections from the genital tract showed, at 2 weeks postchallenge, a marked acute inflammatory reaction in the sham-immunized, C. trachomatis-challenged animals while in the C. trachomatis-immunized, C. trachomatis-challenged mice there was minimal inflammatory reaction. When the animals were mated, only 12% of the mice from the sham-immunized, C. trachomatis-challenged mice were fertile. In contrast, 94 and 80% of the sham-immunized, nonchallenged and C. trachomatis-immunized, C. trachomatis-challenged mice, respectively, were fertile.
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PMID:Protection against infertility in a BALB/c mouse salpingitis model by intranasal immunization with the mouse pneumonitis biovar of Chlamydia trachomatis. 803 6

It has been previously shown with an in vitro neutralization system that monoclonal antibodies (MAbs) to the major outer membrane protein (MOMP) of Chlamydia trachomatis, depending on the isotype of the MAb and the host cell used, can either neutralize or enhance the infectivity of this organism. MAbs to variable domain 4 (VD 4) of MOMP have been described that neutralize the infectivity of C. trachomatis when tested in a system in which either the host cell does not have detectable Fc gammaRIII receptors or complement is added to block the interaction of the MAb with the receptor. However, if Fc gammaRIII receptors are available, immunoglobulin G2b (IgG2b) MAbs to the VD 4 are able to enhance the infectivity of this pathogen. Two MAbs that recognize the sequence TLNPTIA in VD 4 of the MOMP but differ in isotype, E4 (IgG2b) and E21 (IgG1), were used to test whether in vivo the isotype of the MAb modulates the outcome of a vaginal infection in a murine model. A third MAb, CP33 (IgG2b), that recognizes the chlamydial lipopolysaccharide but does not neutralize infectivity of C. trachomatis, was also tested. Elementary bodies (EBs) of C. trachomatis, serovar E (BOUR), were pretreated with the three MAbs and were used to inoculate the vaginas of C3H/HeJ mice which had been pretreated with progesterone. Subsequently mice were monitored over a 5-week period with vaginal cultures. In the groups that were inoculated with EBs pretreated with MAbs directed to VD 4 of MOMP, there was a significant decrease (P < 0.05) in the number of mice infected. Only 30% of the mice were infected in the MAb E4-treated group, and 10% were infected in the MAb E21 group. This was in contrast to the groups inoculated with EBs pretreated with MAb CP33 and control untreated EBs, which resulted in 100 and 79% of the mice infected, respectively. Therefore, in this setting in which EBs were introduced in vivo coated with MAb, there was no enhancement of infection by IgG2b MAbs; rather, the results paralled the in vitro neutralization results, in which cells lacking Fc gammaRIII receptors were employed. Mice were also given the MAbs, as well as purified IgG as a control, by intraperitoneal injection before and after intravaginal inoculation with C. trachomatis. Despite relatively high levels of MAbs in serum and detectable levels of MAbs in the vagina at the time of infection, there was only modest protection in animals receiving MAb E21, with 60% of the mice infected in contrast to 90% of the mice receiving MAb E4, MAb CP33, and IgG. However, by the second week of infection compared to controls, there was a significant increase (P < 0.05) in the amount of chlamydiae recovered from the vaginas of mice that had received the two IgG2b MAbs, E4 and CP33. In summary, the presence of IgG2b MAbs directed to surface components of C. trachomatis at certain times during the course of infection may play a role in enhancing the infectivity of this pathogen.
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PMID:Effect of immunoglobulin G isotype on the infectivity of Chlamydia trachomatis in a mouse model of intravaginal infection. 919 38

The objective of the present study was to define the afferent arm of the mucosal immune system in the lower female reproductive tract. We report here that antigen presentation by vaginal cells is under hormonal control. When vaginal cells from ovariectomized rats treated with estradiol (0.01-10 microg) were incubated with ovalbumin-specific T cells and ovalbumin, a dose-dependent inhibition of antigen presentation was measured. In time course studies, estradiol given to ovariectomized rats inhibited vaginal cell antigen presentation within 24 h after a single injection, relative to that seen in saline controls. To determine whether changes in antigen presentation were attributable to the effect of estradiol on the number of antigen-presenting cells (APCs) in the vagina, tissues were analyzed by immunohistochemistry. Our findings indicate that estradiol inhibited antigen presentation without affecting the number of major histocompatibility complex class II positive cells and at a time when macrophage/dendritic cells/granulocytes in the vagina increase in response to estradiol treatment. Antibody neutralization studies indicated that antigen presentation by vaginal cells from ovariectomized rats is mediated through class II and involves the expression of transmembrane proteins B7.1 and B7.2. In other studies, vaginal APCs interact with thymus APCs to synergistically enhance antigen presentation under conditions in which vaginal antigen presentation is inhibited by estradiol. Analysis of conditioned media indicates that enhancement of thymus antigen presentation involves the release of a soluble factor(s) into the culture media of vaginal cells. When spleen cells were cocultured with vaginal cells from saline-treated rats, proliferation increased in the presence of concanavalin A and/or phytohemagglutinin and decreased with lipopolysaccharide, relative to spleen cells and mitogen alone. In contrast, when incubated with vaginal cells from estradiol-treated rats, spleen cell proliferation was not affected with concanavalin but was inhibited with phytohemagglutinin and lipopolysaccharide. These studies demonstrate that estradiol regulates antigen presentation by vaginal cells and that vaginal cells, in turn, influence antigen presentation, as well as B and T cell proliferation.
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PMID:Antigen-presenting cells in the female reproductive tract: influence of estradiol on antigen presentation by vaginal cells. 1091 75

To identify overlapping and non-overlapping functions for TSP-1 and alphavbeta6, we crossed TSP-1-null and beta6-null mice and compared the phenotype of the double-null mice with those of wild-type and single-null mice. The double-null mice exhibited focal acute and organizing pneumonia that was more severe than the wild-type and single-null mice as well as a significantly higher incidence of inflammation in tissues other than the lung. The TSP-1-null and beta6-null mice exhibited a five to eight-fold increase in granulocyte recruitment to the lung three days after exposure to lipopolysaccharide. They also had abnormalities that were infrequently observed in the wild-type and single-null mice, including heart degeneration (8.35% in wild-type and 28.1% in double-null mice), hyperplasia of the glandular of the stomach (2.8% in wild-type and 21.1% in double-null mice) and endometrial hyperplasia (0% in wild-type and 38.5% in double-null females). Furthermore, the beta6-null and double-null mice displayed a significant elevation in benign and malignant cancers. Stomach papillomas, squamous cell carcinomas of the ear and stomach, and adenocarcinomas of the lungs, vagina/cervix and colon were observed with the highest frequency. These data demonstrate that TSP-1 and alphavbeta6 are involved in regulation of the immune system and epithelial homeostasis. They also indicate that alphavbeta6 functions as a tumor suppressor gene and that activation of TGFbeta by TSP-1 and alphavbeta6 contributes to normal tissue architecture and function.
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PMID:Characterization of integrin beta6 and thrombospondin-1 double-null mice. 1596 61

Salmonella Enteritidis is the predominant serovar associated with egg-borne salmonellosis in humans. The colonization of S. Enteritidis in the vagina may play a role in the production of S. Enteritidis-contaminated eggs. In the first experiment, the in vitro adhesion of S. Enteritidis in vaginal and follicular explants was compared with that of S. Typhimurium by bacteriological isolation methods. The mean number of S. Enteritidis associated with vaginal explants was significantly (P < 0.05) higher than S. Typhimurium associated with vaginal explants and both serovars associated with follicular explants. In the second experiment, the in vitro adhesion and invasion of S. Enteritidis strains in the vaginal epithelium was compared with that of several strains of S. Agona, S. Infantis, S. Hadar, S. Heidelberg, S. Montevideo and S. Typhimurium, by immunohistochemical methods. The mean number of Salmonella in the vaginal epithelium depended on their lipopolysaccharide (LPS) type, with the rank order as follows: LPS type O9 (S. Enteritidis) > LPS type O4 (S. Agona, S. Typhimurium and S. Heidelberg) > LPS type O7 (S. Montevideo and S. Infantis) and LPS type O8 (S. Hadar). This rank order of Salmonella invasiveness is in accordance with the frequency of Salmonella outbreaks involving contaminated eggs. These findings suggest that S. Enteritidis has a higher ability to colonize the vaginal epithelium than other serovars, and the Salmonella LPS type may play an essential role in tropism of the reproductive tract.
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PMID:Specific adhesion and invasion of Salmonella Enteritidis in the vagina of laying hens. 1624 66

Gallinacins (Gal) are antimicrobial peptides that play significant roles in innate immunity in chickens. The aim of this study was to examine whether age of birds and egg-laying activity (laying and non-laying caused by feed-regulation) affect the mRNA expression of Gal-1, -2, and -3 in the vagina of hens, and whether their expressions are changed in response to the stimulation with Salmonella enteritidis (SE) and lipopolysaccharide (LPS). White Leghorn hens were divided into groups of young and old laying hens, and groups of laying and non-laying hens after feed-regulation. Vaginal cells were cultured and stimulated with SE or LPS. Expressions of Gal-1, -2, and -3 mRNA in their vaginal mucosa and cultured cells were examined by quantitative real-time RT-PCR. The expressions of Gal-1, -2, and -3 of the vaginal mucosa were significantly greater in old birds than in young birds. Expression of these Gals in the vagina were decreased in the regressed oviduct of non-laying birds compared with laying birds. The expressions of Gal-1, -2, and -3 in the cultured vaginal cells were increased by stimulation with SE or LPS within 24 h. These results suggest that the mRNA expressions of Gal-1, -2 and -3 in the vagina of laying hens increased with age, whereas they decreased in the regressed oviduct during the non-laying phase. Also, synthesis of these antimicrobial peptides in the vagina may increase in response to SE and LPS to eliminate SE bacteria.
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PMID:Effects of age, egg-laying activity, and Salmonella-inoculation on the expressions of gallinacin mRNA in the vagina of the hen oviduct. 1639 22

The aims of this study were to (i) determine the types of avian beta-defensin genes (AvbetaD) expressed in the hen oviduct and (ii) to examine the effects of lipopolysaccharide (LPS) treatment in vivo on their expression in the vagina. Birds were i.v. treated with LPS (1 mg/kg of BW), and subsequently the oviducts were analyzed 0, 3, 6, 12, or 24 h after LPS administration. The mRNA expression for AvbetaD was examined by reverse transcription-PCR using RNA preparations from the mucosal tissues of all the oviductal segments. Furthermore, changes in their mRNA expression profiles in the vagina were analyzed by semiquantitative reverse transcription-PCR. The AvbetaD-1, -2, -3, -4, -5, -7, -8, -9, -10, -11, and -12 were identified in each oviductal segment from infundibulum to vagina. Among these AvbetaD, the expression of AvbetaD-3, -5, -10, -11, and -12 in the vagina were significantly increased in response to LPS treatment, whereas the others did not show significant changes. These results suggest that all 11 types of AvbetaD are expressed in the hen oviduct and at least 5 of them in the vagina show increased expression in response to LPS.
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PMID:Expression of avian beta-defensins in the oviduct and effects of lipopolysaccharide on their expression in the vagina of hens. 1842 Sep 91


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