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E Balish

Publications and source records attributed to E Balish.

At least 73 records · Page 4Linked to original sources
PubMed1991

Role of CD4+ lymphocytes in resistance to mucosal candidiasis.

The role of CD4+ lymphocytes in resistance of N:NIH(S) III bg/bg nu/+ mice to mucosal candidiasis was evaluated. Alimentary tract colonization with a pure culture of Candida albicans induced a population of lymphocytes in both the Peyer's patches and spleens of bg/bg nu/+ mice, but not bg/bg nu/nu mice, that proliferated and produced interleukin-2 (IL-2) in response to C. albicans antigens. The induction of candida-specific lymphocytes correlated with the clearance of C. albicans from the esophagus and tongue of resistant bg/bg nu/+ mice. Isogenic bg/bg nu/nu mice which do not develop candida-reactive lymphocytes were unable to clear C. albicans from their tongues and esophagi. Treatment of bg/bg nu/+ mice with anti-CD4+ monoclonal antibodies depleted their CD4+ lymphocytes and increased their susceptibility to mucosal candidiasis of the tongue and esophagus. In vivo treatment of bg/bg nu/+ mice with anti-IL-2, anti-gamma interferon (IFN-gamma), or both anti-IL-2 and anti-IFN-gamma monoclonal antibodies did not abrogate their resistance to mucosal candidiasis. Furthermore, treatment of C. albicans-susceptible bg/bg nu/nu mice with IFN-gamma and IL-2 did not protect them from mucosal candidiasis. Thus, CD4+ cells apparently play a critical role in resistance to mucosal candidiasis; however, we were unable to demonstrate a role for IL-2 and IFN-gamma in mediating resistance to mucosal candidiasis.

Animals↗
PubMed1991

Cryptococcosis in beige mice: the effect of congenital defects in innate immunity on susceptibility.

The influence of the beige (bg/bg) mutation on susceptibility to cryptococcosis was assessed by mortality, quantitative culturing, and histopathology of infected organs from bg/bg and bg/+ mice. Immunodeficient bg/bg mice were more susceptible to systemic cryptococcosis than immunocompetent bg/+ mice. Differences in susceptibility of bg/bg and bg/+ mice corresponded with temporal differences in histopathology. In contrast to bg/+ mice, inflammatory responses in infected tissues from bg/bg mice contained less cellular infiltrate, proportionally more polymorphonuclear neutrophils than monocytes and macrophages, and delays in the switch from acute to chronic inflammation. Enhanced growth of Cryptococcus neoformans in the internal organs of bg/bg mice was coincident with delayed inflammatory responses. These quantitative culture and histopathology studies suggest that the defects associated with monocytes and macrophages and polymorphonuclear neutrophils resulted in altered in vivo inflammatory responses and contributed to the enhanced susceptibility of beige mice to C. neoformans.

Animals↗
PubMed1991

Serum antibody response of gnotobiotic athymic and euthymic mice following alimentary tract colonization and infection with Candida albicans.

Colonization and infection evoked specific immunoglobulin responses to Candida albicans antigens in gnotobiotic nu/+ mice which appeared to correlate with clearance of infected mucosal surfaces (tongue and stomach). Conversely, colonized and infected nu/nu mice formed some IgM but no detectable IgG or IgA antibodies against C. albicans antigens. Although chronic mucosal infections of tongue and stomach persisted in nu/nu mice, they were able to resist overwhelming mucosal and systemic infections with C. albicans. Thus, C. albicans specific antibodies may play a role in clearance of mucosal candidiasis (tongue and stomach), but these antibodies do not appear to be necessary for protecting athymic mice against systemic candidiasis of endogenous origin.

Animals↗
PubMed1991

Susceptibility of congenitally immunodeficient mice to a nonencapsulated strain of Cryptococcus neoformans.

The susceptibility of congenitally immunodeficient mice to a nonencapsulated strain of Cryptococcus neoformans (strain M7) was evaluated. Gnotobiotic mice with defined congenital defects in innate immunity (beige) or cell-mediated immunity (athymic) or with combined defects in innate and cellular immunity (beige athymic) were i.v. challenged with C. neoformans M7. The nonencapsulated strain of C. neoformans produced a persistent low-grade infection in the brains of all immunodeficient and immunocompetent mice used in this study. Immunocompetent mice (nu/+;bg/+) and immunodeficient bg/bg mice readily cleared nonencapsulated cryptococci from their kidneys, liver, lungs, and spleen. In contrast to nu/+ mice, nu/nu mice had a reduced capacity to clear nonencapsulated cryptococci from their kidneys and liver after i.v. challenge. Both bg/bg-nu/nu and bg/bg-nu/+ mice developed a low-grade infection in their kidneys, liver, lungs, and spleen, which was maintained throughout the 21-day study. Persistent infections were not due to reversion to an encapsulated state. These data indicate that a capsule may not always be necessary for C. neoformans to survive, in vivo, in tissues of immunodeficient and immunocompetent mice.

Animals↗
PubMed1990

Decreased immunologic responsiveness following intensified vaginal immunization against urinary tract infection.

In an attempt to further increase the protective effect of vaginal immunization against urinary tract infections in Cynomolgus monkeys, the immunogen of killed E. coli was given more times, in larger amounts, and with the adjuvant MDP. Instead of increasing the protective effect, no protective effect on induced cystitis was observed. In addition, rises in urinary and serum immunoglobulins previously observed after vaginal immunization and induced cystitis were lessened. These observations appear to correspond with the classical concepts of immunologic unresponsiveness.

Acetylmuramyl-Alanyl-Isoglutamine↗
PubMed1990

Correlates of cell-mediated immunity in Candida albicans-colonized gnotobiotic mice.

Germfree athymic (nu/nu) and euthymic (nu/+) mice were colonized with a pure culture of Candida albicans. Correlates of cell-mediated immunity (lymphocyte proliferation and footpad responses to C. albicans antigens) and in vivo clearance of mucosal infections were assessed at different time intervals after alimentary tract colonization. C. albicans hyphae infected the dorsal surface of the tongue and the cardial section of the stomach in both nu/nu and nu/+ mice within 1 week after colonization with a pure culture of C. albicans. With time after colonization and infection with C. albicans, nu/+ mice manifested positive lymphocyte proliferation and positive footpad responses to Candida antigens that appeared to correlate with the capacity to clear Candida hyphae from the dorsal surface of the tongue and in the stomach. Conversely, nu/nu mice could not clear mucosal candidosis (in the stomach and on the tongue) and did not manifest either lymphocyte proliferation or footpad swelling in response to C. albicans antigens. These studies indicated that T-cell-mediated immunity may play a role in the acquired resistance of mice to mucosal candidosis. Since neither nu/nu nor nu/+ mice developed a progressive systemic disease, T cells apparently do not play a prominent role in murine resistance to systemic candidosis of endogenous origin.

Animals↗
PubMed1990

Pathogenesis of Cryptococcus neoformans in congenitally immunodeficient beige athymic mice.

Mortality after intravenous challenge with 10(4) Cryptococcus neoformans demonstrated that doubly immunodeficient beige athymic (bg/bg nu/nu) mice were more susceptible to systemic cryptococcosis than either bg/bg or nu/nu mice. Infected bg/bg nu/nu mice also had a shortened lifespan compared with their bg/bg nu/+ littermates. Beige athymic (bg/bg nu/nu) but not bg/bg nu/+mice developed cryptococcal lesions in the skin, demonstrating that C. neoformans is dermatotropic in a T-cell-deficient host. Higher numbers of C. neoformans were isolated from the lungs and spleen of infected bg/bg nu/nu than bg/bg nu/+ mice as early as day 3 after challenge, indicating that in lymphoid-rich organs, T cells can alter the course of systemic cryptococcosis early in the infection. Despite extensive abscess formation in the brains of bg/bg nu/+ mice, dissemination and growth rate of C. neoformans in the brain was similar in both genotypes. The primary histopathological feature in tissues from bg/bg nu/nu mice infected with C. neoformans consisted of foci of encapsulated yeast cells with minimal to no inflammatory response. In contrast to bg/bg nu/nu mice, bg/bg nu/+ mice mounted a vigorous inflammatory response to C. neoformans that progressed from acute to chronic inflammation. Beige athymic mice are a new animal model that will be useful in clarifying the innate and acquired immune factors important in resistance to cryptococcosis.

Animals↗
PubMed1990

Mucosal and systemic candidiasis in congenitally immunodeficient mice.

Colony counts and light microscopy were used to assess the capacity of Candida albicans to colonize, infect the alimentary tract, and cause disseminated disease in athymic (nu/nu), euthymic (nu/+), beige (bg/bg), black (bg/+), beige athymic (bg/bg nu/nu), or beige euthymic (bg/bg nu/+) germfree mice. The alimentary tracts of all six genotypes of germfree mice were quickly colonized after exposure to yeast-phase C. albicans. Only bg/bg nu/nu mice showed obvious morbidity and mortality after mucosal colonization with C. albicans. Histopathology of C. albicans-colonized immunocompetent (nu/+, bg/+) and singly immunodeficient (nu/nu, bg/bg, bg/bg nu/+) mice showed minimal to moderate mucosal infections, whereas doubly immunodeficient (bg/bg nu/nu) mice showed extensive yeast and hyphal infection of the palate, tongue, esophagus, and stomach. A progressive systemic infection in C. albicans-colonized mice occurred only in bg/bg nu/nu mice 12 to 16 weeks after colonization and mucosal infection. Thus, it appears that a combination of defective cell-mediated immunity and phagocytic cell defects (polymorphonuclear leukocytes and/or macrophages) predisposed mice to severe mucosal and systemic candidiasis of endogenous origin. This is the first report of a mouse strain that is not only naturally susceptible to mucosal and systemic candidiasis of endogenous origin but also shows lethality at early (1 to 4 weeks) and late (12 to 16 weeks) times after alimentary tract colonization.

Animals↗
PubMed1990

Adherence of skin bacteria to human epithelial cells.

Aerobic and anaerobic bacteria isolated from human axillae were tested for their capacity to adhere to buccal epithelial cells, immortalized human epithelial (HEp-2) cells, and undifferentiated and differentiated human epithelial cells. In general, both aerobic and anaerobic diphtheroids adhered better to differentiated human epithelial cells than to HEp-2 and undifferentiated human epithelial cells (P less than 0.05). Mannose, galactose, fucose, N-acetyl-D-glucosamine, and fibronectin were also assayed for their capacity to inhibit the adherence of diphtheroids to human epithelial cells. A great deal of variability was observed in the capacity of the latter compounds to inhibit the attachment of aerobic diphtheroids to undifferentiated and differentiated epithelial cells. Overall, mannose appeared to be best at inhibiting the adherence of the aerobic diphtheroids to undifferentiated human epithelial cells. Galactose, fucose, N-acetyl-D-glucosamine, and fibronectin showed a greater capacity to inhibit attachment of aerobic diphtheroids to differentiated than to undifferentiated human epithelial cells. The inhibition of adherence to differentiated human epithelial cells varied with the microorganism and the compound tested; however, the highest and most consistent inhibition of adherence (76.1 to 88.6%) was observed with a 5% solution of N-acetyl-D-glucosamine. The in vitro adherence and adherence inhibition assays presented here demonstrate that a number of adhesins and receptors are involved in the adherence of skin bacteria to human epithelial cells and receptors on human epithelial cells are apparently altered during differentiation.

Bacteria, Aerobic↗
PubMed1990

Inability of human clinical strains of Helicobacter pylori to colonize the alimentary tract of germfree rodents.

Several attempts were made to colonize the alimentary tract and infect germfree BALB/c mice and germfree Sprague-Dawley rats with two human isolates of Helicobacter pylori. The alimentary tracts of mice, sacrificed at intervals between 1 day and 20 weeks after oral challenge, were culture negative for H. pylori. The alimentary tract, kidney, liver, and mesenteric lymph nodes were culture negative for H. pylori 5 h after intravenous challenge. Growth of H. pylori was inhibited by homogenates of murine stomach, small intestine, liver, and mesenteric lymph nodes. Germfree rats and mice do not appear to be readily colonized or infected by human strains of H. pylori.

Animals↗
PubMed1988

Urinary glycosaminoglycan levels following induced cystitis in monkeys.

Urinary glycosaminoglycan (GAG) levels were measured by the Whiteman assay in five monkeys following induction of an E. coli urinary tract infection. Urinary GAG levels rose as the infection developed and returned to baseline levels as the infection resolved. Elevated urinary GAG levels may be a marker for the tissue injury incurred by such infections and may offer insight into their pathophysiology.

Animals↗
PubMed1987

Vaginal immunization against induced cystitis in monkeys.

Cynomolgus monkeys received either vaginal immunization with formalin-killed E. coli or vaginal instillation of excipient without the bacteria. At 2, 7, 14 and 21 days after induction of a urinary tract infection with live E. coli, immunized monkeys showed enhanced clearance of bacteriuria compared to non-immunized controls. Immunized monkeys also showed increased levels of urinary anti-E. coli IgA and IgG after the immunizing and infecting procedures. Induction of heightened local immunity by vaginal immunization may lessen host susceptibility to urinary tract infections.

Administration, Intravaginal↗
PubMed1987

Acquired immunity to Trichophyton mentagrophytes in thymus-grafted or peritoneal exudate cell-injected nude rats.

Congenitally athymic "nude" (RNU/RNU) rats were grafted with syngeneic neonatal thymus glands and 30 days later cutaneously inoculated with Trichophyton mentagrophytes. Nude rats and thymus-grafted nude rats were susceptible to infection with T. mentagrophytes but only thymus-grafted nude rats cleared the dermatophytosis. Clearance of the fungal infection took twice as long (approximately 60 days) in thymus-grafted nude rats when compared with heterozygous euthymic (+/RNU) controls (approximately 35 days). Following clearance of the primary dermatophytosis, peritoneal exudate cells (PEC) were adoptively transferred from either thymus-grafted or heterozygous rats to nude rats. Eight of 12 PEC-recipient nude rats acquired the capacity to resolve T. mentagrophytes-induced dermatophytosis (mean clearance time was approximately 40 days). All heterozygous (+/RNU) rats, thymus-grafted nude rats (4/4), and 8 of 12 PEC-recipient nude rats, which had cleared a primary dermatophytosis also expressed delayed-type hypersensitivity and elevated serum antibody titers to trichophytin antigen. These results demonstrate that immunity to T. mentagrophytes can be acquired in congenitally athymic nude rats following thymus grafting or injection of PEC from syngeneic +/RNU rats; however, injection of PEC from trichophytin-sensitized +/RNU donor rats to nude recipient rats did not result in transfer of specific adoptive immunity to T. mentagrophytes. Interestingly, PEC transfer from non-sensitized +/RNU rats was comparable to thymus grafting in effecting clearance of T. mentagrophytes dermatophytosis. These results suggest that acquired immunity to T. mentagrophytes in the rat is T cell-dependent, and that the absence of functional T lymphocytes and not an epithelial defect results in chronic dermatophytosis in the nude rat.

Animals↗
PubMed1987

Local and systemic antibody responses accompany spontaneous resolution of experimental cystitis in cynomolgus monkeys.

Cynomolgus monkeys were infected intravesically with two different strains of uropathogenic Escherichia coli. A quantitative enzyme-linked immunosorbent assay method was used to monitor secretory and serum immune responses to the induced cystitis. Anti-E. coli secretory immunoglobulin A (sIgA) and IgG urinary antibodies were generated as a result of the cystitis. Urinary sIgA levels against the E. coli strains tested were highest at 25 to 31 days after cystitis induction, and urinary IgG levels were highest at 31 to 45 days after induction. Anti-E. coli IgM was not detected in the urine. The antibody response in serum was characterized by IgM, IgG, and IgA immunoglobulin production. IgM levels in serum rose at 14 days after cystitis induction and were sustained for another 1 to 2 weeks. Increases in serum IgG levels began at 7 to 21 days of infection and persisted in some cases for up to 70 days. Serum IgA to the infecting E. coli was produced within 1 week after cystitis induction and remained at elevated levels throughout the course of the cystitis. These results demonstrate the capacity of primates to spontaneously resolve a cystitis and to mount both local and systemic immune responses against the infecting bacteria.

Animals↗
PubMed1987

Colonization and pathogenesis of Cryptococcus neoformans in gnotobiotic mice.

Congenitally immunodeficient nude (nu/nu) mice and their immunocompetent littermates (nu/+) were used to determine whether the absence of thymus-matured T cells would alter the capacity of Cryptococcus neoformans to colonize their mucosal surfaces or enhance their susceptibility to systemic cryptococcosis, or both, following oral challenge. We present data demonstrating that an encapsulated strain of C. neoformans serotype A colonized the alimentary tracts of germfree, conventional, and antibiotic-treated conventional nu/nu mice. Scanning electron microscopy showed that C. neoformans adhered to the epithelial surfaces of the oral cavities, esophagi, and gastrointestinal tracts of monoassociated nu/nu and nu/+ mice, and culture data showed that there were more viable C. neoformans cells in the alimentary tracts of nu/nu mice than of nu/+ mice. Tetracycline-treated conventional nu/nu, but not nu/+, mice were also colonized with C. neoformans following intragastric challenge. C. neoformans-monoassociated and tetracycline-treated conventional nu/nu mice succumbed to disseminated cryptococcosis with cerebral involvement 3 to 4 weeks after oral challenge, whereas no mortality was observed for similarily challenged nu/+ mice. These results demonstrate that an encapsulated strain of C. neoformans can colonize mucosal surfaces and cause systemic cryptococcosis in immunodeficient nu/nu mice, suggesting that the alimentary tract can be a portal of entry for C. neoformans in an immunodeficient host. These data also indicate that functional T cells play an important role in resistance to systemic cryptococcosis of endogenous origin.

Animals↗
PubMed1986

In vitro and in vivo adherence of uropathogenic Escherichia coli strains.

Twenty-eight Escherichia coli strains isolated from the urine of patients with urinary tract infections were assayed for fimbrial type, in vitro capacity to agglutinate guinea pig red blood cells, and in vivo adherence to rat bladder uroepithelium. A direct correlation was found between hemagglutinating capacity and in vivo adherence. Strains with both Type 1 and P fimbriae showed the greatest adherence in vivo. Of the 28 strains, seven did not manifest either Type 1 or P fimbriae but agglutinated red blood cells and did adhere in vivo. In studies on bacterial adherence and urinary tract infections, both in vivo and in vitro studies may contribute to understanding the relevance of bacterial adhesins in initiating urinary tract infections.

Adhesins, Escherichia coli↗
PubMed1986

Colonization and infection of athymic and euthymic germfree mice by Campylobacter jejuni and Campylobacter fetus subsp. fetus.

Human clinical strains of Campylobacter jejuni and Campylobacter fetus subsp. fetus colonized the gastrointestinal tracts of both athymic (nu/nu) and euthymic (+/nu) germfree mice (BALB/c). Viable Campylobacter spp. (10(9) to 10(10) CFU/g [dry weight] of cecum and colon contents) were isolated on day 3 after oral challenge, and similar large numbers of viable cells were evident at several intervals during a 10-month experiment. The stomachs and upper small intestines of nu/nu and +/nu mice that were monoassociated for 224 days with C. jejuni 45100 contained 3 to 4 logs fewer viable bacteria than did their ceca or colons. Athymic mice that were monoassociated for 224 days with C. fetus subsp. fetus had 2 to 3 logs more viable Campylobacter spp. in their upper gastrointestinal tracts than did their +/nu littermates. Large viable populations (approximately 10(9)/g of contents) of C. fetus subsp. fetus were in the ceca and colons of both nu/nu and +/nu mice. All C. jejuni strains used in this study chronically infected the mesenteric lymph nodes of both nu/nu and +/nu mice. C. jejuni strains 24 and INN 73-83, which were cytotoxic for Chinese hamster ovary cells in vitro, were also more frequently isolated from the livers, spleens, and kidneys of nu/nu mice than was the weak cytotoxin-producing strain 45100. Additionally, heat-labile-enterotoxin-producing C. jejuni INN 73-83 was recovered more frequently from the internal organs of monoassociated +/nu mice than were any other Campylobacter spp. tested. Natural gastrointestinal colonization of neonatal nu/nu and +/nu mice (born to Campylobacter-colonized mothers) with Campylobacter spp. appeared to be delayed until approximately 1 to 2 weeks after birth. Conventionalization of C. jejuni 45100-monoassociated BALB/c mice with a complex mouse fecal microflora eliminated viable C. jejuni from the mesenteric lymph nodes by day 14 and from the cecum by day 78. These findings show that the gnotobiotic BALB/c mouse is a new model for studying acute and chronic host-Campylobacter sp. interactions.

Animals↗