bluuebunny/crossref_metadata_2025_split huggingface dataset:
Porphyromonas gingivalis
Fimbriae Use β
2
Integrin (CD11/CD18) on Mouse Peritoneal Macrophages as a Cellular Receptor, and the CD18 β Chain Plays a Functional Role in Fimbrial Signaling
Authors: Takeshita Akira , Murakami Yukio , Yamashita Yoshinori , Ishida Masami , Fujisawa Seiichiro , Kitano Shigeo , Hanazawa Shigemasa 
Published: March 2020

ABSTRACT

In this study, we demonstrate that
Porphyromonas gingivalis
fimbriae use molecules of β
2
integrin (CD11/CD18) on mouse peritoneal macrophages as cellular receptors and also show that the β chain (CD18) may play a functional role in signalling for the fimbria-induced expression of interleukin-1β (IL-1β) and tumor necrosis factor alpha (TNF-α) genes in the cells. Using a binding assay with
125
I-labeled fimbriae, we observed that fimbrial binding to the macrophages was inhibited by treatment with CD11a, CD11b, CD11c, or CD18 antibody but not by that with CD29 antibody. Western blot assays showed that the fimbriae bound to molecules of β
2
integrin (CD11/CD18) on the macrophages. Furthermore, Northern blot analyses showed that the fimbria-induced expression of IL-1β and TNF-α genes in the cells was inhibited strongly by CD18 antibody treatment and slightly by CD11a, CD11b, or CD11c antibody treatment. Interestingly, intracellular adhesion molecule 1 (ICAM-1), a ligand of CD11/CD18, inhibited fimbrial binding to the cells in a dose-dependent manner. In addition, ICAM-1 clearly inhibited the fimbria-induced expression of IL-1β and TNF-α genes in the cells. However, such inhibitory action was not observed with laminin treatment. These results suggest the importance of β
2
integrin (CD11/CD18) as a cellular receptor of
P. gingivalis
fimbriae in the initiation stage of the pathogenic mechanism of the organism in periodontal disease.
Murine Macrophages Use Oxygen- and Nitric Oxide-Dependent Mechanisms To SynthesizeS-Nitroso-Albumin and To Kill Extracellular Trypanosomes
Authors: Gobert Alain P. , Semballa Silla , Daulouede Sylvie , Lesthelle Sophie , Taxile Murielle , Veyret Bernard , Vincendeau Philippe 
Published: March 2020

ABSTRACTReactive nitrogen intermediates were synthesized spontaneously in cultures of macrophages fromTrypanosoma brucei brucei-infected mice by an inducible nitric oxide (NO) synthase. This was inhibited by the addition of nitro-l-arginine. In this paper, we report the kinetics of the fixation of macrophage-derived NO on bovine serum albumin by using an enzyme-linked immunosorbent assay. S nitrosylation was confirmed by the Saville reaction, using mercuric chloride. It is known that reactive oxygen intermediates (ROI) are also synthesized by stimulated macrophages. The fact that NO is able to bind cysteine only under aerobic conditions led us to investigate the role of macrophage-derived ROI in the formation of S-nitrosylated proteins by activated macrophages. The immunoenzymatic signal decreased by 66 and 30% when superoxide dismutase and catalase, respectively, were added to the culture medium of macrophages from infected mice. In addition, the decrease in S-nitrosylated albumin formation correlated with the protection of extracellular trypanosomes from the cytostatic and cytotoxic activity of NO. Melatonin, a hydroxyl radical scavenger resulting from the decomposition of peroxynitrous acid, had no effect. All these data support the concept that an interaction between NO and ROI promoted the production ofS-nitroso-albumin by activated macrophages from infected mice.
Cloned Lines ofPlasmodium bergheiANKA Differ in Their Abilities To Induce Experimental Cerebral Malaria
Authors: Amani Véronique , Boubou Mariama Idrissa , Pied Sylviane , Marussig Myriam , Walliker David , Mazier Dominique , Rénia Laurent 
Published: March 2020

ABSTRACTInfection withPlasmodium bergheiANKA is usually lethal. The parasite causes in some mouse strains a neurovascular syndrome, experimental cerebral malaria (ECM), involving immunopathological reactions. The effects on the development of ECM of the mouse genetic background have been clearly demonstrated, but nothing is known about the effects of the clonal diversity of the parasite. We showed that various cloned lines derived from a polyclonal line ofP. bergheiANKA caused ECM but that the extent of ECM induction was dependent on the amount of inoculum. Subtle differences in ECM characteristics (survival time and hypothermia) were also observed. We also confirmed, using the 1.49L cloned line, that the mouse genetic background strongly affects ECM.
Identification and Characterization of a Newly Isolated Shiga Toxin 2-Converting Phage from Shiga Toxin-Producing
Escherichia coli
Authors: Watarai Masahisa , Sato Toshio , Kobayashi Midori , Shimizu Takeshi , Yamasaki Shinji , Tobe Toru , Sasakawa Chihiro , Takeda Yoshifumi 
Published: March 2020

ABSTRACT

Shiga toxins 1 (Stx1) and 2 (Stx2) are encoded by toxin-converting bacteriophages of Stx-producing
Escherichia coli
(STEC), and so far two Stx1- and one Stx2-converting phages have been isolated from two STEC strains (A. D. O’Brien, J. W. Newlands, S. F. Miller, R. K. Holmes, H. W. Smith, and S. B. Formal, Science 226:694–696, 1984). In this study, we isolated two Stx2-converting phages, designated Stx2Φ-I and Stx2Φ-II, from two clinical strains of STEC associated with the outbreaks in Japan in 1996 and found that Stx2Φ-I resembled 933W, the previously reported Stx2-converting phage, in its infective properties for
E. coli
K-12 strain C600 while Stx2Φ-II was distinct from them. The sizes of the plaques of Stx2Φ-I and Stx2Φ-II in C600 were different; the former was larger than the latter. The restriction maps of Stx2Φ-I and Stx2Φ-II were not identical; rather, Stx2Φ-II DNA was approximately 3 kb larger than Stx2Φ-I DNA. Furthermore, Stx2Φ-I and Stx2Φ-II showed different phage immunity, with Stx2Φ-I and 933W belonging to the same group. Infection of C600 by Stx2Φ-I or 933W was affected by environmental osmolarity differently from that by Stx2Φ-II. When C600 was grown under conditions of high osmolarity, the infectivity of Stx2Φ-I and 933W was greatly decreased compared with that of Stx2Φ-II. Examination of the plating efficiency of the three phages for the defined mutations in C600 revealed that the efficiency of Stx2Φ-I and 933W for the
fadL
mutant decreased to less than 10
−7
compared with that for C600 whereas the efficiency of Stx2Φ-II decreased to 0.1% of that for C600. In contrast, while the plating efficiency of Stx2Φ-II for the
lamB
mutant decreased to a low level (0.05% of that for C600), the efficiencies of Stx2Φ-I and 933W were not changed. This was confirmed by the phage neutralization experiments with isolated outer membrane fractions from C600,
fadL
mutant, or
lamB
mutant or the purified His
6
-tagged FadL and LamB proteins. Based on the data, we concluded that FadL acts as the receptor for Stx2Φ-I and Stx2Φ-II whereas LamB acts as the receptor only for Stx2Φ-II.
Fas (CD95)-Dependent Cell-Mediated Immunity toListeria monocytogenes
Authors: Jensen Eric R. , Glass Alison A. , Clark William R. , Wing Edward J. , Miller Jeff F. , Gregory Stephen H. 
Published: March 2020

ABSTRACTTwo distinct and complementary pathways, one mediated by perforin and the other dependent upon CD95 (Fas), effect cell-mediated cytotoxicity. We examined the relative roles of these pathways in host defenses against the intracellular bacterial pathogenListeria monocytogenesby using murine listeriosis as a model system. Mice which lacked both perforin and Fas (P0L0) were generated, and their responses to primary and secondary listeriosis were compared to those of wild-type (WT), Fas-deficient (L0), and perforin knockout (P0) mice. Relative to WT mice during primary listeriosis, P0 mice exhibited a reduced capacity to clear the infection from their spleens but not their livers whereas L0 mice had elevated bacterial titers in their livers and a modestly increased titer in their spleens. In contrast, bacterial titers in P0L0 mice were increased approximately 50- to 560-fold in their spleens and 230- to 1,000-fold in their livers; eventual clearance of listeriae from both organs was significantly delayed. Furthermore, the resistance of P0L0 mice to secondary listeriosis was significantly reduced in their spleens and livers compared to that of WT, P0, or L0 mice. In vitro experiments indicated that immune cytotoxic T lymphocytes (CTL) lysedL. monocytogenes-infected hepatocytes primarily via a Fas-dependent, perforin-independent mechanism. The absence of Fas severely abrogated the lysis of infected hepatocytes by immune CD8+CTL. Taken together, these results provide the first evidence for Fas-dependent CTL-mediated lysis ofL. monocytogenes-infected hepatocytes and demonstrate complementary roles for Fas and perforin in host defenses against an intracellular bacterial pathogen.
Simultaneous Induction of Multiple Antigen-Specific Cytotoxic T Lymphocytes in Nonhuman Primates by Immunization with a Mixture of FourPlasmodium falciparumDNA Plasmids
Authors: Wang Ruobing , Doolan Denise L. , Charoenvit Yupin , Hedstrom Richard C. , Gardner Malcolm J. , Hobart Peter , Tine John , Sedegah Martha , Fallarme Victoria , Sacci John B. , Kaur Manjit , Klinman Dennis M. , Hoffman Stephen L. , Weiss Walter R. 
Published: March 2020

ABSTRACTCD8+T cells have been implicated as critical effector cells in protective immunity against malaria parasites developing within hepatocytes. A vaccine that protects against malaria by inducing CD8+T cells will probably have to include multiple epitopes on the same protein or different proteins, because of parasite polymorphism and genetic restriction of T-cell responses. To determine if CD8+T-cell responses against multipleP. falciparumproteins can be induced in primates by immunization with plasmid DNA, rhesus monkeys were immunized intramuscularly with a mixture of DNA plasmids encoding fourP. falciparumproteins or with individual plasmids. All six monkeys immunized with PfCSP DNA, seven of nine immunized with PfSSP2 DNA, and five of six immunized with PfExp-1 or PfLSA-1 DNA had detectable antigen-specific cytotoxic T lymphocytes (CTL) after in vitro restimulation of peripheral blood mononuclear cells. CTL activity was genetically restricted and dependent on CD8+T cells. By providing the first evidence for primates that immunization with a mixture of DNA plasmids induces CD8+T-cell responses against all the components of the mixture, these studies provide the foundation for multigene immunization of humans.
Identification of an Erythrocyte Binding Peptide from the Erythrocyte Binding Antigen, EBA-175, Which Blocks Parasite Multiplication and Induces Peptide-Blocking Antibodies
Authors: Jakobsen P. H. , Heegaard P. M. H. , Koch C. , Wasniowska K. , Lemnge M. M. , Jensen J. B. , Sim B. K. L. 
Published: March 2020

ABSTRACTA biotinylated peptide covering a sequence of 21 amino acids (aa) from the erythrocyte binding antigen (EBA-175) ofPlasmodium falciparumbound to human glycophorin A, an erythrocyte receptor for merozoites, as demonstrated by enzyme-linked immunosorbent assay (ELISA) and to erythrocytes as demonstrated by flow cytometry analysis. The peptide, EBA(aa1076–96), also bound to desialylated glycophorin A and glycophorin B when tested by ELISA. The peptide blocked parasite multiplication in vitro. The glycophorin A binding sequence was further delineated to a 12-aa sequence, EBA(aa1085–96), by testing the binding of a range of truncated peptides to immobilized glycophorin A. Our data indicate that EBA(aa1085–96) is part of a ligand on the merozoite for binding to erythrocyte receptors. This binding suggests that the EBA(aa1085–96) peptide is involved in a second binding step, independent of sialic acid. Antibody recognition of this peptide sequence may protect against merozoite invasion, but only a small proportion of sera from adults from different areas of malaria transmission showed antibody reactivities to the EBA(aa1076–96) peptide, indicating that this sequence is only weakly immunogenic duringP. falciparuminfections in humans. However, Tanzanian children with acute clinical malaria showed high immunoglobulin G reactivity to the EBA(aa1076–96) peptide compared to children with asymptomaticP. falciparuminfections. The EBA(aa1076–96) peptide sequence from EBA-175 induced antibody formation in mice after conjugation of the peptide with purified protein derivative. These murine sera inhibited EBA(aa1076–96) peptide binding to glycophorin A.
Expression of the Peptide Antibiotic Human β-Defensin 1 in Cultured Gingival Epithelial Cells and Gingival Tissue
Authors: Krisanaprakornkit Suttichai , Weinberg Aaron , Perez Christopher N. , Dale Beverly A. 
Published: March 2020

ABSTRACT

Human β-defensin-1 (hBD-1) is a member of the family of small cationic antimicrobial peptides that have been identified in several mucosal epithelia. Because human gingival epithelium is a site that is constantly challenged by oral microorganisms, we examined the expression of hBD-1 in human gingival epithelial and fibroblast cell cultures and tissue samples. Cell cultures were challenged with cell wall extracts of
Porphyromonas gingivalis
or
Fusobacterium nucleatum
,
Escherichia coli
lipopolysaccharide, tumor necrosis factor alpha, or phorbol myristate acetate. hBD-1 mRNA was detected in unstimulated and stimulated cultures by reverse transcription (RT)-PCR using several primer sets specific for hBD-1. Gingival epithelial cells, but not gingival fibroblasts, expressed a product of the predicted size for hBD-1 mRNA. The sequence of the PCR product was identical to that of hBD-1. hBD-1 mRNA expression was not significantly modulated by any of the stimulants tested. Human gingival tissues from noninflamed and inflamed sites were also analyzed by RT-PCR. hBD-1 mRNA was expressed in all tissue samples. The relative expression of hBD-1 mRNA was similar in noninflamed and inflamed tissues obtained from each of four patients undergoing treatment for periodontitis. However, the relative expression of hBD-1 mRNA varied in gingival biopsies obtained from 15 different normal individuals, and the relative hBD-1 expression was unrelated to interleukin-8 expression. Our findings show the constitutive expression of hBD-1 mRNA in cultured epithelial cells and gingival tissues but not gingival fibroblasts. These findings suggest that expression of hBD-1 may play a role as part of the innate host defenses in maintaining normal gingival health.
Interleukin-4 Enhances Pulmonary Clearance ofPseudomonas aeruginosa
Authors: Jain-Vora Shilpa , LeVine Ann Marie , Chroneos Zissis , Ross Gary F. , Hull William M. , Whitsett Jeffrey A. 
Published: March 2020

ABSTRACTTo determine the effects of interleukin-4 (IL-4) on bacterial clearance from the mouse lung, transgenic mice expressing IL-4 in respiratory epithelial cells under the control of the Clara cell secretory protein promoter (CCSP-IL-4 mice) were infected intratracheally withPseudomonas aeruginosa. Survival of CCSP-IL-4 mice following bacterial administration was markedly improved compared with that of control mice. While bacteria proliferated in lungs of wild-type mice, a rapid reduction in the number of bacteria was observed in the IL-4 mice as early as 6 h postinfection. Similarly, intranasal administration of IL-4 enhanced bacterial clearance from the lungs of wild-type mice. While acute and chronic IL-4 increased the numbers of neutrophils in bronchoalveolar lavage fluid, bacterial infection was associated with acute neutrophilic pulmonary infiltration, and this response was similar in the presence or absence of IL-4. Local administration or expression of IL-4 in the mouse lung enhanced pulmonary clearance ofP. aeruginosain vivo and decreased mortality following infection.
Comparison of Loss of Serum Resistance by Defined Lipopolysaccharide Mutants and an Acapsular Mutant of UropathogenicEscherichia coliO75:K5
Authors: Burns Stacy M. , Hull Sheila I. 
Published: March 2020

ABSTRACTIn order to determine the importance of the O75 O antigen versus the K5 capsular antigen and the bimodal distribution of lipopolysaccharides (LPSs) in protection from complement-mediated lysis, mutants were made by insertion of acator anaphAgene in or in place of genes necessary for the synthesis of LPS and/or the K antigen of an O75+K5+uropathogenicEscherichia colistrain, GR-12. Mutations were made in the following genes: therfbDgene (required for the synthesis of TDP-rhamnose), therfbKMgenes (necessary for the synthesis of GDP-mannose), therolgene (regulating O-antigen length), thekfiCgene (encoding a putative glycosyltransferase), and thekfiC-rfbDgenes. The resulting phenotypes were rough (O75−), core plus one partial O-antigen subunit, random distribution of O-antigen chain lengths, acapsular (K5−), and O75−K5−, respectively. All five mutants and GR-12 were analyzed for survival in 80% serum. The GR-12 parent was resistant, exhibiting a 500% increase in numbers. Therol,rfbKM,rfbD, andkfiC-rfbDmutants were sensitive, experiencing 99%, 99.9%, 99.9%, and at least 99.999% killing, respectively, in the first hour. ThekfiCmutant, however, increased in numbers in the first hour but experienced delayed sensitivity, decreasing in viability by 80% in the third hour. Single mutants were complemented with the wild-type gene intrans, showing restoration of the wild-type phenotype and serum resistance. Therefore, the O75 antigen is more important for survival in serum than the K5 antigen, and regulation of the O75 O-antigen chain length is crucial for protection of the bacteria from complement-mediated lysis.
Cloning and Characterization of
tdhA
, a Locus Encoding a TonB-Dependent Heme Receptor from
Haemophilus ducreyi
Authors: Thomas Christopher E. , Olsen Bonnie , Elkins Christopher 
Published: March 2020

ABSTRACT

Haemophilus ducreyi
is unable to synthesize heme and must acquire it from its only known host, humans. We cloned and sequenced a gene encoding an outer membrane receptor for heme. It was designated
tdhA
(for TonB-dependent heme receptor A) since it was related by sequence homology to the family of TonB-dependent receptors. TdhA was strikingly similar to open reading frame HI0113 from the genome of
Haemophilus influenzae
Rd and also shared homology with five other heme receptors, including HxuC, HemR, HmuR, ChuA, and ShuA, from gram-negative bacteria. An
Escherichia coli hemA tonB
mutant strongly expressing
H. ducreyi tdhA
grew on low levels of heme as a source of heme only when an intact
H. ducreyi
Ton system plasmid was present, formally demonstrating functional TonB dependence.
tdhA
was expressed poorly in vitro by
H. ducreyi
and only under conditions of heme limitation. A survey of
H. ducreyi
revealed that all tested strains but one synthesized small amounts of TdhA in vitro under heme-limiting conditions. Surprisingly, an isogenic mutant of
tdhA
as well as its parent, 35000, both required the same high levels of heme for growth (50 μg/ml [77 μM] on agar medium). This result, together with previous findings, suggests that in vitro, the uptake of heme by
H. ducreyi
is mediated by a TonB- and TdhA-independent mechanism, possibly diffusion.
Humoral Immunity to Commensal Oral Bacteria in Human Infants: Salivary Antibodies Reactive with
Actinomyces naeslundii
Genospecies 1 and 2 during Colonization
Authors: Cole Michael F. , Bryan Stacey , Evans Mishell K. , Pearce Cheryl L. , Sheridan Michael J. , Sura Patricia A. , Wientzen Raoul , Bowden George H. W. 
Published: March 2020

ABSTRACT

The secretory immune response in saliva to colonization by
Actinomyces naeslundii
genospecies 1 and 2 was studied in 10 human infants from birth to 2 years of age.
Actinomyces
species were not recovered from the mouths of the infants until approximately 4 months after the eruption of teeth. However, low levels of secretory immunoglobulin A1 (SIgA1) and SIgA2 antibodies reactive with whole cells of
A. naeslundii
genospecies 1 and 2 were detected within the first month after birth. Although there was a fivefold increase in the concentration of SIgA between birth and age 2 years, there were no differences between the concentrations of SIgA1 and SIgA2 antibodies reactive with
A. naeslundii
genospecies 1 and 2 over this period. When the concentrations of SIgA1 and SIgA2 antibodies reactive with whole cells of
A. naeslundii
genospecies 1 and 2 were normalized to the concentrations of SIgA1 and SIgA2 in saliva, the
A. naeslundii
genospecies 1- and 2-reactive SIgA1 and SIgA2 antibodies showed a significant decrease from birth to 2 years of age. The fine specificities of
A. naeslundii
genospecies 1- and 2-reactive SIgA1 and SIgA2 antibodies were examined by Western blotting of envelope proteins. Similarities in the molecular masses of proteins recognized by SIgA1 and SIgA2 antibodies, both within and between subjects over time, were examined by cluster analysis and showed considerable variability. Taken overall, our data suggest that among the mechanisms
Actinomyces
species employ to persist in the oral cavity are the induction of a limited immune response and clonal replacement with strains differing in their antigen profiles.
Involvement of C3a and C5a in Interleukin-8 Secretion by Human Polymorphonuclear Cells in Response to Capsular Material ofCryptococcus neoformans
Authors: Vecchiarelli Anna , Retini Cinzia , Casadevall Arturo , Monari Claudia , Pietrella Donatella , Kozel Thomas R. 
Published: March 2020

ABSTRACTIn a previous paper we demonstrated that human polymorphonuclear cells (PMN) in the presence of normal human serum (NHS) secrete proinflammatory cytokines in response toCryptococcus neoformansor its major capsular component, glucuronoxylomannan (GXM). The hypothesis that activation of the complement system could be responsible for the observed phenomenon is supported by the fact that encapsulated and acapsularC. neoformansisolates are activators of the complement system and, in particular, large encapsulated isolates are powerful activators. In the present study we demonstrate that (i) interleukin-8 (IL-8) release in response to acapsular or encapsulated strains ofC. neoformansis significantly reduced in the presence of heat-inactivated serum rather than NHS and is completely abrogated in the absence of human serum; (ii) GXM-induced IL-8 release is strictly dependent on the presence of NHS, is inhibited by specific antibodies to either C3a and C5 complement components, and is completely abrogated by the combined use of these antibodies; (iii) the addition of purified C3a and C5a directly stimulates IL-8 release by PMN; and (iv) monoclonal antibody to GXM in combination with GXM or encapsulatedC. neoformanspotentiates IL-8 release by PMN. These data shed light on the mechanism involved in GXM-induced IL-8 secretion by PMN, provide an additional potential role for complement in the control ofC. neoformansinfections, and suggest a complex interplay between the complement system, humoral immunity, and cytokine regulation.