Degradation of Chlamydia trachomatis in human polymorphonuclear leukocytes: an ultrastructural study of peroxidase-positive phagolysosomes

Yong, Elenita C.; Y, E; Chen, W J; Kuo, Cho‐Chou

doi:10.1128/iai.53.2.427-431.1986

Cited by 27 publications

(15 citation statements)

References 15 publications

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“…But we were unable to confirm their finding that degranulation is initiated (24). We indirectly confirmed that lysosomal fusion is normal in the early phase of infection (25), as evidenced by a normal degranulation response to FMLP. Each of the three serovars, however, selectively impaired the respiratory burst upon activation with FMLP but differed from influenza virus in the mode of neutrophil deactivation (8).…”

Section: Discussioncontrasting

confidence: 64%

Inhibition of human neutrophil NADPH oxidase by Chlamydia serovars E, K, and L2

Tauber¹,

Pavlotsky²,

Lin³

et al. 1989

Infect Immun

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The effects of Chlamydia trachomatis (serovars E, K, and L2) on human neutrophil activation were examined with respect to the organisms both as primary agonists and as agents that modulate cell responses to a second stimulus. Unopsonized chlamydiae alone, at ratios of 1.5 to 100 organisms per cell, failed to elicit changes in intracellular calcium or membrane depolarization or to stimulate the respiratory burst or degranulation during 60 min of incubation. Each of these functions except the respiratory burst was also normally activated when chlamydia-infected neutrophils were subsequently stimulated with formylmethionyl leucine phenylalanine or phorbol myristate acetate; the respiratory burst was inhibited 30 to 65%. Inhibition was dependent on live organisms and was maximal within 5 min of incubation. The organisms had no effect on the superoxide (02-) assay, and the site of chlamydial inhibition was determined at the level of the NADPH oxidase itself, not at an intermediate step in the activation cascade. The mechanism of enzyme inactivation could not be determined. These results show that unopsonized chlamydiae do not elicit responses from infected neutrophils and suggest that microbicidal mechanisms other than those dependent on elaboration of toxic oxygen-derived species are required to inactivate chlamydiae.

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Section: Discussioncontrasting

confidence: 64%

Inhibition of human neutrophil NADPH oxidase by Chlamydia serovars E, K, and L2

Tauber¹,

Pavlotsky²,

Lin³

et al. 1989

Infect Immun

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show abstract

“…BMNs were fixed in 2.5% glutaraldehyde in 0.1 M phosphate buffer at pH 7.4 and 4°C and then stained with DAB solution (2.5 mM diaminobenzidine and 0.02% H 2 O 2 in 0.1 M cacodylate, pH 7.2) for 1 h to enhance the electron density of peroxidase-containing vesicles [35]. The cells were postfixed in 1% osmium tetroxide for 1 h at 4°C and then dehydrated with ethanol before being embedded in resin (Quetol-812; Nisshin EM, Tokyo, Japan).…”

Section: Electron Microscopymentioning

confidence: 99%

“…2). Azurophilic granules can be distinguished from other granules by their electron density when stained with DAB, which reacts with endogenous MPO [35]. We analyzed the number of DAB-positive granules in the neutrophils.…”

Section: Azurophilic Granule Exocytosis Is Enhanced In Hv1/vsop-deficmentioning

confidence: 99%

The voltage-gated proton channel Hv1/VSOP inhibits neutrophil granule release

Okochi

Aratani

Adissu

et al. 2015

Journal of Leukocyte Biology

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Neutrophil granule exocytosis is crucial for host defense and inflammation. Neutrophils contain 4 types of granules, the exocytotic release of which is differentially regulated. This exocytosis is known to be driven by diverse mediators, including calcium and nucleotides, but the precise molecular mechanism remains largely unknown. We show in the present study that voltage-gated proton (Hv) channels are necessary for the proper release of azurophilic granules in neutrophils. On activation of NADPH oxidase by PMA and IgG, neutrophils derived from Hvcn1 gene knockout mouse exhibited greater secretion of MPO and elastase than WT cells. In contrast, release of LTF enriched in specific granules was not enhanced in these cells. The excess release of azurophilic granules in Hv1/VSOP-deficient neutrophils was suppressed by inhibiting NADPH oxidase activity and, in part, by valinomycin, a potassium ionophore. In addition, Hv1/VSOP-deficient mice exhibited more severe lung inflammation after intranasal Candida albicans infection than WT mice. These findings suggest that the Hv channel acts to specifically dampen the release of azurophilic granules through, in part, the suppression of increased positive charges at the plasma membrane accompanied by the activation of NADPH oxidase in neutrophils.

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“…Also, PMNs have been shown to take up and degrade chlamydiae via the intracellular antimicrobial peroxidase system. 36 In the case of FcR-mediated uptake of chlamydiae into DC and macrophages, the outcome is probably enhanced processing and presentation of chlamydial antigens for T-cell activation. 37±39 Although the FcR-bearing macrophages and DC have been shown to be involved in anti-chlamydial immunity, 31±33,35,40±44 the present study reveals that a major mechanism for the role of these cells is enhanced antigen presentation for Th1 induction (Fig.…”

Section: Discussionmentioning

confidence: 99%

Fc receptor regulation of protective immunity against Chlamydia trachomatis

et al. 2002

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SUMMARYThe prevailing paradigm for designing potentially ef®cacious vaccines against the obligate intracellular bacterium, Chlamydia trachomatis, advocates regimens capable of inducing a mucosal antigen-speci®c T helper type 1 (Th1) response. However, recent reports indicate that rapid and ef®cient clearance of a secondary infection also requires certain B-cell functions. We investigated the hypothesis that Fc receptor (FcR)-mediated antibody effector mechanisms are important B-cell-related functions involved in controlling a chlamydial genital reinfection. Microbiological analysis of genital chlamydial infection in FcR knockout (FcRKO) mice lacking the activatory FccRI (CD64) and FcRcIII (CD16), as well as the inhibitory FccRIIB1 (CD32), revealed a greater intensity of secondary infection (i.e. bacterial shedding) in FcRx/x as compared to FcR +/+ mice; however, the course of the primary infection was indistinguishable in both animals. Pathologically, FcRKO mice suffered greater ascending infection than immunocompetent wild-type (WT) mice after a secondary infection. Immunological evaluation indicated that the presence of speci®c anti-chlamydial antibodies enhanced chlamydial antigen presentation for induction of a Th1 response by FcRx/x , antigen-presenting cells. In addition, speci®c anti-chlamydial antibodies augmented both macrophage killing of infected epithelial cells by antibody-dependent cellular cytotoxicity (ADCC) and macrophage inhibition of productive growth of chlamydiae in co-cultures. These results indicate that B cells participate in anti-chlamydial immunity via FcR-mediated effector functions of antibodies, which are operative during reinfections. Such effector functions include ADCC, and possibly enhanced uptake, processing and presentation of chlamydial antigens for rapid induction of a Th1 response, all facilitating the early clearance of an infection. These ®ndings suggest that a future anti-chlamydial vaccine should elicit both humoral and T-cell-mediated immune responses for optimal memory response and vaccine ef®cacy.

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Degradation of Chlamydia trachomatis in human polymorphonuclear leukocytes: an ultrastructural study of peroxidase-positive phagolysosomes

Cited by 27 publications

References 15 publications

Inhibition of human neutrophil NADPH oxidase by Chlamydia serovars E, K, and L2

Inhibition of human neutrophil NADPH oxidase by Chlamydia serovars E, K, and L2

The voltage-gated proton channel Hv1/VSOP inhibits neutrophil granule release

Fc receptor regulation of protective immunity against Chlamydia trachomatis

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