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Academic literature on the topic 'Anti-mycobacterial Effectors'

Author: Grafiati
Published: 6 September 2023

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Journal articles on the topic "Anti-mycobacterial Effectors"

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Driss, Virginie, Fanny Legrand, Emmanuel Hermann, Sylvie Loiseau, Yann Guerardel, Laurent Kremer, Estelle Adam, Gaëtane Woerly, David Dombrowicz, and Monique Capron. "TLR2-dependent eosinophil interactions with mycobacteria: role of α-defensins." Blood 113, no. 14 (April 2, 2009): 3235–44. http://dx.doi.org/10.1182/blood-2008-07-166595.

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AbstractPeripheral blood and tissue eosinophilia are a prominent feature in allergic diseases and during helminth infections. Eosinophil recruitment also frequently occurs upon mycobacterial infections, particularly in lung granuloma. However, the mechanism by which eosinophils interact with mycobacteria remains largely unknown. Because eosinophils recently have been shown to be involved in innate immune responses, we investigated the direct interactions of eosinophils with Mycobacterium bovis BCG as a study model. We show that live BCG attracts human eosinophils and induces reactive oxygen species (ROS) synthesis, granule protein release, and tumor necrosis factor (TNF)–α secretion. Using anti-TLR2 neutralizing antibodies before exposure of eosinophils to BCG, we showed a critical role of TLR2 signaling in ROS and eosinophil peroxidase release. BCG-induced eosinophil activation is mediated through the p38 mitogen-activated protein (MAP) kinase and nuclear factor (NF)–κB pathways. In addition, a mycobacterial wall component, lipomannan, induced a TLR2-dependent eosinophil activation. In addition, we showed that eosinophils express and produce α-defensins upon stimulation with BCG and lipomannan and that α-defensins could inhibit mycobacterial growth in synergy with eosinophil cationic protein. These results suggest a role for human eosinophils as direct effectors in TLR2-mediated innate immunity against mycobacteria and confer to these cells potent cytotoxic functions through defensin and eosinophil cationic protein production.
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2

Sano, Keisuke, Haruaki Tomioka, Katsumasa Sato, Chiaki Sano, Hideyuki Kawauchi, Shanshan Cai, and Toshiaki Shimizu. "Interaction of Antimycobacterial Drugs with the Anti-Mycobacterium avium Complex Effects of Antimicrobial Effectors, Reactive Oxygen Intermediates, Reactive Nitrogen Intermediates, and Free Fatty Acids Produced by Macrophages." Antimicrobial Agents and Chemotherapy 48, no. 6 (June 2004): 2132–39. http://dx.doi.org/10.1128/aac.48.6.2132-2139.2004.

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ABSTRACT The profiles of the interaction of antimycobacterial drugs with macrophage (MΦ) antimicrobial mechanisms have yet to be elucidated in detail. We examined the effects of various antimycobacterial drugs on the anti-Mycobacterium avium complex (MAC) antimicrobial activity of reactive oxygen intermediates (ROIs), especially of an H2O2-halogen (H2O2-Fe2+-NaI)-mediated bactericidal system, reactive nitrogen intermediates (RNIs), and free fatty acids (FFAs), which are known as central antimicrobial effectors of host MΦs against mycobacterial pathogens. We have found that certain drugs, such as rifampin (RIF), rifabutin (RFB), isoniazid (INH), clofazimine (CLO), and some fluoroquinolones, strongly or moderately reduced the anti-MAC activity of the H2O2-Fe2+-NaI system, primarily by inhibiting the generation of hypohalite ions and in part by interfering with the halogenation reaction of bacterial cell components due to the H2O2-Fe2+-NaI system. This phenomenon is specific to the H2O2-Fe2+-NaI system, since these drugs did not reduce the anti-MAC activity of RNIs and FFAs. From the perspective of the chemotherapy of MAC infections, the present findings indicate an important possibility that certain antimycobacterial drugs, such as rifamycins (RIF and RFB), INH, CLO, and also some types of fluoroquinolones, may interfere with the ROI-mediated antimicrobial mechanisms of host MΦs against intracellular MAC organisms.
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Mattila, Joshua, Olabisi Ojo, Philana Lin, and JoAnne Flynn. "Macrophages and neutrophils in necrotic granulomas from cynomolgus macaques and humans localize to distinct microenvironments and express nitric oxide synthase and arginase enzymes. (117.11)." Journal of Immunology 188, no. 1_Supplement (May 1, 2012): 117.11. http://dx.doi.org/10.4049/jimmunol.188.supp.117.11.

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Abstract Macrophages are abundant in granulomas, the hallmark lesion of tuberculosis (TB), where they engage in activities critical for mycobacterial control. The assortment of macrophage functions, ranging from being the primary anti-mycobacterial effector cell to the primary mycobacterial host cell, underscores the complexity of macrophages in this system. Despite their importance, the molecular phenotypes and functions of granuloma macrophages in human TB are not well understood. In this study, we examined a variety of macrophage markers in non-human primate and human granulomas to better describe macrophage diversity and spatial organization. We identified three myeloid cell markers, including CD68, CD163, and HAM56, that stained populations of macrophages occupying discrete positions in necrotic granulomas that may be relevant to granuloma function. Neutrophils expressed high levels of calprotectin, a small bacteriostatic protein sometimes associated with macrophages, and also localized to specific positions in necrotic granulomas. In addition to phenotypic markers, we identified cell-specific expression of nitric oxide synthase isoforms (iNOS and eNOS) and arginase isoforms (arg1 and arg2) expression in granulomas by biochemical, molecular and immunohistochemical techniques. Both macrophages and neutrophils were determined to express NOS and arg enzymes, including co-expression, suggesting these enzymes with opposing effects act in concert to maintain mycobacterial control.
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Huang, Shouxiong, Manju Sharma, Shuangmin Zhang, Liang Niu, and Xiang Zhang. "Innate-like activation of mucosal-associated invariant T cells in mycobacterial infection." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 114.12. http://dx.doi.org/10.4049/jimmunol.200.supp.114.12.

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Abstract Unlike conventional T cells, mucosal-associated invariant T (MAIT) T cells respond to microbial riboflavin precursor metabolites presented by major histocompatibility complex (MHC)-like molecule MHC-related protein 1 (MR1). Recently, a high percentage of CD8+ T cells reactive to Mycobacterium tuberculosis in humans were identified as MAIT cells instead of conventional MHC class I-restricted T cells. To understand the activation mechanism and effector functions of MAIT cells in mycobacterial infections, we used mycobacterial-incubated human dendritic cells and MR1-overexpressed cells to stimulate primary and clonal human MAIT cells. As a result, the enzyme-linked immunospot assay showed a quick activation kinetics of MAIT cells within hours of mycobacterial stimulation in an MR1-dependent manner. Flow cytometry analysis demonstrated that mycobacterial-incubated antigen presenting cells quickly stimulated primary human MAIT cells to develop a dominant CD69+CD26+phenotype. Activated MAIT cells displayed an enhanced expression of cytokines TNFa, IFNg, IL-17, and granulysin, demonstrating a potential to induce pro-inflammatory and cytolytic responses. Further transcriptomic analysis of the CD69+CD26+subset revealed an integrated activation pathway from conventional CD8+ T cells and natural killer (NK) cells. Especially, activated MAIT cells showed an enhanced gene expression of mitogen-activated protein kinase (MAPK) signaling molecules, NF-kB, T-bet, RORg, and PLZF transcription factors, and pro-inflammatory cytokines and cytolytic molecules. Taken together, our data support that MAIT cells are quickly activated through an innate-like activation mechanism to induce anti-mycobacterial responses.
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Moni, Esther Del florence Ndedi, Patrick Hervé Diboue Betote, Christelle Wayoue Kom, Chimène Félicite Mekoulou Benga, Armelle Deutou Tchamgoue, and Maximilienne Ascension Nyegue. "Inhibitory effects of hydroethanolic extracts from three Cameroonian medicinal plants on proteins inflammation and growth of multi-resistant strains of Mycobacterium tuberculosis." Journal of Drug Delivery and Therapeutics 11, no. 4-S (August 15, 2021): 15–21. http://dx.doi.org/10.22270/jddt.v11i4-s.4930.

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The present work aimed to determine the phytochemical components and evaluate the in vitro anti-inflammatory and anti-mycobacterial effects of hydroethanolic extracts of Allium sativum L bulbs, Drypetes gossweileri S. MOORE stem-barks and Pentadiplandra brazzeana Baill roots against several resistant strains of Mycobacterium tuberculosis. The phytochemical screenings of extracts were carried out according the colorimetric and precipitation tests to reveal the presence of phytochemical compounds. The anti-inflammatory effects of extracts were evaluated using in vitro Bovine Serum Albumin denaturation and proteinase inhibitory action assays. The inhibitory parameters of hydro-ethanol extracts were evaluated by the microdilution method agaisnt Mycobacterium tuberculosis. The phytochemical screening of hydro-ethanol extracts revealed the presence of phenols, polyphenols, flavonoids, alkaloids, cathechic tannins, triterpens, steroids, anthocyanins and leucoanthocyanins. The anti-inflammatory activity of hydro-ethanol extracts of D. gossweileri, P. brazzeana and A. sativum have shown the inhibitory concentrations 50 (IC50) values ranging from 356.70, 183.30 and 226.30 mg/mL for BSA denaturation and 31.92, 33.62 and 56.93 mg/mL for proteinase inhibitory action respectively. The hydroethanolic extracts of D. gossweileri, P. brazzeana and A. sativum exhibited moderate and weak anti-mycobacterial activities with the minimum inhibitory concentrations (MICs) ranging from 312.5 to 2500 μg/mL. A. sativum hydro-ethanol extract has shown the highest anti-mycobacterial activity with MIC of 312.5 μg/mL against isoniazid resistant of M. tuberculosis and extremely resistant drug strain of M. tuberculosis. These results suggest that hydro-ethanol extracts of A. sativum, D. gossweileri and P. brazzeana are efficient against tuberculosis caused by multi-resistant Mycobacterium tuberculosis strains and are able to resorb the inflammation induced during infection. Keywords: Anti-inflammatory activity, Anti-mycobacterial effect, Hydroethanolic extracts, Medicinal plants, Phytochemical screening.
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Hong, Min-Sun, Eun-Soon Son, Sung-Joong Lee, Sun-Kyoung Lee, Ye-Jin Lee, Sun-Dae Song, Sang-Nae Cho, Clifton E. III Barry, and Seok-Yong Eum. "Anti-mycobacterial Effects of the Extract of Humulus japonicus." Korean Journal of Food Science and Technology 46, no. 1 (February 28, 2014): 94–99. http://dx.doi.org/10.9721/kjfst.2014.46.1.94.

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7

Kirman, Joanna, Kathy McCoy, Sarah Hook, Melanie Prout, Brett Delahunt, Ian Orme, Anthony Frank, and Graham Le Gros. "CTLA-4 Blockade Enhances the Immune Response Induced by Mycobacterial Infection but Does Not Lead to Increased Protection." Infection and Immunity 67, no. 8 (August 1, 1999): 3786–92. http://dx.doi.org/10.1128/iai.67.8.3786-3792.1999.

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ABSTRACT The murine immune response to a pulmonary mycobacterial infection is slow to develop, allowing bacterial numbers to increase in the lung for several weeks after infection. We sought to enhance the protective immune response induced during Mycobacterium bovis BCG infection by administering an antibody that blocks the interaction of CTLA-4 with its ligands, CD80 and CD86. We found that injection of anti-CTLA-4 monoclonal antibody (MAb) greatly enhanced and accelerated the immune response, as measured by increased cellularity of the draining mediastinal lymph nodes, and enhanced antigen-inducible proliferation and gamma interferon production by mediastinal lymphocytes in vitro. However, despite the apparently enhanced immune response in the mediastinal lymph node following treatment with anti-CTLA-4 MAb, there was no improvement in clearance of mycobacteria in the lungs, liver, or spleen. Examination of the primary site of infection, the lung, revealed that CTLA-4 blockade had no effect on the number or function of lymphocytes infiltrating the infected lung tissue. Taken together, these data suggest that in vivo CTLA-4 blockade enhances mycobacterial-infection-induced lymphocyte expansion and effector cell cytokine production in the draining lymph node but does not alter the number or function of lymphocytes at the primary site of infection and therefore does not lead to enhanced clearance of the infection.
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8

Spencer, Charles T., Getahun Abate, Azra Blazevic, and Daniel F. Hoft. "Mycobacteria Induce Protective Effector Functions in a Subset of Nonprotective Phosphoantigen-reactive γ9δ2 T cells (43.21)." Journal of Immunology 178, no. 1_Supplement (April 1, 2007): S40. http://dx.doi.org/10.4049/jimmunol.178.supp.43.21.

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Abstract Human γ9δ2 T cells expand and produce protective cytokine and cytolytic responses during mycobacterial infection. γ9δ2 T cells are also stimulated by nonpeptidic phosphoantigens (i.e-IPP, HMB-PP), expressed by intracellular mycobacteria and infected cells. Therefore, purified phosphoantigens could be useful components of new vaccines or immunotherapeutics by stimulating protective γ9δ2 T cells. However, it is unclear whether γ9δ2 T cells induced by phosphoantigens can protect against mycobacterial replication. We show that while BCG-expanded γ9δ2 T cells potently inhibit intracellular mycobacterial growth, IPP/HMB-PP-expanded γ9δ2 T cells fail to inhibit intracellular mycobacteria, although both lyse Daudi targets. TLR co-stimulation during IPP expansion also failed to induce anti-mycobacterial γ9δ2 T cells. TCR spectratyping and CDR3 sequencing demonstrated that BCG-expanded γ9δ2 T cells expressed significantly less TCR sequence diversity than IPP-expanded γ9δ2 T cells. BCG-expanded γ9δ2 T cells respond similarly to BCG- and IPP-stimulation, while IPP-expanded γ9δ2 T cells responded poorly to BCG. BCG appears to stimulate an antigen-specific focusing event in γ9δ2 T cells while IPP acts like a mitogen with broad γ9δ2 T cell reactivity. The antigens and/or co-stimulatory signals required to induce protective γ9δ2 T cells remain to be identified. Support: NIH R01-AI-48391, VTEU NO1-AI-25464
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Shurygina, A. P. S., N. V. Zabolotnykh, T. I. Vinogradova, K. A. Vasilyev, Zh V. Buzitskaya, and M. A. Stukova. "Lung memory T-cell response in mice following intranasal immunization with influenza vector expressing mycobacterial proteins." Russian Journal of Infection and Immunity 10, no. 3 (August 7, 2020): 506–14. http://dx.doi.org/10.15789/2220-7619-iol-1232.

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Improving specific prevention of tuberculosis continues to be a top priority in phthisiology. “Prime-boost” vaccination schemes aim to maintain adequate levels of specific immunity while forming long-term protection. They are based on sequential use of BCG vaccine and new vaccine candidates expressing protective mycobacterial proteins. The development of new tuberculosis prevention approaches requires an understanding of how the anti-tuberculosis immune response forms and which mechanisms provide TB protection. Since tuberculosis is an airborne infection, vaccine effectiveness largely depends on mucosal immunity based on the formation of long-lived, functionally-active memory T-lymphocytes in the respiratory tract. We have previously shown that the influenza vector expressing ESAT-6 and Ag85A mycobacterial proteins (Flu/ESAT-6_Ag85A) in vaccination scheme of intranasal boost immunization resulted in significant increase of BCG's protective effect according to key indicators aggregate data in experimental tuberculosis infection. The aim of this work was to study the effect of intranasal immunization with the Flu/ESAT-6_Ag85A influenza vector on the formation of antigen-specific central and effector memory T cells and the cytokine-producing activity of effector T cells (TEM) in BCG standard and “BCG prime — influenza vector boost” vaccination schemes in mice. Intranasal immunization with the influenza vector has been shown to increase the proportion of antigen-specific CD4+ central memory T cells (TCM) in the pool of activated lymphocytes of lung and spleen reaching significant differences from the BCG group in the percentage of spleen CD4+ TCM (p < 0.01). In contrast to BCG, vaccination with the studied vaccine candidate was accompanied by accumulation of highly differentiated CD8 effector cells in lung, the target organ during tuberculosis infection. Comparative evaluation of the cell-mediated, post-vaccine immune response after immunization with influenzavector-based vaccine candidate (intranasal/mucosal) or BCG vaccine (subcutaneous) showed advantages in the mucosal group: in formation of functionally active subpopulations of effector CD4 and CD8 T lymphocytes (CD44highCD62Llow) in lungs secreting IL-2 as well as polyfunctional cells capable of coproducing two cytokines (IFNγ/TNFα or IFNγ/IL-2) or three cytokines (IFNγ/TNFα/IL-2). Due to their more pronounced effector function, polyfunctional T-lymphocytes can be considered to be potential immunological markers of protective immunity in tuberculosis.
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Via, L. E., R. A. Fratti, M. McFalone, E. Pagan-Ramos, D. Deretic, and V. Deretic. "Effects of cytokines on mycobacterial phagosome maturation." Journal of Cell Science 111, no. 7 (April 1, 1998): 897–905. http://dx.doi.org/10.1242/jcs.111.7.897.

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One of the major mechanisms permitting intracellular pathogens to parasitize macrophages is their ability to alter maturation of the phagosome or affect its physical integrity. These processes are opposed by the host innate and adaptive immune defenses, and in many instances mononuclear phagocytes can be stimulated with appropriate cytokines to restrict the growth of the microorganisms within the phagosomal compartment. Very little is known about the effects that cytokines have on phagosome maturation. Here we have used green fluorescent protein (GFP)-labeled mycobacteria and a fixable acidotropic probe, LysoTracker Red DND-99, to monitor maturation of the mycobacterial phagosome. The macrophage compartments that stained with the LysoTracker probe were examined first. This dye was found to colocalize preferentially with the late endosomal and lysosomal markers rab7 and Lamp1, and with a fluid phase marker chased into the late endosomal compartments. In contrast, LysoTracker showed only a minor overlap with the early endosomal marker rab5. Pathogenic mycobacteria are believed to reside in nonacidified vacuoles sequestered away from late endosomal compartments as a part of their intracellular survival strategy. We examined the status of mycobacterial phagosomes in macrophages from IL-10 knockout mice, in quiescent cells, and in mononuclear phagocytes stimulated with the macrophage-activating cytokine IFN-(gamma). When macrophages were derived from the bone marrow of transgenic IL-10 mice lacking this major deactivating cytokine, colocalization of GFP-fluorescing mycobacteria with the LysoTracker staining appeared enhanced, suggestive of increased acidification of the mycobacterial phagosome relative to macrophages from normal mice. When bone marrow-derived macrophages from normal mice or a J774 murine macrophage cell line were stimulated with IFN-(gamma) and LPS, this resulted in increased colocalization of mycobacteria and LysoTracker, but no statistically significant enhancement was observed in IL-10 transgenic animals. These studies are consistent with the interpretation that proinflammatory and anti-inflammatory cytokines affect maturation of mycobacterial phagosomes. Although multiple mechanisms are likely to be at work, we propose the existence of a direct link between cytokine effects on the host cell and phagosome maturation in the macrophage.
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Books on the topic "Anti-mycobacterial Effectors"

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Fazal, Nadeem. Effector mechanisms of human anti-mycobacterial immunity. Birmingham: University of Birmingham, 1994.

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Conference papers on the topic "Anti-mycobacterial Effectors"

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Madikizela, B., and L. McGaw. "Anti-mycobacterial, cytotoxicity and genotoxicity effects of five traditionally used anti-tuberculosis plants in South Africa." In GA 2017 – Book of Abstracts. Georg Thieme Verlag KG, 2017. http://dx.doi.org/10.1055/s-0037-1608563.

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