Macrophage—Mycobacterium tuberculosis interactions: role of complement receptor 3

Velasco-Velázquez, Marco A.; Barrera, Diana; González-Arenas, Aliesha; Rosales, Carlos; Agramonte-Hevia, José

doi:10.1016/s0882-4010(03)00099-8

Cited by 84 publications

(71 citation statements)

References 50 publications

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“…Once in the alveoli, the bacilli interact with alveolar macrophages through a multitude of different receptors (15,53,113,158,232). Once these innate immune cells are triggered, numerous cytokines and chemokines are released, the activation of a type 1 Thelper cell-mediated immune response occurs, and, ultimately, a granuloma is formed.…”

Section: Overview Of Pathogenesismentioning

confidence: 99%

Central Nervous System Tuberculosis: Pathogenesis and Clinical Aspects

et al. 2008

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SUMMARY Tuberculosis of the central nervous system (CNS) is a highly devastating form of tuberculosis, which, even in the setting of appropriate antitubercular therapy, leads to unacceptable levels of morbidity and mortality. Despite the development of promising molecular diagnostic techniques, diagnosis of CNS tuberculosis relies largely on microbiological methods that are insensitive, and as such, CNS tuberculosis remains a formidable diagnostic challenge. Insights into the basic neuropathogenesis of Mycobacterium tuberculosis and the development of an appropriate animal model are desperately needed. The optimal regimen and length of treatment are largely unknown, and with the rising incidence of multidrug-resistant strains of M. tuberculosis, the development of well-tolerated and effective antibiotics remains a continued need. While the most widely used vaccine in the world largely targets this manifestation of tuberculosis, the BCG vaccine has not fulfilled the promise of eliminating CNS tuberculosis. We put forth this review to highlight the current understanding of the neuropathogenesis of M. tuberculosis, to discuss certain epidemiological, clinical, diagnostic, and therapeutic aspects of CNS tuberculosis, and also to underscore the many unmet needs in this important field.

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Section: Overview Of Pathogenesismentioning

confidence: 99%

Central Nervous System Tuberculosis: Pathogenesis and Clinical Aspects

et al. 2008

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“…2A) or TNF production (Supplemental Fig. 2B CD11b/CD18 (CR3, Mac-1) is an integrin strongly expressed on neutrophils and that acts as a receptor for mycobacteria (41). CD11b is also able to activate Syk to trigger anti-inflammatory properties in innate cells (42).…”

Section: Dcs Infected With Live Bcg Instruct Neutrophils To Produce Imentioning

confidence: 99%

Mycobacteria-Infected Dendritic Cells Attract Neutrophils That Produce IL-10 and Specifically Shut Down Th17 CD4 T Cells through Their IL-10 Receptor

Doz

Lombard

Carreras

et al. 2013

The Journal of Immunology

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Neutrophils participate in the control of mycobacterial infection both by directly eliminating bacilli and by interacting with macrophages and dendritic cells (DCs). Despite host defenses, slow-growing mycobacteria can persist in the host for decades, mostly inside macrophages and DCs, and eventually destroy tissues after exacerbated inflammation. IL-17A–driven neutrophil recruitment may participate in this process. We report that mouse bone marrow–derived DCs infected with live Mycobacterium bovis Bacillus Calmette-Guérin (BCG) produced large amounts of CXCL1 and CXCL2, and attracted neutrophils. After physical contact with DCs infected with live BCG, the neutrophils produced large quantities of the immunosuppressive cytokine IL-10 via the MyD88 and spleen tyrosine kinase pathways. The CD11b integrin was involved in this neutrophil–DC interaction and allowed IL-10 production. TCR OVA transgenic mice immunized with a BCG strain producing OVA mounted an OVA-specific Th17 and Th1 CD4 response. Interestingly, IL-10–producing neutrophils specifically shut down IL-17A production by Th17 CD4 cells, but not IFN-γ production by Th1 cells. This was due to Th17 CD4 cell–restricted expression of the receptor for IL-10. After neutrophil depletion, total mouse lung cells produced less IL-10 but more IL-17A; IFN-γ production was not affected. Therefore, we suggest that during mycobacterial infection, regulatory neutrophils are instructed by infected reservoir DCs to produce IL-10 that specifically targets IL-10Rα–expressing Th17 CD4 T cells. This could be important to control the otherwise exuberant Th17 response.

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“…This interaction is mediated by several M receptors in association with ligands on the bacterium, including the complement receptors CR1, CR3, and CR4, (1)(2)(3)(4)(5)(6), Fc␥Rs (7), mannose/glucan receptors (1,8), CD14 (9,10), scavenger receptors (4), and surfactant protein receptors A (11,12) and D (13). It has also been shown that CD43 (leukosialin; sialophorin) may be important in promoting a stable interaction of mycobacteria with M (14).…”

mentioning

confidence: 99%

CD43 Is Required for Optimal Growth Inhibition of Mycobacterium tuberculosis in Macrophages and in Mice

Randhawa

Ziltener

Merzaban

et al. 2005

The Journal of Immunology

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We explored the role of macrophage (Mφ) CD43, a transmembrane glycoprotein, in the pathogenesis of Mycobacterium tuberculosis. Using gene-deleted mice (CD43−/−), we assessed the association of the bacterium with distinct populations of Mφ and found that CD43−/− Mφ bound less M. tuberculosis than CD43+/+ Mφ. Increased infective doses did not abrogate this difference. However, reduced association due to the absence of CD43 could be overcome by serum components. Mφ from heterozygote mice, which express 50% of wild-type CD43, bound more bacteria than CD43−/− but less than CD43+/+, proving that the gene dose of CD43 correlates with binding of M. tuberculosis. Furthermore, the reduced ability of CD43−/− Mφ to bind bacteria was restricted to mycobacterial species. We also found that the survival and replication of M. tuberculosis within Mφ was enhanced significantly in the absence of CD43, making this the first demonstration that the mechanism of mycobacterial entry influences its subsequent growth. Most importantly, we show here that the absence of CD43 in mice aerogenically infected with M. tuberculosis results in an increased bacterial load during both the acute and chronic stages of infection and more rapid development of granulomas, with greater lung involvement and distinctive cellularity.

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Macrophage—Mycobacterium tuberculosis interactions: role of complement receptor 3

Cited by 84 publications

References 50 publications

Central Nervous System Tuberculosis: Pathogenesis and Clinical Aspects

Central Nervous System Tuberculosis: Pathogenesis and Clinical Aspects

Mycobacteria-Infected Dendritic Cells Attract Neutrophils That Produce IL-10 and Specifically Shut Down Th17 CD4 T Cells through Their IL-10 Receptor

CD43 Is Required for Optimal Growth Inhibition of Mycobacterium tuberculosis in Macrophages and in Mice

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