Mycobacterium tuberculosis with different virulence reside within intact phagosomes and inhibit phagolysosomal biogenesis in alveolar macrophages of patients with pulmonary tuberculosis

Ufimtseva, Elena; Eremeeva, Natalya; Bayborodin, Sergey I.; Umpeleva, Tatiana; Vakhrusheva, Diana; Skornyakov, Sergey

doi:10.1016/j.tube.2018.12.002

Cited by 12 publications

(34 citation statements)

References 43 publications

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“…This apparent difference in the impact of clinical pathology on the expression of C1q is obviously due to core differences between the physiopathology of TB and LF. Indeed, since C1q is produced by phagocytotic cells such as macrophages and dendritic cells (Castellano et al 2004; Loos et al 1989), LF worms and microfilaria (> 1100 μm) that are too large to be phagocyted (Gray and Lawrence 2002) may have less impact on the C1q producing phagocytic cells compared to Mycobacterium tuberculosis which persistence mechanism consists in inhibiting the intracellular maturation of phagolysosome in these cells (Ufimtseva et al 2019). Aging is another factor known to affect the expression of C1q (Kouser et al 2015).…”

Section: Discussionmentioning

confidence: 99%

IgG4 antibodies from patients with asymptomatic bancroftian filariasis inhibit the binding of IgG1 and IgG2 to C1q in a Fc-Fc-dependent mechanism

2019

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A striking feature of lymphatic filariasis (LF) is the clinical heterogeneity among exposed individuals. While endemic normals (EN) remain free of infection despite constant exposure to the infective larvae, a small group of patients, generally microfilaria free (Mf-) develops severe pathology (CP) such as lymphedema or hydrocele. Another group of infected individuals remains asymptomatic while expressing large amounts of microfilariae (Mf+). This Mf+ group is characterized by an immune-suppressed profile with high levels of anti-inflammatory cytokines and elevated IgG4. This particular immunoglobulin is unable to activate the complement. The complement system plays a critical role in both innate and adaptive immunity. However, its importance and regulation during LF is not fully understood. Using affinity chromatography and solid-phase-enzyme-immunoassays, we investigated the ability of antibody isotypes from LF clinical groups to bind C1q, the first element of the complement’s classical pathway. The results indicate that while C1q is similarly expressed in all LF clinical groups, IgG1–2 in the plasma from Mf+ individuals presented significantly lower affinity to C1q compared to EN, Mf−, and CP. In addition, selective depletion of IgG4 significantly enhanced the affinity of IgG1–2 to C1q in Mf+ individuals. Strikingly, no effect was seen on the ability of IgG3 to bind C1q in the same conditions. More interestingly, papain-generated IgG4-Fc-portions interacted with Fc portions of IgG1–2 as revealed by far-western blot analysis. These data suggest that while being unable to bind C1q, IgG4 inhibits the first steps of the complement classical pathway by IgG1 or IgG2 via Fc-Fc interactions.Electronic supplementary materialThe online version of this article (10.1007/s00436-019-06451-2) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

IgG4 antibodies from patients with asymptomatic bancroftian filariasis inhibit the binding of IgG1 and IgG2 to C1q in a Fc-Fc-dependent mechanism

2019

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“…Mtb can survive and replicate in alveolar macrophages (Ufimtseva et al, 2019), evading host defence mechanisms and developing the latent disease. Considering that phagocytes can localize and internalize foreign substances, such as polymeric particles, this fact could guide particles to the interior of macrophages, leading to an exciting approach to the treatment of intracellular infections affecting the mononuclear phagocytic system.…”

Section: Graphical Abstractmentioning

confidence: 99%

Recent advances in PLGA micro/nanoparticle delivery systems as novel therapeutic approach for drug-resistant tuberculosis

Shao¹,

Shěn²,

Liu³

2022

Front. Bioeng. Biotechnol.

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Tuberculosis is a severe infectious disease caused by Mycobacterium tuberculosis and is a significant public health concern globally. The World Health Organization (WHO) recommends a combination regimen of several drugs, such as rifampicin (RIF), isoniazid (INH), pyrazinamide (PZA), and ethambutol (ETB), to treat tuberculosis. However, these drugs have low plasma concentrations after oral administration and require multiple high doses, which may lead to the occurrence and development of drug-resistant tuberculosis. Micro/Nanotechnology drug delivery systems have considerable potential in treating drug-resistant tuberculosis, allowing the sustained release of the drug and delivery of the drug to a specific target. These system properties could improve drug bioavailability, reduce the dose and frequency of administration, and solve the problem of non-adherence to the prescribed therapy. This study systematically reviewed the recent advances in PLGA micro/nanoparticle delivery systems as a novel therapeutic approach for drug-resistant tuberculosis.

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“…Mycobacterium tuberculosis ( Mtb ) is the etiologic agent of TB. It can invade various organ systems of the body, using macrophages as the main host cells, causing bone TB, TB pneumonia, tuberculous meningitis, and pulmonary TB (PTB) 3 . Among them, PTB accounts for 75% of TB cases and greatly increases mortality 4 .…”

Section: Introductionmentioning

confidence: 99%

“…It can invade various organ systems of the body, using macrophages as the main host cells, causing bone TB, TB pneumonia, tuberculous meningitis, and pulmonary TB (PTB). 3 Among them, PTB accounts for 75% of TB cases and greatly increases mortality. 4 Symptom assessment, radiological examination, and microbiological examination are the commonly used diagnostic methods, but they have different drawbacks.…”

Section: Introductionmentioning

confidence: 99%

Diagnostic value of lncRNA NORAD in pulmonary tuberculosis and its regulatory role in Mycobacterium tuberculosis infection of macrophages

Sun

Zhang

et al. 2022

Microbiology and Immunology

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Pulmonary tuberculosis (PTB) infection is a chronic inflammatory response caused by Mycobacterium tuberculosis (Mtb). The purpose of this study was to confirm the value of long noncoding RNA NORAD (noncoding RNA activated by DNA damage) in the diagnosis of PTB and to explore its mechanism in Mtb-infected macrophages. NORAD serum levels were estimated by qRT-PCR in 90 patients with PTB and 85 healthy individuals. Receiver operating characteristic curves were plotted to assess the diagnostic value of NORAD in PTB. Human and murine macrophages were infected with Mtb strain H37Rv. CCK-8 (a cell counting kit) and ELISA detected viability of macrophages and inflammatory cytokine secretion, respectively. A dual-luciferase reporter assay was performed to analyze the relationship between NORAD and microRNA (miR)-618. NORAD was significantly elevated in patients with PTB, and its positivity was correlated with levels of inflammatory cytokines IL-1 β (r = 0.854), TNF-α (r = 0.617), and IL-6 (r = 0.585). With an area under the curve of 0.918, and sensitivity and specificity of 80.0% and 89.4%, respectively, NORAD remarkedly differentiated patients with PTB from healthy individuals. Furthermore, Mtb infection significantly increased NORAD levels in THP-1 and RAW264.7 cells and increased their viability and inflammation (P < 0.001). However, this increased effect was weakened by reduced NORAD levels. Dual-luciferase reporter assay results confirmed that miR-618 in macrophages is a target miRNA for NORAD and can be negatively regulated by it. Moreover, elevated miR-618 suppressed macrophage viability and inflammation in Mtb infection. NORAD is a potential diagnostic biomarker for PTB and is involved in Mtb-infected macrophage activity and inflammation by targeting miR-618.

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Mycobacterium tuberculosis with different virulence reside within intact phagosomes and inhibit phagolysosomal biogenesis in alveolar macrophages of patients with pulmonary tuberculosis

Cited by 12 publications

References 43 publications

IgG4 antibodies from patients with asymptomatic bancroftian filariasis inhibit the binding of IgG1 and IgG2 to C1q in a Fc-Fc-dependent mechanism

IgG4 antibodies from patients with asymptomatic bancroftian filariasis inhibit the binding of IgG1 and IgG2 to C1q in a Fc-Fc-dependent mechanism

Recent advances in PLGA micro/nanoparticle delivery systems as novel therapeutic approach for drug-resistant tuberculosis

Diagnostic value of lncRNA NORAD in pulmonary tuberculosis and its regulatory role in Mycobacterium tuberculosis infection of macrophages

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