Internalization of Mycobacterium tuberculosis by macropinocytosis in non-phagocytic cells

Garcı́a-Pérez, Blanca Estela; Mondragón-Flores, Ricardo; Luna-Herrera, Julieta

doi:10.1016/s0882-4010(03)00089-5

Cited by 93 publications

(87 citation statements)

References 32 publications

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“…First, it is apparent that mycobacteria exist in the phagosome of macrophages. However, the subcellular localization of mycobacteria within epithelial cells has not been established, although mycobacteria have been shown to be localized in endosomes or macropinosomes (37,38). Our results revealed colocalization of mycobacteria and dextran, indicating that mycobacteria exist in the endosome-like vacuole within epithelial cells.…”

Section: Discussionmentioning

confidence: 59%

Lipocalin 2-Dependent Inhibition of Mycobacterial Growth in Alveolar Epithelium

Saiga

Nishimura

Kuwata

et al. 2008

The Journal of Immunology

127

134

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Mycobacterium tuberculosis invades alveolar epithelial cells as well as macrophages. However, the role of alveolar epithelial cells in the host defense against M. tuberculosis remains unknown. In this study, we report that lipocalin 2 (Lcn2)-dependent inhibition of mycobacterial growth within epithelial cells is required for anti-mycobacterial innate immune responses. Lcn2 is secreted into the alveolar space by alveolar macrophages and epithelial cells during the early phase of respiratory mycobacterial infection. Lcn2 inhibits the in vitro growth of mycobacteria through sequestration of iron uptake. Lcn2-deficient mice are highly susceptible to intratracheal infection with M. tuberculosis. Histological analyses at the early phase of mycobacterial infection in Lcn2-deficient mice reveal increased numbers of mycobacteria in epithelial cell layers, but not in macrophages, in the lungs. Increased intracellular mycobacterial growth is observed in alveolar epithelial cells, but not in alveolar macrophages, from Lcn2-deficient mice. The inhibitory action of Lcn2 is blocked by the addition of endocytosis inhibitors, suggesting that internalization of Lcn2 into the epithelial cells is a prerequisite for the inhibition of intracellular mycobacterial growth. Taken together, these findings highlight a pivotal role for alveolar epithelial cells during mycobacterial infection, in which Lcn2 mediates anti-mycobacterial innate immune responses within the epithelial cells.

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Section: Discussionmentioning

confidence: 59%

Lipocalin 2-Dependent Inhibition of Mycobacterial Growth in Alveolar Epithelium

Saiga

Nishimura

Kuwata

et al. 2008

The Journal of Immunology

127

134

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“…In contrast, the mechanisms associated with M. tuberculosis infection of the CNS and the specific cells targeted for invasion are mostly unknown. Although studies have described microglia as the preferred cell population infected by M. tuberculosis bacilli during CNS-TB pathogenesis (18,19,20), the ubiquitous nature of M. tuberculosis enables it to infect different cell types, which include both phagocytic and nonphagocytic cells (8,9). Previous studies that investigated the relationship between M. tuberculosis bacilli and cells of the CNS have typically focused on microglia as the principal cellular target for infection (18,34), while astroglia were infected to a lesser extent (19).…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have investigated and reported on different cell types that are targeted by M. tuberculosis bacilli for invasion (8,9,10,11). Among these, macrophages are well described as preferred host cells despite their primary protective function in innate immune responses; the evolutionary development of specific immune evasion mechanisms allows M. tuberculosis to exist within what is essentially a hostile environment.…”

mentioning

confidence: 99%

Neurons Are Host Cells for Mycobacterium tuberculosis

et al. 2014

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“…Mtb was shown in vitro to enter type 1 pneumocytes by macropinocytosis. 82 The M cells overlying the luminal aspect of bronchiolar-associated lymphoid tissue is also a proposed site of entry for Mtb. 199 As mentioned in Table 1, ESAT-6 is cytolytic for type 1 pneumocytes, 118 and necrosis of alveolar epithelium was shown to be a characteristic of virulent Mtb infection.…”

Section: Cellular Responsementioning

confidence: 99%

The Pathology ofMycobacterium tuberculosisInfection

Sakamoto

2012

Vet Pathol

113

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Mycobacterium tuberculosis is an old enemy of the human race, with evidence of infection observed as early as 5000 years ago. Although more host-restricted than Mycobacterium bovis, which can infect all warm-blooded vertebrates, M. tuberculosis can infect, and cause morbidity and mortality in, several veterinary species as well. As M. tuberculosis is one of the earliest described bacterial pathogens, the literature describing this organism is vast and overwhelming. This review strives to distill what is currently known about this bacterium and the disease it causes for the veterinary pathologist.

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Internalization of Mycobacterium tuberculosis by macropinocytosis in non-phagocytic cells

Cited by 93 publications

References 32 publications

Lipocalin 2-Dependent Inhibition of Mycobacterial Growth in Alveolar Epithelium

Lipocalin 2-Dependent Inhibition of Mycobacterial Growth in Alveolar Epithelium

Neurons Are Host Cells for Mycobacterium tuberculosis

The Pathology ofMycobacterium tuberculosisInfection

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