Human β-Defensin 2 Is Expressed and Associated with<i>Mycobacterium tuberculosis</i>during Infection of Human Alveolar Epithelial Cells

Rivas-Santiago, Bruno; Schwander, Stephan; Sarabia, Carmen; Diamond, Gill; Klein-Patel, Marcia E.; Hernández-Pando, Rogelio; Ellner, Jerrold J.; Sada, Eduardo

doi:10.1128/iai.73.8.4505-4511.2005

Cited by 155 publications

(147 citation statements)

References 46 publications

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“…6B). In contrast, the mRNA for hBD2 was reproducibly upregulated by infection with M. tuberculosis at 20% oxygen (2.0 6 0.3-fold) (20), and it was much more pronounced at 1% oxygen (5.3 6 1.8-fold; p , 0.001) (Fig. 6C, n = 14).…”

Section: Regulation Of Vdr and Antimicrobial Peptides At Low Oxygen Tmentioning

confidence: 82%

Hypoxia Triggers the Expression of Human β Defensin 2 and Antimicrobial Activity against Mycobacterium tuberculosis in Human Macrophages

Nickel

Busch

Mayer

et al. 2012

The Journal of Immunology

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Low oxygen tension is a metabolic hallmark of chronic infection. To investigate the influence of hypoxia on macrophage biology, we analyzed the interaction between the intracellular pathogen Mycobacterium tuberculosis and primary human macrophages. Although the metabolic activity of extracellular M. tuberculosis was reduced at oxygen levels between 0.5 and 10%, the bacilli remained viable throughout the 4 d of culture. Phagocytosis of virulent M. tuberculosis and the pathogen-induced release of inflammatory cytokines by macrophages were not affected by oxygen levels as low as 1%. However, we detected the upregulation of an antimicrobial effector pathway mediated by the vitamin D receptor and human β defensin 2. This finding was functionally relevant, because intracellular mycobacterial growth was inhibited by 58 ± 8% at 1% O2. We conclude that a hypoxic microenvironment, which is characteristic of infected tissue, supports the efficacy of antimicrobial immunity, in part by the upregulation of the antimicrobial peptide human β defensin 2.

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Section: Regulation Of Vdr and Antimicrobial Peptides At Low Oxygen Tmentioning

confidence: 82%

Hypoxia Triggers the Expression of Human β Defensin 2 and Antimicrobial Activity against Mycobacterium tuberculosis in Human Macrophages

Nickel

Busch

Mayer

et al. 2012

The Journal of Immunology

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“…Crucially, AECs control the composition of ASL. ASL contains anti‐microbial peptides that have been implicated in Mtb resistance, such as β‐defensin 2 (Rivas‐Santiago et al ., 2005), cathelicidin (LL‐37) (Rivas‐Santiago et al ., 2008) and hepcidin (Sow et al ., 2011), as well as a variety of cytokines and chemokines that are secreted by AECs to recruit and activate phagocytes (reviewed in Li et al ., 2012). …”

Section: Cells Involved In the Innate Immune Response To Tb In Humansmentioning

confidence: 99%

“…In contrast, infection of type II epithelial cells by Mtb has been extensively studied in vitro , and Mtb DNA has been detected within these cells in post‐mortem studies (Hernández‐Pando et al ., 2000). Similar to AECs, these cells produce anti‐microbial molecules (Rivas‐Santiago et al ., 2005). Additionally, type II cells produce and secrete pulmonary surfactant, hydrolytic enzymes and hydrolases in the extracellular lining of the lung.…”

Section: Cells Involved In the Innate Immune Response To Tb In Humansmentioning

confidence: 99%

The innate immune response in human tuberculosis

2015

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Summary M ycobacterium tuberculosis (Mtb) infection can be cleared by the innate immune system before the initiation of an adaptive immune response. This innate protection requires a variety of robust cell autonomous responses from many different host immune cell types. However, Mtb has evolved strategies to circumvent some of these defences. In this mini‐review, we discuss these host–pathogen interactions with a focus on studies performed in human cells and/or supported by human genetics studies (such as genome‐wide association studies).

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“…139 Both mouse and human lung and tracheal epithelial cells have been shown to express defensins after infection with Mtb, with data supporting a protective role by these cationic peptides. 177,178 Dendritic cells in the lung can phagocytose Mtb that has crossed the epithelial barrier. Mtb enters by binding the receptor DC-SIGN via the cell wall component ManLAM, with a lesser role played by CR3 and MR. 196 After phagocytosis, the DCs mature and migrate to regional lymph nodes, where they present mycobacterial antigens in the context of major histocompatibility complex (MHC) molecules, as well as CD1, to prime CD4 þ and CD8 þ T cells.…”

Section: Cellular Responsementioning

confidence: 99%

The Pathology of Mycobacterium tuberculosis Infection

Sakamoto

2012

Vet Pathol

122

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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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Human β-Defensin 2 Is Expressed and Associated withMycobacterium tuberculosisduring Infection of Human Alveolar Epithelial Cells

Cited by 155 publications

References 46 publications

Hypoxia Triggers the Expression of Human β Defensin 2 and Antimicrobial Activity against Mycobacterium tuberculosis in Human Macrophages

Hypoxia Triggers the Expression of Human β Defensin 2 and Antimicrobial Activity against Mycobacterium tuberculosis in Human Macrophages

The innate immune response in human tuberculosis

The Pathology of Mycobacterium tuberculosis Infection

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