Neutrophil Extracellular Traps Exhibit Antibacterial Activity against Burkholderia pseudomallei and Are Influenced by Bacterial and Host Factors

Riyapa, Donporn; Buddhisa, Surachat; Korbsrisate, Sunee; Cuccui, Jon; Wren, Brendan W.; Stevens, Mark P.; Ato, Manabu; Lertmemongkolchai, Ganjana

doi:10.1128/iai.00806-12

Cited by 81 publications

(72 citation statements)

References 43 publications

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“…Mutant strains deficient in either of these components induce higher levels of NET production, which result in increased bacterial killing by NETs compared with wild-type bacteria (37). Increased NET production was mirrored by higher levels of phagocytosis of the mutants with an elevated oxidative burst, implying that the type III protein secretion system and capsular polysaccharide 1 attenuate NET release through inhibition of the NADPH oxidase pathway.…”

Section: Burkholderia Pseudomallei: Net Inhibitionmentioning

confidence: 84%

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Storisteanu¹,

Pocock²,

Cowburn

et al. 2017

Am J Respir Cell Mol Biol

101

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The release of neutrophil extracellular traps (NETs) is a major immune mechanism intended to capture pathogens. These histoneand protease-coated DNA structures are released by neutrophils in response to a variety of stimuli, including respiratory pathogens, and have been identified in the airways of patients with respiratory infection, cystic fibrosis, acute lung injury, primary graft dysfunction, and chronic obstructive pulmonary disease. NET production has been demonstrated in the lungs of mice infected with Staphylococcus aureus, Klebsiella pneumoniae, and Aspergillus fumigatus. Since the discovery of NETs over a decade ago, evidence that "NET evasion" might act as an immune protection strategy among respiratory pathogens, including group A Streptococcus, Bordetella pertussis, and Haemophilus influenzae, has been growing, with the majority of these studies being published in the past 2 years. Evasion strategies fall into three main categories: inhibition of NET release by down-regulating host inflammatory responses; degradation of NETs using pathogen-derived DNases; and resistance to the microbicidal components of NETs, which involves a variety of mechanisms, including encapsulation. Hence, the evasion of NETs appears to be a widespread strategy to allow pathogen proliferation and dissemination, and is currently a topic of intense research interest. This article outlines the evidence supporting the three main strategies of NET evasion-inhibition, degradation, and resistance-with particular reference to common respiratory pathogens.

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Section: Burkholderia Pseudomallei: Net Inhibitionmentioning

confidence: 84%

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Storisteanu¹,

Pocock²,

Cowburn

et al. 2017

Am J Respir Cell Mol Biol

101

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“…During the early phases of infection, macrophages and neutrophils provide essential innate defense against B. pseudomallei. However, macrophages also provide a potential intracellular niche for B. pseudomallei persistence and replication (5)(6)(7)(8)(9)(10)(11).…”

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confidence: 99%

Migration of Dendritic Cells Facilitates Systemic Dissemination of Burkholderia pseudomallei

et al. 2014

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Burkholderia pseudomallei, the etiological agent for melioidosis, is an important cause of community-acquired sepsis in northern Australia and northeast Thailand. Due to the rapid dissemination of disease in acute melioidosis, we hypothesized that dendritic cells (DC) could act as a vehicle for dissemination of B. pseudomallei. Therefore, this study investigated the effect of B. pseudomallei infection on DC migration capacity and whether migration of DC enabled transportation of B. pseudomallei from the site of infection. B. pseudomallei stimulated significantly increased migration of bone marrow-derived DC (BMDC), both in vitro and in vivo, compared to uninfected BMDC. Furthermore, migration of BMDC enabled significantly increased in vitro trafficking of B. pseudomallei and in vivo dissemination of B. pseudomallei to secondary lymphoid organs and lungs of C57BL/6 mice. DC within the footpad infection site of C57BL/6 mice also internalized B. pseudomallei and facilitated dissemination. Although DC have previously been shown to kill intracellular B. pseudomallei in vitro, the findings of this study demonstrate that B. pseudomallei-infected DC facilitate the systemic spread of this pathogen.

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“…They also reported that depletion of Gr-1 ϩ cells increased the susceptibility of mice to B. pseudomallei and resulted in a drastic reduction in TNF-␣, IL-6, and IFN-␥ levels. Neutrophil extracellular traps may also be involved in the response to B. pseudomallei infection (78). Collectively, these data suggest that neutrophils play a major role in the innate defense against melioidosis.…”

Section: Discussionmentioning

confidence: 79%

Burkholderia pseudomallei Capsule Exacerbates Respiratory Melioidosis but Does Not Afford Protection against Antimicrobial Signaling or Bacterial Killing in Human Olfactory Ensheathing Cells

et al. 2016

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g Melioidosis, caused by the bacterium Burkholderia pseudomallei, is an often severe infection that regularly involves respiratory disease following inhalation exposure. Intranasal (i.n.) inoculation of mice represents an experimental approach used to study the contributions of bacterial capsular polysaccharide I (CPS I) to virulence during acute disease. We used aerosol delivery of B. pseudomallei to establish respiratory infection in mice and studied CPS I in the context of innate immune responses. CPS I improved B. pseudomallei survival in vivo and triggered multiple cytokine responses, neutrophil infiltration, and acute inflammatory histopathology in the spleen, liver, nasal-associated lymphoid tissue, and olfactory mucosa (OM). To further explore the role of the OM response to B. pseudomallei infection, we infected human olfactory ensheathing cells (OECs) in vitro and measured bacterial invasion and the cytokine responses induced following infection. Human OECs killed >90% of the B. pseudomallei in a CPS I-independent manner and exhibited an antibacterial cytokine response comprising granulocyte colony-stimulating factor, tumor necrosis factor alpha, and several regulatory cytokines. In-depth genome-wide transcriptomic profiling of the OEC response by RNA-Seq revealed a network of signaling pathways activated in OECs following infection involving a novel group of 378 genes that encode biological pathways controlling cellular movement, inflammation, immunological disease, and molecular transport. This represents the first antimicrobial program to be described in human OECs and establishes the extensive transcriptional defense network accessible in these cells. Collectively, these findings show a role for CPS I in B. pseudomallei survival in vivo following inhalation infection and the antibacterial signaling network that exists in human OM and OECs.

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Neutrophil Extracellular Traps Exhibit Antibacterial Activity against Burkholderia pseudomallei and Are Influenced by Bacterial and Host Factors

Cited by 81 publications

References 43 publications

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Evasion of Neutrophil Extracellular Traps by Respiratory Pathogens

Migration of Dendritic Cells Facilitates Systemic Dissemination of Burkholderia pseudomallei

Burkholderia pseudomallei Capsule Exacerbates Respiratory Melioidosis but Does Not Afford Protection against Antimicrobial Signaling or Bacterial Killing in Human Olfactory Ensheathing Cells

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