Filamentous morphology of bacteria delays the timing of phagosome morphogenesis in macrophages

Prashar, Akriti; Bhatia, Sonam; Gigliozzi, Darren; Martin, Tonya; Duncan, Carla; Guyard, Cyril; Terebiznik, Mauricio R.

doi:10.1083/jcb.201304095

Cited by 56 publications

(103 citation statements)

References 70 publications

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“…It was recently reported that filamentous Legionella pneumophila cells are harder for professional phagocytes to engulf (91). These filaments are slowly phagocytized along the long axis of the cell, resulting in prolonged phagocytic cups that fail to develop complete hydrolytic activity, thus allowing escape of the pathogen from phagosomal killing in a filament length-dependent manner (91). Similar findings have also been reported for uropathogenic E. coli (UPEC), where bacillary cells are preferentially killed over their filamentous counterparts (85).…”

Section: Bigger Is Bettersupporting

confidence: 65%

“…One common theme that has emerged is the use of filamentation to evade phagocytosis-mediated killing by the host. It was recently reported that filamentous Legionella pneumophila cells are harder for professional phagocytes to engulf (91). These filaments are slowly phagocytized along the long axis of the cell, resulting in prolonged phagocytic cups that fail to develop complete hydrolytic activity, thus allowing escape of the pathogen from phagosomal killing in a filament length-dependent manner (91).…”

Section: Bigger Is Bettermentioning

confidence: 99%

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Staying in Shape: the Impact of Cell Shape on Bacterial Survival in Diverse Environments

Yang

Blair

Salama

2016

Microbiol Mol Biol Rev

245

192

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SUMMARYBacteria display an abundance of cellular forms and can change shape during their life cycle. Many plausible models regarding the functional significance of cell morphology have emerged. A greater understanding of the genetic programs underpinning morphological variation in diverse bacterial groups, combined with assays of bacteria under conditions that mimic their varied natural environments, from flowing freshwater streams to diverse human body sites, provides new opportunities to probe the functional significance of cell shape. Here we explore shape diversity among bacteria, at the levels of cell geometry, size, and surface appendages (both placement and number), as it relates to survival in diverse environments. Cell shape in most bacteria is determined by the cell wall. A major challenge in this field has been deconvoluting the effects of differences in the chemical properties of the cell wall and the resulting cell shape perturbations on observed fitness changes. Still, such studies have begun to reveal the selective pressures that drive the diverse forms (or cell wall compositions) observed in mammalian pathogens and bacteria more generally, including efficient adherence to biotic and abiotic surfaces, survival under low-nutrient or stressful conditions, evasion of mammalian complement deposition, efficient dispersal through mucous barriers and tissues, and efficient nutrient acquisition.

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Section: Bigger Is Bettersupporting

confidence: 65%

Section: Bigger Is Bettermentioning

confidence: 99%

Staying in Shape: the Impact of Cell Shape on Bacterial Survival in Diverse Environments

Yang

Blair

Salama

2016

Microbiol Mol Biol Rev

245

192

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“…These filaments display both increased size and aspect ratio, and consequentially their phagocytosis by neutrophils and macrophages is decreased (Horvath et al, 2011; Moller et al, 2012). Even when phagocytosis occurs, it is delayed, leading to disturbed phagosome maturation and decreased killing of ingested filaments (Prashar et al, 2013). One can easily imagine a similar process happening during the slow ingestion of large S. aureus clumps, potentially contributing to survival of staphylococci after phagocytosis.…”

Section: Role Of Clumping/agglutination In Diseasementioning

confidence: 99%

Staphylococcus aureus Aggregation and Coagulation Mechanisms, and Their Function in Host–Pathogen Interactions

Crosby

Kwieciński

Horswill

2016

Advances in Applied Microbiology

121

100

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The human commensal bacterium Staphylococcus aureus can cause a wide range of infections ranging from skin and soft tissue infections to invasive diseases like septicemia, endocarditis, and pneumonia. Muticellular organization almost certainly contributes to S. aureus pathogenesis mechanisms. While there has been considerable focus on biofilm formation and its role in colonizing prosthetic joints and indwelling devices, less attention has been paid to non-surface attached group behavior like aggregation and clumping. S. aureus is unique in its ability to coagulate blood, and it also produces multiple fibrinogen-binding proteins that facilitate clumping. Formation of clumps, which are large, tightly-packed groups of cells held together by fibrin(ogen), has been demonstrated to be important for S. aureus virulence and immune evasion. Clumps of cells are able to avoid detection by the host’s immune system due to a fibrin(ogen) coat that acts as a shield, and the size of the clumps facilitates evasion of phagocytosis. In addition, clumping could be an important early step in establishing infections that involve tight clusters of cells embedded in host matrix proteins, such as soft tissue abscesses and endocarditis. In this review we discuss clumping mechanisms and regulation, as well as what is known about how clumping contributes to immune evasion.

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“…It has been observed that adhering Dr-positive E. coli forms filamentous forms at the cell surface of CHO-hDAF-␣5␤1 (189) or CHO-hDAF (234) cells. Filamentous bacteria residing within the phagosome escaped phagosomal killing as the bacteria manipulated the phagosome compartment by blocking the acquisition of hydrolytic components (235,236). Even though the intracellular vacuole-containing Dr-positive E. coli in HeLa cells lack the characteristics of a degradative compartment (189), no filamentous forms of Afa-or Dr-positive E. coli residing intracellularly have ever been observed.…”

Section: Other Factorsmentioning

confidence: 99%

Pathogenesis of Human Diffusely Adhering Escherichia coli Expressing Afa/Dr Adhesins (Afa/Dr DAEC): Current Insights and Future Challenges

Servin

2014

Clin Microbiol Rev

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SUMMARY The pathogenicity and clinical pertinence of diffusely adhering Escherichia coli expressing the Afa/Dr adhesins (Afa/Dr DAEC) in urinary tract infections (UTIs) and pregnancy complications are well established. In contrast, the implication of intestinal Afa/Dr DAEC in diarrhea is still under debate. These strains are age dependently involved in diarrhea in children, are apparently not involved in diarrhea in adults, and can also be asymptomatic intestinal microbiota strains in children and adult. This comprehensive review analyzes the epidemiology and diagnosis and highlights recent progress which has improved the understanding of Afa/Dr DAEC pathogenesis. Here, I summarize the roles of Afa/Dr DAEC virulence factors, including Afa/Dr adhesins, flagella, Sat toxin, and pks island products, in the development of specific mechanisms of pathogenicity. In intestinal epithelial polarized cells, the Afa/Dr adhesins trigger cell membrane receptor clustering and activation of the linked cell signaling pathways, promote structural and functional cell lesions and injuries in intestinal barrier, induce proinflammatory responses, create angiogenesis, instigate epithelial-mesenchymal transition-like events, and lead to pks -dependent DNA damage. UTI-associated Afa/Dr DAEC strains, following adhesin-membrane receptor cell interactions and activation of associated lipid raft-dependent cell signaling pathways, internalize in a microtubule-dependent manner within urinary tract epithelial cells, develop a particular intracellular lifestyle, and trigger a toxin-dependent cell detachment. In response to Afa/Dr DAEC infection, the host epithelial cells generate antibacterial defense responses. Finally, I discuss a hypothetical role of intestinal Afa/Dr DAEC strains that can act as “silent pathogens” with the capacity to emerge as “pathobionts” for the development of inflammatory bowel disease and intestinal carcinogenesis.

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Filamentous morphology of bacteria delays the timing of phagosome morphogenesis in macrophages

Abstract: Uptake of bacterial filaments by macrophages is characterized by a prolonged phagocytic cup stage and diminished microbicidal activity during phagosome maturation.

Cited by 56 publications

References 70 publications

Staying in Shape: the Impact of Cell Shape on Bacterial Survival in Diverse Environments

Staying in Shape: the Impact of Cell Shape on Bacterial Survival in Diverse Environments

Staphylococcus aureus Aggregation and Coagulation Mechanisms, and Their Function in Host–Pathogen Interactions

Pathogenesis of Human Diffusely Adhering Escherichia coli Expressing Afa/Dr Adhesins (Afa/Dr DAEC): Current Insights and Future Challenges

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