<i>Bordetella pertussis</i>entry into respiratory epithelial cells and intracellular survival

Lamberti, Yanina Andrea; Gorgojo, Juan Pablo; Massillo, Cintia; Rodrı́guez, Marı́a Eugenia

doi:10.1111/2049-632x.12072

Cited by 35 publications

(41 citation statements)

References 66 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The invasion at 4 h post infection was quite low (0.032% ± 0.01) and thereafter increased exponentially with highest rates witnessed at 24 h post infection (2.28% ± 0.19). Such long infection periods and/or comparable invasion frequencies have earlier been reported for many bacterial pathogens, including mycoplasmas, which were predominantly known to be extracellular but were subsequently shown to have alternative intracellular lifestyle ( Martin and Mohr, 2000; Dusanic et al, 2009; Marques et al, 2010; Buim et al, 2011; Hopfe et al, 2013; Lamberti et al, 2013 ). The percentage invasion frequency differed slightly for the three cell types.…”

Section: Resultssupporting

confidence: 59%

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

Hegde¹,

Hegde²,

Spergser³

et al. 2014

International Journal of Medical Microbiology

View full text Add to dashboard Cite

Generally regarded as extracellular pathogens, molecular mechanisms of mycoplasma persistence, chronicity and disease spread are largely unknown. Mycoplasma agalactiae, an economically important pathogen of small ruminants, causes chronic infections that are difficult to eradicate. Animals continue to shed the agent for several months and even years after the initial infection, in spite of long antibiotic treatment. However, little is known about the strategies that M. agalactiae employs to survive and spread within an immunocompetent host to cause chronic disease. Here, we demonstrate for the first time its ability to invade cultured human (HeLa) and ruminant (BEND and BLF) host cells. Presence of intracellular mycoplasmas is clearly substantiated using differential immunofluorescence technique and quantitative gentamicin invasion assays. Internalized M. agalactiae could survive and exit the cells in a viable state to repopulate the extracellular environment after complete removal of extracellular bacteria with gentamicin. Furthermore, an experimental sheep intramammary infection was carried out to evaluate its systemic spread to organs and host niches distant from the site of initial infection. Positive results obtained via PCR, culture and immunohistochemistry, especially the latter depicting the presence of M. agalactiae in the cytoplasm of mammary duct epithelium and macrophages, clearly provide the first formal proof of M. agalactiae's capability to translocate across the mammary epithelium and systemically disseminate to distant inner organs. Altogether, the findings of these in vitro and in vivo studies indicate that M. agalactiae is capable of entering host cells and this might be the strategy that it employs at a population level to ward off the host immune response and antibiotic action, and to disseminate to new and safer niches to later egress and once again proliferate upon the return of favorable conditions to cause persistent chronic infections.

show abstract

Section: Resultssupporting

confidence: 59%

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

Hegde¹,

Hegde²,

Spergser³

et al. 2014

International Journal of Medical Microbiology

View full text Add to dashboard Cite

show abstract

“…Although B. pertussis is considered an extracellular pathogen, several studies have documented internalization within myeloid cells and survival in lysosomal compartments as a strategy for the bacterium to evade host defense. [36][37][38] Thus, in these circumstances, bacterial DNA may activate TLR9 in myeloid cells. Moreover, B. pertussis has been shown to use a type III secretion system to inject effector proteins into the eukaryotic cytosol.…”

Section: Discussionmentioning

confidence: 99%

Plasmacytoid dendritic cell-derived IFNα modulates Th17 differentiation during early Bordetella pertussis infection in mice

Smith

You

et al. 2016

Mucosal Immunology

View full text Add to dashboard Cite

Whooping cough is a highly contagious respiratory disease caused by Bordetella pertussis (B. pertussis). T helper 17 (Th17) cells have a central role in the resolution of the infection. Emerging studies document that type I interferons (IFNs) suppress Th17 differentiation and interleukin (IL)-17 responses in models of infection and chronic inflammation. As plasmacytoid dendritic cells (pDCs) are a major source of type I IFNs, we hypothesize that during B. pertussis infection in mice, pDC-derived IFNα inhibits a rapid increase in Th17 cells. We found that IFNα-secreting pDCs appear in the lungs during the early stages of infection, while a robust rise of Th17 cells in the lungs is detected at 15 days post-infection or later. The presence of IFNα led to reduced Th17 differentiation and proliferation in vitro. Furthermore, in vivo blocking of IFNα produced by pDCs during infection with B. pertussis infection resulted in early increase of Th17 frequency, inflammation, and reduced bacterial loads in the airways of infected mice. Taken together, the experiments reported here describe an inhibitory role for pDCs and pDC-derived IFNα in modulating Th17 responses during the early stages of B. pertussis infection, which may explain the prolonged nature of whooping cough.

show abstract

“…Some pathogens have developed ways to reside within the epithelium, such as Bordetella which uses host tubulin activity to enter the epithelial cells. This entry provides protection not only against antibiotic treatment but also against host antimicrobial peptides (28). Pathogens also avoid fusion with acidic lysosomes, which are filled with enzymes that can lyse the bacterial cell wall by manipulating cellular trafficking.…”

Section: How Pathogens Circumvent Phagocytic Abilitymentioning

confidence: 99%

Mechanisms of Epithelial Immunity Evasion by Respiratory Bacterial Pathogens

et al. 2020

View full text Add to dashboard Cite

Bacterial lung infections are major healthcare challenges killing millions of people worldwide and resulting in a huge economic burden. Both basic and clinical research have elucidated host mechanisms that contribute to the bacterial clearance where an indispensable role of immune cells has been established. However, the role of respiratory epithelial cells in bacterial clearance has garnered limited attention due to their weak inflammatory or phagocytic ability compared to immune cells such as macrophages and neutrophils. These studies often underappreciate the fact that epithelial cells are the most abundant cells in the lung, not only serving as building blocks but also providing immune protection throughout the lung. Epithelial cells function either independently to eradicate the pathogen or communicate with immune cells to orchestrate pathogen clearance. The epithelial cells have multiple mechanisms that include mucus production, antimicrobial peptide production, muco-ciliary clearance, and phagocytosis, all of which contribute to their direct antibacterial function. Secretion of cytokines to recruit immune cells and potentiate their antimicrobial activities is a pathway by which the epithelium contributes to bacterial clearance. Successful pathogens outsmart epithelial resistance and find a way to replicate in sufficient numbers to establish infections in the airway or lung epithelial surfaces. In this mini-review, we discuss evidences that establish important roles for epithelial host defense against invading respiratory bacterial pathogens and demonstrate how pathogens outsmart these epithelial immune mechanisms to successfully establish infection. Finally, we discuss briefly how to boost epithelial immunity to improve outcomes in bacterial lung infections.

show abstract

Bordetella pertussisentry into respiratory epithelial cells and intracellular survival

Cited by 35 publications

References 66 publications

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

In vitro and in vivo cell invasion and systemic spreading of Mycoplasma agalactiae in the sheep infection model

Plasmacytoid dendritic cell-derived IFNα modulates Th17 differentiation during early Bordetella pertussis infection in mice

Mechanisms of Epithelial Immunity Evasion by Respiratory Bacterial Pathogens

Contact Info

Product

Resources

About