Adherence to, Invasion by, and Cytokine Production in Response to Serotype VIII Group B Streptococci

Mikamo, Hiroshige; Johri, Atul Kumar; Paoletti, Lawrence C.; Madoff, Lawrence C.; Onderdonk, Andrew B.

doi:10.1128/iai.72.8.4716-4722.2004

Cited by 26 publications

(25 citation statements)

References 49 publications

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“…Airway epithelial cells also interact with microbial pathogens, which should be rapidly killed or otherwise they may easily reach the bloodstream. There are reports showing that infection of airway epithelial cells by pathogens such as Streptococcus pneumoniae, Mycoplasma pneumoniae and group B streptococci triggers the secretion of IL-8 and increases the surface levels of ICAM-1 (Doran et al, 2002;Mikamo et al, 2004;Murdoch et al, 2002;Yang et al, 2002). These responses have been related to the recruitment of neutrophils into airways (Look et al, 1992;Tosi et al, 1992Tosi et al, , 1992, which is a common histological finding in patients with pneumonia independently of the infecting micro-organism.…”

Section: Introductionmentioning

confidence: 99%

The uptake of a Klebsiella pneumoniae capsule polysaccharide mutant triggers an inflammatory response by human airway epithelial cells

et al. 2006

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The means by which airway epithelial cells sense a bacterial infection and which intracellular signalling pathways are activated upon infection are poorly understood. A549 cells and human primary airway cells (NHBE) were used to investigate the response to infection with Klebsiella pneumoniae. Infection of A549 and NHBE with K. pneumoniae 52K10, a capsule polysaccharide (CPS) mutant, increased the surface levels of ICAM-1 and caused the release of IL-8. By contrast, the wild-type strain did not elicit these responses. Consistent with a functional role for these responses, there was a correlation between ICAM-1 levels and the number of adherent leukocytes on the epithelial cell surface. In addition, treatment of neutrophils with IL-8 enhanced their ability to kill K. pneumoniae. Strain 52K10 was internalized by A549 cells more efficiently than the wild-type, and when infections with 52K10 were performed in the presence of cytochalasin D the inflammatory response was abrogated. These findings suggest that cellular activation is mediated by bacterial internalization and that CPS prevents the activation through the blockage of bacterial adhesion and uptake. Collectively, the results indicate that bacterial internalization by airway epithelial cells could be the triggering signal for the activation of the innate immune system of the airway. Infection of A549 cells by 52K10 was shown to trigger the nuclear translocation of NF-kB. Evidence is presented showing that 52K10 activated IL-8 production through Toll-like receptor (TLR) 2 and TLR4 pathways and that A549 cells could use soluble CD14 as TLR co-receptor. INTRODUCTIONOne of the largest epithelial surfaces of humans is located in the respiratory tract, which needs to be protected without compromising its functionality. In addition to serving as a physical barrier, airway epithelial cells react against insults such as cigarette smoke or air pollutants, mounting an inflammatory response. This response includes the production of pro-inflammatory and chemoattractant cytokines and the cell-surface expression of the adhesion molecule ICAM-1 (CD54) (Bayram et al., 1998;Hellermann et al., 2002;Hoshino et al., 2001;Mio et al., 1997;Pathmanathan et al., 2003;. Airway epithelial cells also interact with microbial pathogens, which should be rapidly killed or otherwise they may easily reach the bloodstream. There are reports showing that infection of airway epithelial cells by pathogens such as Streptococcus pneumoniae, Mycoplasma pneumoniae and group B streptococci triggers the secretion of IL-8 and increases the surface levels of ICAM-1 (Doran et al., 2002;Mikamo et al., 2004;Murdoch et al., 2002;Yang et al., 2002). These responses have been related to the recruitment of neutrophils into airways (Look et al., 1992;Tosi et al., 1992Tosi et al., , 1992, which is a common histological finding in patients with pneumonia independently of the infecting micro-organism. The current evidence shows that IL-8 targets neutrophils to sites of attack through its chemoattractant and activat...

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Section: Introductionmentioning

confidence: 99%

The uptake of a Klebsiella pneumoniae capsule polysaccharide mutant triggers an inflammatory response by human airway epithelial cells

et al. 2006

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“…However, it is not clear whether the inhibition of apoptosis by the RSV SH protein during RSV infection is due to inhibition of the TNF-␣ pathway. A549 cells, which can produce TNF-␣ but are not sensitive to TNF-␣-induced death (13,20), also displayed an increased level of apoptosis after RSV⌬SH infection compared with that for wild-type infection, suggesting that, while the RSV SH protein may play a role in the TNF-␣ pathway, it may inhibit apoptosis by an alternative mechanism as well.…”

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confidence: 99%

Function of the Respiratory Syncytial Virus Small Hydrophobic Protein

Fuentes¹,

Tran²,

Luthra³

et al. 2007

J Virol

182

174

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Respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, encodes a small hydrophobic (SH) protein of unknown function. Parainfluenza virus 5 (PIV5), a prototypical paramyxovirus, also encodes an SH protein, which inhibits tumor necrosis factor alpha (TNF-␣) signaling. In this study, recombinant PIV5 viruses without their own SH but containing RSV SH (from RSV strain A2 or B1) in its place (PIV5⌬SH-RSV SH) and RSV lacking its own SH (RSV⌬SH) were generated and analyzed. The results indicate that the SH protein of RSV has a function similar to that of PIV5 SH and that it can inhibit TNF-␣ signaling.Human respiratory syncytial virus (RSV) is the leading cause of lower respiratory tract infections in infants and young children (17). RSV, along with the prototype paramyxovirus parainfluenza virus 5 (PIV5; formerly known as simian virus 5), is a member of the Paramyxoviridae family, which includes important human and animal pathogens. Both RSV and PIV5 encode small hydrophobic (SH) proteins, which are type II transmembrane proteins. The SH protein of RSV contains 64 (RSV subgroup A) or 65 (RSV subgroup B) amino acid residues (Fig. 1A) (3)(4)(5)14). Some studies have suggested that the RSV SH protein may have a role in viral fusion (9, 19) or in changing membrane permeability (15). However, RSV lacking the SH gene (RSV⌬SH) is viable, causes syncytium formation, and grows as well as the wild-type virus (1, 10, 11), indicating that the SH protein is not necessary for virus entry into host cells or syncytium formation (19). RSV⌬SH is attenuated in animals, indicating that RSV plays an important role in viral pathogenesis (1). Interestingly, recombinant PIV5 lacking the SH gene (rPIV5⌬SH) has a similar phenotype: it has normal growth in vitro, but it is attenuated in vivo (7). Studies of rPIV5⌬SH have shown that the SH protein is necessary for the inhibition of tumor necrosis factor alpha (TNF-␣)-induced apoptosis in L929 cells (12). Recent work suggests that the SH protein of mumps virus is a functional counterpart of the PIV5 SH protein (22), even though the PIV5 and mumps SH proteins have no sequence homology. We hypothesized that the SH protein of RSV may be functionally similar to other SH proteins from members of the Paramyxoviridae family. To test this hypothesis, recombinant viruses that contained the RSV SH gene of strain A2 or B1 in place of the PIV5 SH gene were produced and confirmed by reverse transcription (RT)-PCR (Fig. 1B). The rPIV5 and rPIV5⌬SH viruses grow to similar titers, although rPIV5⌬SH virus grows slightly faster in the first stages of infection (Fig. 1C) (6, 22). Growth of the rPIV5⌬SH-RSV SH recombinant viruses was comparable to that of rPIV5 and rPIV5⌬SH up to 2 days postinfection (dpi). Occasionally, a delay in the growth of one or both of the recombinant viruses was observed, but by 24 or 36 h the viruses had always reached titers comparable to that of the wild-type virus (Fig. 1C). The plaques formed by the rPIV5, rPIV5⌬SH, and rPIV5⌬SH-RSV SH viruses in BHK cells were of a...

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“…It has a large (80-m 2 ) surface area (38) for spore contact. Several bacterial infectious agents, including Legionella pneumophila and group B streptococci, as well as several viral infectious agents, including respiratory syncytial virus and adenovirus, stimulate lung epithelia to release cytokines and chemokines that activate and recruit inflammatory cells and antigen-presenting cells which are important in the transition to adaptive immunity (1,20,24,32).…”

Section: Discussionmentioning

confidence: 99%

Human Lung Innate Immune Response toBacillus anthracisSpore Infection

Chakrabarty

Booth

et al. 2007

Infect Immun

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Bacillus anthracis, the causative agent of inhalational anthrax, enters a host through the pulmonary system before dissemination. We have previously shown that human alveolar macrophages participate in the initial innate immune response to B. anthracis spores through cell signal-mediated cytokine release. We proposed that the lung epithelia also participate in the innate immune response to this pathogen, and we have developed a human lung slice model to study this process. Exposure of our model to B. anthracis (Sterne) spores rapidly activated the mitogen-activated protein kinase signaling pathways ERK, p38, and JNK. In addition, an RNase protection assay showed induction of mRNA of several cytokines and chemokines. This finding was reflected at the translational level by protein peak increases of 3-, 25-, 9-, 34-, and 5-fold for interleukin-6 (IL-6), tumor necrosis factor alpha, IL-8, macrophage inflammatory protein 1␣/␤, and monocyte chemoattractant protein 1, respectively, as determined by an enzyme-linked immunosorbent assay. Inhibition of individual pathways by UO126, SP600125, and SB0203580 decreased induction of chemokines and cytokines by spores, but this depended on the pathways inhibited and the cytokines and chemokines induced. Combining all three inhibitors reduced induction of all cytokines and chemokines tested to background levels. An immunohistochemistry analysis of IL-6 and IL-8 revealed that alveolar epithelial cells and macrophages and a few interstitial cells are the source of the cytokines and chemokines. Taken together, these data showed the activation of the pulmonary epithelium in response to B. anthracis spore exposure. Thus, the lung epithelia actively participate in the innate immune response to B. anthracis infection through cell signal-mediated elaboration of cytokines and chemokines.

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Adherence to, Invasion by, and Cytokine Production in Response to Serotype VIII Group B Streptococci

Cited by 26 publications

References 49 publications

The uptake of a Klebsiella pneumoniae capsule polysaccharide mutant triggers an inflammatory response by human airway epithelial cells

The uptake of a Klebsiella pneumoniae capsule polysaccharide mutant triggers an inflammatory response by human airway epithelial cells

Function of the Respiratory Syncytial Virus Small Hydrophobic Protein

Human Lung Innate Immune Response toBacillus anthracisSpore Infection

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