PacBio sequencing of the plyNCR marker for pneumococcal strain resolution
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB45241 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| Other | ||||
| ERR5985330.fastq.gz | Fastqsanger.gz | |||
| ERR5987040.fastq.gz | Fastqsanger.gz | |||
| ERR5987050.fastq.gz | Fastqsanger.gz | |||
| ERR5987060.fastq.gz | Fastqsanger.gz |
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Project description:Secondary bacterial pneumonia following influenza infection is a significant cause of mortality worldwide. Upper respiratory tract pneumococcal carriage is important as both determinants of disease and population transmission. The immunological mechanisms that contain pneumococcal carriage are well-studied in mice but remain unclear in humans. Loss of this control of carriage following influenza infection is associated with secondary bacterial pneumonia during seasonal and pandemic outbreaks. We used a human type 6B pneumococcal challenge model to show that carriage acquisition induces early degranulation of resident neutrophils and recruitment of monocytes to the nose. Monocyte function associated with clearance of pneumococcal carriage. Prior nasal infection with live attenuated influenza virus induced inflammation, impaired innate function and altered genome-wide nasal gene responses to pneumococcal carriage. Levels of the cytokine IP-10 promoted by viral infection at the time of pneumococcal encounter was positively associated with bacterial density. These findings provide novel insights in nasal immunity to pneumococcus and viral-bacterial interactions during co-infection.
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Project description:Influenza A virus (IAV) predisposes individuals to secondary infections with the bacterium Streptococcus pneumoniae (the pneumococcus). Infections may manifest as pneumonia, sepsis, meningitis or otitis media (OM). It remains controversial as to whether secondary pneumococcal disease is due to the induction of an aberrant immune response or IAV induced immunosuppression. Moreover, as the majority of studies have been performed in the context of pneumococcal pneumonia, it remains unclear how far these findings can be extrapolated to other pneumococcal disease phenotypes. Here, we demonstrate that the viral hemagglutinin (HA) mediates bacterial OM by inducing a pro-inflammatory response in the middle ear cavity in a replication-dependent manner. Importantly, our findings show that it is the inflammatory response that mediates pneumococcal replication; not viral suppression of the immune system or epithelial damage. This study provide the first evidence that HA induced inflammation drives pneumococcal replication in the middle ear cavity, which has important consequences to the treatment of pneumococcal OM.
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Project description:Patients with inflammatory bowel disease (IBD) will be assessed for immunologic response to pneumococcal vaccination. Patients with IBD meet criteria as outlined by the Centers for Disease Control (CDC) for pneumococcal vaccination, yet the investigators have found that pneumococcal vaccination in this population is under-utilized. It is unknown whether or not IBD or IBD-related medications impact the immune response to this recommended vaccine.
Three groups of 25 patients each will be recruited. The first group will consist of outpatients with IBD who are receiving infliximab (Remicade TM) while on concommitant immunosuppressive therapy (with either 6MP, azathioprine, or methotrexate). This group is intended to represent a common ‘heavily immunosuppressed’ patient group with IBD.
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Project description:Streptococcus pneumoniae is a major cause of invasive diseases, such as pneumoniae, meningitis and sepsis resulting in high mortality. The molecular mechanisms and disease developing mechanism underlying pneumococcal infection remain unknown. Previously, we reported that S. pneumoniae β-galactosidase (BgaA) is evolutionarily conserved and contributes to pneumococcal pathogenesis in mouse sepsis model. BgaA is also known to play a role in pneumococcal growth, resistance to human neutrophil opsonophagocytic killing, bacterial adherence to human epithelial cells. In this study, since the detailed role that BgaA plays in sepsis remain unknown, we focused on the role of BgaA in pneumococcal sepsis. Our in vitro assays showed that BgaA promoted bacterial association with human lung epithelial and vascular endothelium cells. BgaA also contributes to pneumococcal survival with human blood by suppressing neutrophils killing, whereas BgaA did not affect pneumococcal survival in mouse blood. In a mouse sepsis model, mice infected with S. pneumoniae bgaA deletion mutant strain exhibited up-regulated host innate immunity pathways, and suppressed tissue damages and blood coagulation as compared to mice infected with the wild-type strain. These results suggest that BgaA works as a multifunctional virulence factor for inducing host tissue damages and blood coagulation. BgaA could be an attractive target for drug and vaccine development.
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