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Pneumonia I: Introduction

Pneumonia I: Introduction

Pneumonia is an infection of the lower respiratory tract that leads to inflammation of the lung parenchyma, often resulting in the accumulation of inflammatory exudate in the alveoli and airways. Unlike the watery, low-protein fluid exudate in pulmonary edema, the exudate in this case is a thick fluid rich in immune cells, proteins, and debris produced during infection and inflammation.This impairs gas exchange and can lead to consolidation of lung tissue. The infection may be caused by a...

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Related Experiment Video

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Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma

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NLRP3 and ASC differentially affect the lung transcriptome during pneumococcal pneumonia.

Miriam H van Lieshout¹, Brendon P Scicluna, Sandrine Florquin

¹1 Center of Infection and Immunity, Amsterdam, The Netherlands; and.

American Journal of Respiratory Cell and Molecular Biology

|October 30, 2013

Summary

The apoptosis-associated speck-like protein containing a caspase activation and recruitment domain (ASC) adaptor is crucial for controlling Streptococcus pneumoniae pneumonia. ASC deficiency leads to increased bacterial spread and mortality, suggesting roles beyond the NLRP3 inflammasome.

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A Fast and Reliable Pipeline for Bacterial Transcriptome Analysis Case study: Serine-dependent Gene Regulation in Streptococcus pneumoniae

A Fast and Reliable Pipeline for Bacterial Transcriptome Analysis Case study: Serine-dependent Gene Regulation in Streptococcus pneumoniae

Published on: April 25, 2015

Area of Science:

Immunology
Microbiology
Genetics

Background:

Streptococcus pneumoniae causes community-acquired pneumonia, a major global mortality cause.
Inflammasomes, multiprotein complexes regulating inflammation, involve sensors like NLRP3 and adaptors like ASC.
Understanding inflammasome roles in bacterial pneumonia is critical for developing targeted therapies.

Purpose of the Study:

To investigate the distinct roles of NLRP3 and ASC in host defense against S. pneumoniae pneumonia.
To compare bacterial pathogenesis and innate immune responses in wild-type, Nlrp3(-/-), and Asc(-/-) mice.
To identify key immune mediators differentially regulated by NLRP3 and ASC during infection.

Main Methods:

Comparative analysis of bacterial growth, dissemination, and survival in wild-type, Nlrp3(-/-), and Asc(-/-) mice infected with S. pneumoniae.
Whole-genome transcriptional profiling of lung tissue to assess early inflammatory responses.
Quantification of cytokine and immune cell marker expression.

Main Results:

Asc(-/-) mice exhibited significantly increased bacterial dissemination and mortality compared to Nlrp3(-/-) mice.
Both Nlrp3(-/-) and Asc(-/-) mice showed impaired cytokine responses.
Transcriptional profiling revealed differential expression of IL-17, GM-CSF, and integrin-αM, with notable attenuation in Asc(-/-) mice.

Conclusions:

ASC plays a critical role in controlling S. pneumoniae dissemination and lethality, potentially through both NLRP3-dependent and -independent inflammasome pathways.
ASC's function extends beyond NLRP3 inflammasomes, involving regulation of adaptive immune responses.
These findings highlight ASC as a key regulator in pneumonia pathogenesis and suggest novel therapeutic targets.