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Atypical Pneumonia

Atypical Pneumonia

Atypical pneumonia, often caused by Mycoplasma pneumoniae, is a form of pulmonary infection that differs from the classical presentation of bacterial pneumonia in both its cause and clinical symptoms. Mycoplasma pneumoniae is a pleomorphic bacterium notable for its lack of a rigid cell wall. This structural characteristic imparts resistance to beta-lactam antibiotics and significantly influences the bacterium’s behavior within the human host.Other pathogens responsible for the disease include...

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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...

Pneumonia I: Introduction

Pneumonia I: Introduction

Pneumonia is an acute respiratory infection that targets the lungs, specifically the alveoli. These tiny air sacs, essential for oxygen exchange, become engorged with pus and fluid, severely hindering breathing, decreasing oxygen absorption, and causing significant pain and discomfort during respiration.
Risk Factors
Various factors influence the likelihood of developing pneumonia. Age plays a crucial role, with infants, children under two, and individuals over 65 at increased risk due to their...

Pneumonia II: Pathophysiology

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:

Pneumonia III: Complications and Assessment

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Pneumonia poses the potential for numerous complications that warrant consideration. These complications include the following:

Adherens Junctions

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Visualization of Streptococcus pneumoniae within Cardiac Microlesions and Subsequent Cardiac Remodeling

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Dectin immunoadhesins and pneumocystis pneumonia.

David M Ricks¹, Kong Chen, Mingquan Zheng

¹Department of Genetics, Louisiana State University Health Sciences Center, New Orleans, Louisiana, USA.

Infection and Immunity

|July 10, 2013

Summary

Researchers developed novel immunoadhesins targeting Pneumocystis jirovecii

Area of Science:

Mycology
Immunology
Pharmacology

Background:

Pneumocystis jirovecii is an opportunistic pathogen causing severe disease in immunocompromised individuals.
Immune reconstitution inflammatory syndrome (IRIS) can arise during recovery from immunosuppression, complicating Pneumocystis infections.
The fungal cell wall component β-(1,3)-glucan is a target for immune modulation and antifungal strategies.

Purpose of the Study:

To develop and characterize novel immunoadhesins targeting β-(1,3)-glucan for potential therapeutic applications against Pneumocystis.
To evaluate the in vitro and in vivo efficacy of Dectin-1:Fc immunoadhesins in targeting Pneumocystis and modulating inflammatory responses.

Main Methods:

Development of immunoadhesins by fusing the Dectin-1 carbohydrate binding domain to murine IgG (mIgG) Fc regions.

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In vitro assays to assess β-glucan binding affinity, cytokine production inhibition, and P. murina viability.

In vivo studies using a murine model of Pneumocystis infection and IRIS to evaluate therapeutic effects.

Main Results:

Dectin-1:Fc immunoadhesins demonstrated high-affinity binding to β-glucan and specificity for Pneumocystis asci.
Dectin-1:mIgG2a Fc reduced P. murina viability via complement-dependent mechanisms.
Dectin-1:mIgG1 Fc reduced fungal burden in vivo and ameliorated hypoxemia in an IRIS model.

Conclusions:

Targeting β-glucan with Dectin-1:Fc immunoadhesins offers a promising strategy for treating Pneumocystis infections.
These engineered molecules can modulate the immune response, potentially mitigating IRIS complications.
Fc subtype variation influences the effector functions, suggesting tailored therapeutic approaches.