The immune interplay between the host and the pathogen in Aspergillus fumigatus lung infection.

Biomed Res Int

Departamento de Análises Clínicas, Toxicológicas e Bromatológicas, Faculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Avenida Do Café, 14040-903 Ribeirão Preto, SP, Brazil.

Published: March 2014


Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

The interplay between Aspergillus fumigatus and the host immune response in lung infection has been subject of studies over the last years due to its importance in immunocompromised patients. The multifactorial virulence factors of A. fumigatus are related to the fungus biological characteristics, for example, structure, ability to grow and adapt to high temperatures and stress conditions, besides capability of evading the immune system and causing damage to the host. In this context, the fungus recognition by the host innate immunity occurs when the pathogen disrupts the natural and chemical barriers followed by the activation of acquired immunity. It seems clear that a Th1 response has a protective role, whereas Th2 reactions are often associated with higher fungal burden, and Th17 response is still controversial. Furthermore, a fine regulation of the effector immunity is required to avoid excessive tissue damage associated with fungal clearance, and this role could be attributed to regulatory T cells. Finally, in this work we reviewed the aspects involved in the complex interplay between the host immune response and the pathogen virulence factors, highlighting the immunological issues and the importance of its better understanding to the development of novel therapeutic approaches for invasive lung aspergillosis.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3745895PMC
http://dx.doi.org/10.1155/2013/693023DOI Listing

Publication Analysis

Top Keywords

interplay host
8
aspergillus fumigatus
8
lung infection
8
host immune
8
immune response
8
virulence factors
8
host
5
immune
4
immune interplay
4
host pathogen
4

Similar Publications

Objective: Leishmaniasis, caused by protozoan parasites of the spp., presents significant global health challenges, with visceral leishmaniasis (VL) and cutaneous leishmaniasis forms causing severe morbidity and mortality. Macrophages serve as primary host cells, where spp.

View Article and Find Full Text PDF

SUMO-modified Tripartite Motif Protein 28 (TRIM28; KAP1) plays a crucial role in repressing endogenous retroelement (ERE) transcription. We previously provided evidence that loss of SUMO-modified TRIM28 triggered by influenza A virus (IAV) infection promotes activation of host antiviral immunity via a mechanism involving derepression of EREs and production of immunostimulatory RNAs. While the IAV NS1 protein might limit consequences of such activation via its dsRNA-binding activity, we hypothesized that other human pathogenic viruses could have evolved more direct strategies to counteract this potential ERE-based defense system.

View Article and Find Full Text PDF

Vertebrate animals and many small DNA and single-stranded RNA viruses that infect vertebrates have evolved to suppress genomic CpG dinucleotides. All organisms and most viruses additionally suppress UpA dinucleotides in protein-coding RNA. Synonymously recoding viral genomes to introduce CpG or UpA dinucleotides has emerged as an approach for viral attenuation and vaccine development.

View Article and Find Full Text PDF

A Viral RNA Silencing Suppressor Modulates Reactive Oxygen Species Levels to Induce the Autophagic Degradation of Dicer-Like and Argonaute-Like Proteins.

Adv Sci (Weinh)

September 2025

State Key Laboratory of Crop Stress Biology for Arid Areas and College of Plant Protection, Northwest A&F University, Yangling, Shaanxi, 712100, P. R. China.

Mounting evidence indicates that viruses exploit elevated reactive oxygen species (ROS) levels to promote replication and pathogenesis, yet the mechanistic underpinnings of this viral strategy remain elusive for many viral systems. This study uncovers a sophisticated viral counter-defense mechanism in the Cryphonectria hypovirus 1 (CHV1)-Fusarium graminearum system, where the viral p29 protein subverts host redox homeostasis to overcome antiviral responses. That p29 directly interacts with and inhibits the enzymatic activity of fungal NAD(P)H-dependent FMN reductase 1 (FMR1), leading to increased ROS accumulation and subsequent autophagy activation is demonstrated.

View Article and Find Full Text PDF

The human microbiota is composed of a complex community of microorganisms essential for maintaining host homeostasis, especially in the gastrointestinal tract. Emerging evidence suggests that dysbiosis is linked to various cancers, including colorectal cancer (CRC). The microbiota contributes to CRC development and progression by influencing inflammation, genotoxic stress, and key cell growth, proliferation, and differentiation pathways.

View Article and Find Full Text PDF