Immune Netw.  2019 Oct;19(5):e31. 10.4110/in.2019.19.e31.

The Interplay between Host Immunity and Respiratory Viral Infection in Asthma Exacerbation

• Hossain FM
• Choi JY
• Uyangaa E
• Park SO
• Eo SK

• KMID: 2461195
• DOI: http://doi.org/10.4110/in.2019.19.e31

Abstract

Asthma is one of the most common and chronic diseases characterized by multidimensional immune responses along with poor prognosis and severity. The heterogeneous nature of asthma may be attributed to a complex interplay between risk factors (either intrinsic or extrinsic) and specific pathogens such as respiratory viruses, and even bacteria. The intrinsic risk factors are highly correlated with asthma exacerbation in host, which may be mediated via genetic polymorphisms, enhanced airway epithelial lysis, apoptosis, and exaggerated viral replication in infected cells, resulting in reduced innate immune response and concomitant reduction of interferon (types I, II, and III) synthesis. The canonical features of allergic asthma include strong Th2-related inflammation, sensitivity to non-steroidal anti-inflammatory drugs (NSAIDs), eosinophilia, enhanced levels of Th2 cytokines, goblet cell hyperplasia, airway hyper-responsiveness, and airway remodeling. However, the NSAID-resistant non-Th2 asthma shows a characteristic neutrophilic influx, Th1/Th17 or even mixed (Th17-Th2) immune response and concurrent cytokine streams. Moreover, inhaled corticosteroid-resistant asthma may be associated with multifactorial innate and adaptive responses. In this review, we will discuss the findings of various in vivo and ex vivo models to establish the critical heterogenic asthmatic etiologies, host-pathogen relationships, humoral and cell-mediated immune responses, and subsequent mechanisms underlying asthma exacerbation triggered by respiratory viral infections.

Keyword

Asthma exacerbation; Respiratory tract infection; Innate immunity; Adaptive immunity

MeSH Terms

Adaptive Immunity
Airway Remodeling
Apoptosis
Asthma*
Bacteria
Chronic Disease
Cytokines
Eosinophilia
Goblet Cells
Hyperplasia
Immunity, Innate
Inflammation
Interferons
Neutrophils
Polymorphism, Genetic
Prognosis
Respiratory Hypersensitivity
Respiratory Tract Infections
Risk Factors
Rivers
Cytokines
Interferons