# Exacerbations and Management of Asthma in Viral Lower Respiratory Tract Infections: The Significance of Immunoglobulin E

**Authors:** Mandana Akhavan, Parastoo Yousefi, Alireza Tabibzadeh

PMC · DOI: 10.1002/iid3.70386 · Immunity, Inflammation and Disease · 2026-02-25

## TL;DR

The paper explores how high IgE levels may worsen asthma during viral infections and how targeting IgE could help manage asthma symptoms.

## Contribution

The study highlights the role of IgE in asthma exacerbations during viral infections and discusses biological treatments targeting IgE.

## Key findings

- Elevated IgE levels are linked to worsened asthma symptoms during viral lower respiratory tract infections.
- Th2 inflammatory pathways are upregulated during viral infections, leading to increased asthma exacerbations.
- Viral infections can disrupt Th1/Th2 cytokine balance, increasing allergen exposure and asthma severity.

## Abstract

Viral‐respiratory infections are the most prevalent illness among humans. A viral infection affecting lower respiratory tract infections (LRTI) is a critical health concern worldwide. The COVID‐19 pandemic has significantly impacted respiratory health, particularly in individuals with asthma. Other viral respiratory infections and asthma are critical concerns, either. The current study aimed to discuss how elevated IgE levels can influence viral LRTI and potentially exacerbate asthma symptoms, as well as biological treatments targeting IgE in managing asthma.

The search was conducted in electronical databases (including PubMed, Scopus, Google Scholar, and so on). all obtained documents were listed and reviewed by two independent authors. All relevant studies were included and used for final assessment and data collection.

IgE is a crucial mediator in the pathophysiology of asthma, particularly in type 2‐high (T2‐high) asthma, where it drives allergic responses and airway inflammation. The interaction between COVID‐19 and asthma has illustrated that asthmatic patients may experience increased respiratory symptoms following COVID‐19 infection. Interestingly, T2‐high asthmatics may have had some protection against severe COVID‐19 outcomes, highlighting the need for a nuanced understanding of asthma management during and after the pandemic.

Viral infections, particularly those caused by human rhinoviruses, are a significant trigger for asthma exacerbations. These infections can lead to heightened serum IgE levels, which play a vital role in the immune response and the worsening of asthma symptoms. The Th2 inflammatory pathway is frequently upregulated during these infections, associated with increased production of cytokines such as IL‐4, IL‐5, and IL‐13, which aggravate asthma symptoms. Additionally, viral infections can compromise the airway epithelium, resulting in greater exposure to allergens and irritants, and disrupt the balance between Th1 and Th2 cytokines, leading to more severe exacerbations.

## Linked entities

- **Proteins:** IGHE (immunoglobulin heavy constant epsilon), IL4 (interleukin 4), IL5 (interleukin 5), IL13 (interleukin 13)
- **Diseases:** asthma (MONDO:0004979), COVID-19 (MONDO:0100096)

## Full-text entities

- **Genes:** CPT1A (carnitine palmitoyltransferase 1A) [NCBI Gene 1374] {aka CPT I, CPT1, CPT1-L, CPTI-L, L-CPT1}, IL5RA (interleukin 5 receptor subunit alpha) [NCBI Gene 3568] {aka CD125, CDw125, HSIL5R3, IL5R}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, IGHE (immunoglobulin heavy constant epsilon) [NCBI Gene 3497] {aka IgE}, GABARAPL1 (GABA type A receptor associated protein like 1) [NCBI Gene 23710] {aka APG8-LIKE, APG8L, ATG8, ATG8B, ATG8L, GEC1}, DUSP10 (dual specificity phosphatase 10) [NCBI Gene 11221] {aka MKP-5, MKP5}, AHR (aryl hydrocarbon receptor) [NCBI Gene 196] {aka FVH3, RP85, bHLHe76}, STAT6 (signal transducer and activator of transcription 6) [NCBI Gene 6778] {aka D12S1644, HIES6, IL-4-STAT, STAT6B, STAT6C}, IL25 (interleukin 25) [NCBI Gene 64806] {aka IL17E}, ZBTB10 (zinc finger and BTB domain containing 10) [NCBI Gene 65986] {aka RINZF}, ACE2 (angiotensin converting enzyme 2) [NCBI Gene 59272] {aka ACEH}, NEU1 (neuraminidase 1) [NCBI Gene 4758] {aka NANH, NEU, SIAL1}, IL17A (interleukin 17A) [NCBI Gene 3605] {aka CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17}, IL17RB (interleukin 17 receptor B) [NCBI Gene 55540] {aka CRL4, EVI27, IL17BR, IL17RH1}, MAPK8 (mitogen-activated protein kinase 8) [NCBI Gene 5599] {aka JNK, JNK-46, JNK1, JNK1A2, JNK21B1/2, PRKM8}, CD8A (CD8 subunit alpha) [NCBI Gene 925] {aka CD8, CD8alpha, IMD116, Leu2, p32}, CASP2 (caspase 2) [NCBI Gene 835] {aka CASP-2, ICH1, MRT80, NEDD-2, NEDD2, PPP1R57}, IL4R (interleukin 4 receptor) [NCBI Gene 3566] {aka CD124, IL-4RA, IL4RA}, IL13 (interleukin 13) [NCBI Gene 3596] {aka IL-13, P600}, IL5 (interleukin 5) [NCBI Gene 3567] {aka EDF, IL-5, TRF}, FCER1A (Fc epsilon receptor Ia) [NCBI Gene 2205] {aka FCE1A, FCERIA, FcERI}, IFNG (interferon gamma) [NCBI Gene 3458] {aka IFG, IFI, IMD69}, IL4 (interleukin 4) [NCBI Gene 3565] {aka BCGF-1, BCGF1, BSF-1, BSF1, IL-4}
- **Diseases:** airway inflammation (MESH:D007249), LRTI (MESH:D012141), vasculitis (MESH:D014657), respiratory diseases (MESH:D012140), asthmatic (MESH:D013224), Hong Kong flu (MESH:D007251), cyanosis (MESH:D003490), breathlessness (MESH:D004417), RSV infection (MESH:D018357), swelling (MESH:D004487), Allergic asthma (MESH:D001249), common (MESH:D020326), respiratory (MESH:D012131), Pneumonia (MESH:D011014), atopy (MESH:C564133), COPD (MESH:D029424), ARDS (MESH:D012128), respiratory symptoms (MESH:D012818), Viral Infections (MESH:D014777), deaths (MESH:D003643), nasal congestion (MESH:D009668), COVID-19 (MESH:D000086382), infected (MESH:D007239), cardiovascular complications (MESH:D002318), osteoporosis (MESH:D010024), cytotoxicity (MESH:D064420), cough (MESH:D003371), wheezing (MESH:D012135), allergic (MESH:D004342), hemolytic anemia (MESH:D000743), bronchial lesions (MESH:D001982), bronchiolitis (MESH:D001988), communicable diseases (MESH:D003141), chronic (MESH:D002908), Long COVID (MESH:D000094024), tissue damage (MESH:D017695), influenza type A and B. (MESH:D008583)
- **Chemicals:** Benralizumab (MESH:C571386), favipiravir (MESH:C462182), remdesivir (MESH:C000606551), Ribavirin (MESH:D012254), Motavizumab (MESH:C506968), OCS (-), zanamivir (MESH:D053243), Baloxavir (MESH:C000628402), Nirsevimab (MESH:C000709769), oseltamivir (MESH:D053139), lopinavir/ritonavir (MESH:C558899), Mepolizumab (MESH:C434107), Bamlanivimab (MESH:C000711749), Palivizumab (MESH:D000069455), molnupiravir (MESH:C000656703), Laninamivir (MESH:C546918), Omalizumab (MESH:D000069444), viramidine (MESH:C026956)
- **Species:** Mus musculus (house mouse, species) [taxon 10090], Human rhinovirus sp. (species) [taxon 169066], Enterovirus (genus) [taxon 12059], Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Gammacoronavirus (genus) [taxon 694013], H1N1 subtype (serotype) [taxon 114727], Respiratory syncytial virus (no rank) [taxon 12814], Orthomyxoviridae (family) [taxon 11308], Adenoviridae (family) [taxon 10508], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

89 references — full list in the complete paper: https://tomesphere.com/paper/PMC12933411/full.md

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Source: https://tomesphere.com/paper/PMC12933411