Role of asthma, age, TLR7 and leukocyte subsets
Viral respiratory infections are usually benign but can trigger asthma exacerbations. The factors associated with upper respiratory tract infection (cold) frequency are not fully understood, nor is it clear whether such factors differ between women and men.
To determine which immunological and clinical variables associate with the frequency of self-reported respiratory infections (colds), 150 asthma cases and 151 controls were recruited. Associations between antiviral immune response variables: toll-like receptor (TLR)7/8 gene expression, plasmacytoid dendritic cell (pDC) numbers and interferon-Î±, tumour necrosis factor and interleukin-12 production, and asthma were then examined that might explain cold frequency.
People with asthma cases reported more colds per year (median 3Â versusÂ 2; p<0.001) and had lower baseline TLR7 gene expression (odds ratio 0.12; p=0.02) than controls. Associations between many variables and cold frequency differed between women and men. In women, high blood neutrophil counts (Î²=0.096, p=0.002), and younger age (Î²=âˆ’0.017, p<0.001), but not exposure to children, were independently associated with more frequent colds. In men, low TLR7 expression (Î²=âˆ’0.96, p=0.041) and high CLEC4C gene expression (a marker of pDC; Î²=0.88, p=0.008) were independently associated with more frequent colds. Poor asthma symptom control was independently associated with reduced TLR8 gene expression (Î²=âˆ’1.4, p=0.036) and high body mass index (Î²=0.041, p=0.004).
Asthma, age and markers of inflammation and antiviral immunity in peripheral blood are associated with frequent colds. Interestingly, the variables associated with cold frequency differed between women and men.
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Conflict of interest: L.M. Murray reports grants from Asthma Foundation of Queensland, during the conduct of the study.
Conflict of interest: S.T. Yerkovich has nothing to disclose.
Conflict of interest: M.A. Ferreira has nothing to disclose.
Conflict of interest: J.W. Upham reports grants from AstraZeneca, during the conduct of the study; grants and personal fees from AstraZeneca and GSK, personal fees from Novartis and Boehringer Ingelheim, outside the submitted work.
Support statement: This work was supported by the NHMRC (Australia; grant APP1128010), Asthma Australia and an unrestricted grant from AstraZeneca. Funding information for this article has been deposited with theÂ Crossref Funder Registry.
- ReceivedÂ December 19, 2019.
- AcceptedÂ May 17, 2020.
- Copyright Â©ERS 2020
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