Increased type 2 inflammation post rhinovirus infection in patients with moderate asthma

Southworth, Thomas; Pattwell, Caroline; Khan, Noor; Mowbray, Sarah F.; Strieter, Robert M.; Erpenbeck, Veit J.; Singh, Dave

doi:10.1016/j.cyto.2019.154857

Cited by 26 publications

(23 citation statements)

References 15 publications

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“…Surprisingly, IL-17C protein was not detected in the apical wash samples but was consistently measured in the basolateral medium following HRV infection. This may have implications for in vivo studies, as the polarized basolateral release of IL-17C could mean that IL-17C, in contrast to IL-17A and IL-17E (Southworth et al, 2019), may be difficult to detect in airway surface secretions recovered by lavage or aspiration. This vectorial distribution of IL-17C is not a generalized phenomenon, as other cytokines induced by HRV, including IFN-λ, CXCL10, and HBD2, could be detected in both the apical and basolateral secretions (Warner et al, 2019) (and data not shown), although levels were not necessarily equivalent FIGURE 4 | Basolateral IL-17C release can be induced in response to multiple serotypes of human rhinovirus as can CXCL1.…”

Section: Discussionmentioning

confidence: 99%

Rhinovirus Induces Basolateral Release of IL-17C in Highly Differentiated Airway Epithelial Cells

Jamieson

Wiehler

Michi

2020

Front. Cell. Infect. Microbiol.

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Human rhinovirus (HRV) is a major trigger of acute exacerbations of both asthma and chronic obstructive pulmonary disease. The airway epithelium is the primary site of HRV infection, and responds by releasing proinflammatory and antimicrobial cytokines. Epithelial cells release IL-17C in response to exposure to bacterial, viral, and fungal pathogens. We previously demonstrated a role for HRV in IL-17C production from undifferentiated epithelial cells, and showed that IL-17C could play a role in neutrophil recruitment. To extend these observations, highly differentiated human bronchial epithelial cells (HBE) were infected apically with HRV to assess the effect of dose, time, viral replication, and strain on the IL-17C response. Cellular lysates, and basolateral and apical secretions were analyzed for IL-17C and CXCL1 protein release following HRV or IL-17C stimulation. Upon HRV infection, IL-17C protein was exclusively released basolaterally in a dose-, time-, and viral replication-dependent manner. Several strains of rhinovirus were capable of inducing IL-17C release. Enriched columnar epithelial cell populations contained significantly higher viral titer, and expressed significantly more IL-17C mRNA than enriched basal cell populations. In addition, the kinetic profile of IL-17C release following HRV treatment closely mimics viral shedding kinetics, further implicating the role of rhinovirus replication in IL-17C production. Basolateral treatment of HBEs with IL-17C resulted in a dose-dependent increase in basolateral CXCL1 production. In summary, replicating rhinovirus drives basolateral IL-17C protein release from both apical and basal epithelial cells, which may then act in an autocrine/paracrine manner to promote basolateral CXCL1 protein release.

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Section: Discussionmentioning

confidence: 99%

Rhinovirus Induces Basolateral Release of IL-17C in Highly Differentiated Airway Epithelial Cells

Jamieson

Wiehler

Michi

2020

Front. Cell. Infect. Microbiol.

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“…In vitro studies have suggested that corticosteroids may impair antiviral innate immune responses [15,16] and that ICS use leads to delayed virus clearance [17]. Other studies, however, have shown normal responses in patients on ICS [18]. It is important to note that most studies have been carried out with rhinovirus and there may be differences in the response to other viruses.…”

Section: @Erspublicationsmentioning

confidence: 99%

Inhaled corticosteroids and COVID-19: a systematic review and clinical perspective

2020

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“…The increased risk of respiratory infection with ICS may be due to impairment in innate immune responses with a reduction in neutrophil recruitment [7,8] and a delay in viral clearance in COPD patients [9]. Nonetheless, impairment in immune response was not replicated in a recent study among asthmatic patients on ICS [10]. It is, however, possible that the effect of ICS may vary depending on the type of respiratory infection and patient factors such as the severity of their respiratory condition as well as the physicochemical properties of ICS.…”

Section: Use Of Corticosteroids In Asthma and Copd Patients Without Cmentioning

confidence: 99%

Use of corticosteroids in asthma and COPD patients with or without COVID-19

Hasan

Capstick

Zaidi

et al. 2020

Respiratory Medicine

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The potential detrimental effects of steroids on the immune system to fight viral infections had always been a concern for patients on long term steroids in chronic conditions. A recent warning from WHO on systemic corticosteroid use amid COVID-19 raised suspicion among public and healthcare professionals regarding the safety of steroid use during the SARS-CoV-2 pandemic. The corticosteroids (inhaled and oral) are commonly prescribed in the management of asthma and COPD patients and any unsolicited changes in medications use may lead to potentially severe exacerbations and may risk patient lives. This article provides a critical review of clinical evidence and offers a detailed discussion on the safety and efficacy of corticosteroids in asthma and COPD patients, both with and without COVID-19.

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Increased type 2 inflammation post rhinovirus infection in patients with moderate asthma

Cited by 26 publications

References 15 publications

Rhinovirus Induces Basolateral Release of IL-17C in Highly Differentiated Airway Epithelial Cells

Rhinovirus Induces Basolateral Release of IL-17C in Highly Differentiated Airway Epithelial Cells

Inhaled corticosteroids and COVID-19: a systematic review and clinical perspective

Use of corticosteroids in asthma and COPD patients with or without COVID-19

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