Acute changes in serum immune markers due to swimming in a chlorinated pool

Vlaanderen, Jelle; Veldhoven, Karin van; Font-Ribera, Laia; Villanueva, Cristina M.; Víneis, Paolo; Kogevinas, Manolis; Vermeulen, Roel

doi:10.1289/isee.2016.3661

Cited by 1 publication

(1 citation statement)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2,5 However, there have been reports of an increased prevalence of asthma in individuals exposed to chronic low-dose chlorine, such as swimmers, swimming pool workers, and cleaning staff. [6][7][8][9][10] This suggests that long-term exposure to chlorine gas even at low concentrations may affect the respiratory system. While the effects of high concentrations of acute chlorine exposure have been extensively studied, there have been only a few studies on the effects of low-dose chronic chlorine exposure on asthmatic airways.…”

Section: Introductionmentioning

confidence: 99%

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Shim

Lee

Park

et al. 2019

Allergy

View full text Add to dashboard Cite

Background Chlorine is widely used in daily life as disinfectant. However, chronic exposure to chlorine products aggravates allergic TH2 inflammation and airway hyperresponsiveness (AHR). Innate lymphoid cells (ILCs) in airways contribute to the inception of asthma in association with virus infection, pollution, and excess of nutrient, but it is not known whether chronic chlorine exposure can activate innate immune cells. The aim of this study was to evaluate the impact of chlorine inhalation on the innate immunity such as ILCs and macrophages in relation with the development of asthma by using murine ovalbumin (OVA) sensitization/challenge model. Methods Six‐week‐old female BALB/c mice were sensitized and challenged with OVA in the presence and absence of chronic low‐dose chlorine exposure by inhalation of naturally vaporized gas of 5% sodium hypochlorite solution. AHR, airway inflammatory cells, from BALF and the population of ILCs and macrophages in the lung were evaluated. Results The mice exposed to chlorine with OVA (Cl + OVA group) showed enhanced AHR and eosinophilic inflammation compared to OVA‐treated mice (OVA group). The population of TH2 cells, ILC2s, and ILC3s increased in Cl + OVA group compared with OVA group. CD11cint macrophages also remarkably increased in Cl + OVA group compared with OVA group. The deletion of macrophages by clodronate resulted in reduction of ILC2s and ILC3s population which was restored by adoptive transfer of CD11cint macrophages. Conclusions Chronic chlorine inhalation contributes to the exacerbation of airway inflammation in asthmatic airway by mobilizing pro‐inflammatory macrophage into the lung as well as stimulating group 2 and 3 ILCs.

show abstract

Section: Introductionmentioning

confidence: 99%

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Shim

Lee

Park

et al. 2019

Allergy

View full text Add to dashboard Cite

show abstract

Acute changes in serum immune markers due to swimming in a chlorinated pool

Cited by 1 publication

References 29 publications

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Contact Info

Product

Resources

About

Acute changes in serum immune markers due to swimming in a chlorinated pool

Cited by 1 publication

References 29 publications

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11cintermediate macrophages

Contact Info

Product

Resources

About

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages

Aggravation of asthmatic inflammation by chlorine exposure via innate lymphoid cells and CD11c^intermediate macrophages