Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.

Early life respiratory insults, such as viral infections or hyperoxia, often increase asthma susceptibility later in life. The mechanisms underlying this increased susceptibility are not fully understood. IL-33 has been shown to be critically involved in allergic airway diseases. IL-33 expression in...

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Autores principales:	Koji Iijima, Takao Kobayashi, Koji Matsumoto, Kenzo Ohara, Hirohito Kita, Li Y Drake
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2021
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/8674b6cc803c40de941da94a8e24fa89
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spelling	oai:doaj.org-article:8674b6cc803c40de941da94a8e24fa892021-12-02T20:05:26ZTransient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.1932-620310.1371/journal.pone.0252199https://doaj.org/article/8674b6cc803c40de941da94a8e24fa892021-01-01T00:00:00Zhttps://doi.org/10.1371/journal.pone.0252199https://doaj.org/toc/1932-6203Early life respiratory insults, such as viral infections or hyperoxia, often increase asthma susceptibility later in life. The mechanisms underlying this increased susceptibility are not fully understood. IL-33 has been shown to be critically involved in allergic airway diseases. IL-33 expression in the neonatal lung can be increased by various respiratory insults associated with asthma development. Therefore, we investigated whether and how early life increases in IL-33 impact allergic airway responses later in life. Using a novel IL-33 transgenic mouse model, in which full-length IL-33 was inducible overexpressed in lung epithelial cells, we transiently upregulated lung IL-33 expression in neonatal mice for one week. After resting for 4-6 weeks, mice were intranasally exposed to a single-dose of recombinant IL-33 or the airborne allergen Alternaria. Alternatively, mice were exposed to Alternaria and ovalbumin multiple times for one month. We found that a transient increase in IL-33 expression during the neonatal period promoted IL-5 and IL-13 production when mice were later exposed to a single-dose of IL-33 or Alternaria in adulthood. However, increased IL-33 expression during the neonatal period did not affect airway inflammation, type 2 cytokine production, lung mucus production, or antigen-specific antibody responses when adult mice were exposed to Alternaria and ovalbumin multiple times. These results suggest that transient increased IL-33 expression early in life may have differential effects on allergic airway responses in later life, preferentially affecting allergen-induced acute type 2 cytokine production.Koji IijimaTakao KobayashiKoji MatsumotoKenzo OharaHirohito KitaLi Y DrakePublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 16, Iss 5, p e0252199 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Koji Iijima Takao Kobayashi Koji Matsumoto Kenzo Ohara Hirohito Kita Li Y Drake Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.
description	Early life respiratory insults, such as viral infections or hyperoxia, often increase asthma susceptibility later in life. The mechanisms underlying this increased susceptibility are not fully understood. IL-33 has been shown to be critically involved in allergic airway diseases. IL-33 expression in the neonatal lung can be increased by various respiratory insults associated with asthma development. Therefore, we investigated whether and how early life increases in IL-33 impact allergic airway responses later in life. Using a novel IL-33 transgenic mouse model, in which full-length IL-33 was inducible overexpressed in lung epithelial cells, we transiently upregulated lung IL-33 expression in neonatal mice for one week. After resting for 4-6 weeks, mice were intranasally exposed to a single-dose of recombinant IL-33 or the airborne allergen Alternaria. Alternatively, mice were exposed to Alternaria and ovalbumin multiple times for one month. We found that a transient increase in IL-33 expression during the neonatal period promoted IL-5 and IL-13 production when mice were later exposed to a single-dose of IL-33 or Alternaria in adulthood. However, increased IL-33 expression during the neonatal period did not affect airway inflammation, type 2 cytokine production, lung mucus production, or antigen-specific antibody responses when adult mice were exposed to Alternaria and ovalbumin multiple times. These results suggest that transient increased IL-33 expression early in life may have differential effects on allergic airway responses in later life, preferentially affecting allergen-induced acute type 2 cytokine production.
format	article
author	Koji Iijima Takao Kobayashi Koji Matsumoto Kenzo Ohara Hirohito Kita Li Y Drake
author_facet	Koji Iijima Takao Kobayashi Koji Matsumoto Kenzo Ohara Hirohito Kita Li Y Drake
author_sort	Koji Iijima
title	Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.
title_short	Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.
title_full	Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.
title_fullStr	Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.
title_full_unstemmed	Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.
title_sort	transient il-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.
publisher	Public Library of Science (PLoS)
publishDate	2021
url	https://doaj.org/article/8674b6cc803c40de941da94a8e24fa89
work_keys_str_mv	AT kojiiijima transientil33upregulationinneonatalmouselungpromotesacutebutnotchronictype2immuneresponsesinducedbyallergenlaterinlife AT takaokobayashi transientil33upregulationinneonatalmouselungpromotesacutebutnotchronictype2immuneresponsesinducedbyallergenlaterinlife AT kojimatsumoto transientil33upregulationinneonatalmouselungpromotesacutebutnotchronictype2immuneresponsesinducedbyallergenlaterinlife AT kenzoohara transientil33upregulationinneonatalmouselungpromotesacutebutnotchronictype2immuneresponsesinducedbyallergenlaterinlife AT hirohitokita transientil33upregulationinneonatalmouselungpromotesacutebutnotchronictype2immuneresponsesinducedbyallergenlaterinlife AT liydrake transientil33upregulationinneonatalmouselungpromotesacutebutnotchronictype2immuneresponsesinducedbyallergenlaterinlife
_version_	1718375492500848640

Transient IL-33 upregulation in neonatal mouse lung promotes acute but not chronic type 2 immune responses induced by allergen later in life.

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