<b>IL-33 mediates multi-walled carbon nanotube (MWCNT)-induced airway hyper-reactivity via the mobilization of innate helper cells in the lung</b>

Beamer, Celine A.; Girtsman, Teri; Seaver, Benjamin P.; Finsaas, Krissy J.; Migliaccio, Christopher T.; Perry, Victoria Kristina; Rottman, James B.; Smith, Dirk E.; Holian, Andrij

doi:10.3109/17435390.2012.702230

Cited by 67 publications

(93 citation statements)

References 74 publications

(107 reference statements)

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“…In addition, a blocking anti‐ST2 antibody or an isotype‐matched control antibody were used during feeding of the diet in ApoE −/− mice (ApoE −/− , anti‐ST2 or ApoE −/− , isotype control). Efficacy of the blocking anti‐ST2 antibody was demonstrated previously 12, 13. At the beginning of the cholesterol‐rich diet, body weight was not different between the groups (Supporting Information Table S1), but there was some variation of serum total cholesterol levels between the groups.…”

Section: Resultsmentioning

confidence: 68%

Atherosclerosis severity is not affected by a deficiency in IL‐33/ST2 signaling

Martin

Palmer

Rodriguez

et al. 2015

Immunity Inflam & Disease

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Interleukin (IL)‐33 is a cytokine of the IL‐1 family, which signals through the ST2 receptor. Previous work demonstrated that the systemic administration of recombinant IL‐33 reduces the development of atherosclerosis in apolipoprotein E‐deficient (ApoE−/−) mice by inducing a Th1‐to‐Th2 shift. The objective of our study was to examine the role of endogenous IL‐33 and ST2 in atherosclerosis. ApoE−/−, IL‐33−/−ApoE−/−, and ST2−/−ApoE−/− mice were fed with a cholesterol‐rich diet for 10 weeks. Additionally, a group of ApoE−/− mice was injected with a neutralizing anti‐ST2 or an isotype control antibody during the period of the cholesterol‐rich diet. Atherosclerotic lesion development was measured by Oil Red O staining in the thoracic‐abdominal aorta and the aortic sinus. There were no significant differences in the lipid‐staining area of IL‐33−/−ApoE−/−, ST2−/−ApoE−/−, or anti‐ST2 antibody‐treated ApoE−/− mice, compared to ApoE−/− controls. The absence of IL‐33 signaling had no major and consistent impact on the Th1/Th2 cytokine responses in the supernatant of in vitro‐stimulated lymph node cells. In summary, deficiency of the endogenously produced IL‐33 and its receptor ST2 does not impact the development of atherosclerosis in ApoE‐deficient mice.

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Section: Resultsmentioning

confidence: 68%

Atherosclerosis severity is not affected by a deficiency in IL‐33/ST2 signaling

Martin

Palmer

Rodriguez

et al. 2015

Immunity Inflam & Disease

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“…For example, alveolar macrophages and the pulmonary epithelium play a crucial role in immune responses induced by pulmonary exposure to CBN, 13,[23][24][25] whereas iv administration of CBN may initiate an immune response through the activation of circulating leukocytes. 26 Our previous studies demonstrated that MWCNT instilled through oropharyngeal aspiration induces IL-33 production in the lung.…”

Section: Discussionmentioning

confidence: 99%

Intravenously delivered graphene nanosheets and multiwalled carbon nanotubes induce site-specific Th2 inflammatory responses via the IL-33/ST2 axis

Wang

Podila²,

Shannahan³

et al. 2013

IJN

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Abstract:Carbon-based nanomaterials (CBN), such as graphene nanosheets (GNS) and multiwalled carbon nanotubes (MWCNT), have been proposed for potential nanomedicine applications such as biomedical devices and carriers for drug delivery. However, our current understanding regarding the systemic toxicity of these CBN through intravenous (iv) injection is limited. In this study, we compare the immune response resulting from GNS and MWCNT exposure. We hypothesize that iv administration of GNS and MWCNT would result in divergent systemic inflammatory responses due to physicochemical differences between these two CBN. In the lungs of C57BL/6 mice, GNS actuate a Th2 immune response 1 day following iv administration, which consists of neutrophilic influx and a significant increase in interleukin (IL)-5, IL-13, IL-33, and its soluble receptor (sST2) in the bronchoalveolar lavage fluid. MWCNT elicited a significant increase in the messenger ribonucleic acid expression of cytokines in the spleen including IL-4 and IL-33, which are associated with an increase in splenic cell differentiation (CD)4 + and CD8 + T-cells in C57BL/6 mice following iv injection. The observed Th2 responses in both the lung and spleen are absent in ST2 -/-mice administrated GNS or MWCNT, suggesting a critical role for IL-33. In conclusion, the use of GNS or MWCNT as nanocarriers for drug delivery may result in Th2 immune responses that are mediated through the IL-33/ST2 axis and therefore may promote adverse allergic reactions.

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“…A targeting construct that replaced exons 1-6 was injected into 129 ES cells, and chimeras were backcrossed onto the C57BL/6 background >10 generations and confirmed using a 377 SNP panel for microsatellite analysis. All experiments were conducted with age-and sexmatched WT or IL-33-deficient mice on a C57BL/6 background obtained from Taconic and have been described elsewhere (51). N. brasiliensis was maintained in the laboratory using established protocols (23).…”

Section: Methodsmentioning

confidence: 99%

IL-33 drives biphasic IL-13 production for noncanonical Type 2 immunity against hookworms

Hung

Lewkowich

Dawson

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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Parasitic helminths are a major cause of chronic human disease, affecting more than 3 billion people worldwide. Host protection against most parasitic helminths relies upon Type 2 cytokine production, but the mechanisms that regulate interleukin (IL) 4 and 13 production from CD4 + T helper 2 cells (T H 2) and innate lymphoid type 2 cells (ILC2s) remain incompletely understood. The epithelial cell-derived cytokines IL-25 and IL-33 promote Type 2 responses, but the extent of functional redundancy between these cytokines is unclear and whether Type 2 memory relies upon either IL-25 or IL-33 is unknown. Herein, we demonstrate a pivotal role for IL-33 in driving primary and anamnestic immunity against the rodent hookworm Nippostrongylus brasiliensis. IL-33-deficient mice have a selective defect in ILC2-derived IL-13 during both primary and secondary challenge infections but generate stronger canonical CD4 + T helper 2 cells responses (IL-4, IgE, mast cells, and basophils) than WT controls. Lack of IL-13 production in IL-33-deficient mice impairs resistin-like molecule beta (RELMβ) expression and eosinophil recruitment, which are two mechanisms that eliminate N. brasiliensis parasites from infected hosts. Thus, IL-33 is requisite for IL-13 but not IL-4-driven Type 2 responses during hookworm infection. mucosal immunity | gastrointestinal nematode | inflammation

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IL-33 mediates multi-walled carbon nanotube (MWCNT)-induced airway hyper-reactivity via the mobilization of innate helper cells in the lung

Cited by 67 publications

References 74 publications

Atherosclerosis severity is not affected by a deficiency in IL‐33/ST2 signaling

Atherosclerosis severity is not affected by a deficiency in IL‐33/ST2 signaling

Intravenously delivered graphene nanosheets and multiwalled carbon nanotubes induce site-specific Th2 inflammatory responses via the IL-33/ST2 axis

IL-33 drives biphasic IL-13 production for noncanonical Type 2 immunity against hookworms

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