Toxicity and Mechanisms of Engineered Nanoparticles in Animals with Established Allergic Asthma

Figures & data

Table 1 The Occurrence Count and Centrality Score of Keywords in the Co-Occurrence Analysis for the 194 Articles Related to Allergic Asthma and Nanoparticles in the Web of Science Core Collection. Information is Provided for the Keywords with Occurrence Counts Greater Than 10

Keywords	Occurrence Count	Centrality Score	Year of the First Occurrence
Asthma	49	0.18	2010
Airway inflammation	35	0.18	2006
Nanoparticle	26	0.11	2013
Oxidative stress	20	0.11	2007
Allergic asthma	19	0.07	2009
Dendritic cell	18	0.35	2008
Murine model	18	0.08	2012
Diesel exhaust particle	17	0.13	2008
Expression	17	0.10	2003
Inflammation	17	0.08	2013
Air pollution	15	0.10	2008
Allergic airway inflammation	15	0.09	2008
Toxicity	15	0.09	2010
In vitro	15	0.07	2008
Response	14	0.22	2010
Cell	14	0.13	2008
Exposure	14	0.05	2009
Particle	13	0.10	2014
Immune response	13	0.06	2013
Mechanism	11	0.06	2013
Drug delivery	11	0.05	2006
Ultrafine particle	10	0.10	2010
Allergic inflammation	10	0.07	2010
Activation	10	0.04	2009
Antigen	10	0.03	2009
Carbon nanotube	10	0.02	2007

Table 2 Top 25 Keywords with the Strongest Occurrence Bursts in the Keyword Burst Analysis for the 194 Articles Related to Allergic Asthma and Nanoparticles in the Web of Science Core Collection

Keywords	Strength	Begin	End	2003–2022
Oxidative stress	2.54	2007	2011	▂▂▂▂▃▃▃▃▃▂▂▂▂▂▂▂▂▂▂▂
Carbon nanotube	1.69	2007	2014	▂▂▂▂▃▃▃▃▃▃▃▃▂▂▂▂▂▂▂▂
Diesel exhaust particle	5.99	2008	2012	▂▂▂▂▂▃▃▃▃▃▂▂▂▂▂▂▂▂▂▂
Antigen presenting cell	2.31	2009	2012	▂▂▂▂▂▂▃▃▃▃▂▂▂▂▂▂▂▂▂▂
Cytokine expression	2.29	2009	2013	▂▂▂▂▂▂▃▃▃▃▃▂▂▂▂▂▂▂▂▂
Bacterial endotoxin	2.20	2009	2011	▂▂▂▂▂▂▃▃▃▂▂▂▂▂▂▂▂▂▂▂
Lung inflammation	2.00	2009	2012	▂▂▂▂▂▂▃▃▃▃▂▂▂▂▂▂▂▂▂▂
Particulate matter	1.95	2009	2010	▂▂▂▂▂▂▃▃▂▂▂▂▂▂▂▂▂▂▂▂
Ultrafine particle	1.82	2010	2013	▂▂▂▂▂▂▂▃▃▃▃▂▂▂▂▂▂▂▂▂
Alveolar macrophage	1.66	2011	2016	▂▂▂▂▂▂▂▂▃▃▃▃▃▃▂▂▂▂▂▂
Hyperresponsiveness	2.51	2012	2013	▂▂▂▂▂▂▂▂▂▃▃▂▂▂▂▂▂▂▂▂
Epithelial cell	2.00	2012	2015	▂▂▂▂▂▂▂▂▂▃▃▃▃▂▂▂▂▂▂▂
Mice	3.55	2013	2014	▂▂▂▂▂▂▂▂▂▂▃▃▂▂▂▂▂▂▂▂
Mouse model	3.02	2013	2015	▂▂▂▂▂▂▂▂▂▂▃▃▃▂▂▂▂▂▂▂
Particle	2.62	2014	2017	▂▂▂▂▂▂▂▂▂▂▂▃▃▃▃▂▂▂▂▂
Exposure	1.83	2014	2015	▂▂▂▂▂▂▂▂▂▂▂▃▃▂▂▂▂▂▂▂
Disease	2.04	2015	2018	▂▂▂▂▂▂▂▂▂▂▂▂▃▃▃▃▂▂▂▂
lung	3.32	2016	2018	▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▃▂▂▂▂
Apoptosis	1.67	2016	2018	▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▃▂▂▂▂
Mechanism	3.15	2017	2018	▂▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▂▂▂▂
Nanoparticle	3.11	2017	2022	▂▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▃▃▃▃
Regulatory T cell	2.23	2018	2022	▂▂▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▃▃▃
Antigen	2.03	2018	2019	▂▂▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▂▂▂
Inflammation	2.28	2019	2022	▂▂▂▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▃▃
Delivery	2.47	2020	2022	▂▂▂▂▂▂▂▂▂▂▂▂▂▂▂▂▂▃▃▃

Figure 1 The visual network of the keyword co-occurrence analysis for the 194 articles related to allergic asthma and nanoparticles in the Web of Science Core Collection. Colored squares represent different keywords extracted from the articles. The size and color of a specific square represent the occurrence count and the year of the first occurrence of the corresponding keyword, respectively. Labels are provided for the squares of keywords with occurrence counts greater than 10.

Table 3 The Occurrence Count and Centrality Score of Keywords in the Co-Occurrence Analysis for the 54 Articles Discussed in Detail in This Review. Information is Provided for the Keywords with Occurrence Counts Greater Than 5

Keywords	Occurrence Count	Centrality Score	Year of the First Occurrence
Airway inflammation	16	0.19	2010
Asthma	14	0.20	2010
Exposure	13	0.12	2009
Expression	10	0.08	2007
Lung	9	0.26	2012
Oxidative stress	9	0.09	2005
Carbon nanotube	8	0.22	2007
Immune response	8	0.17	2014
Mouse model	8	0.38	2013
Murine model	8	0.00	2005
Particle	8	0.25	2009
Allergic asthma	7	0.03	2012
Epithelial cell	7	0.11	2012
Inflammation	7	0.12	2012
Toxicity	7	0.01	2011
Allergic airway inflammation	6	0.06	2009
Disease	6	0.00	2011
Response	6	0.05	2009
Activation	5	0.02	2010
Cell	5	0.04	2012
Dendritic cell	5	0.19	2005
Inhalation exposure	5	0.18	2012

Figure 2 The visual network of the keyword co-occurrence analysis for the 54 articles discussed in detail in this review. Colored squares represent different keywords extracted from the articles. The size and color of a specific square represent the occurrence count and the year of the first occurrence of the corresponding keyword, respectively. Labels are provided for the squares of keywords with occurrence counts greater than 5.

Figure 3 The number of articles closely related to the effects of NPs on the development and exacerbation of allergic asthma. An article investigating both Au and TiO₂ NPs is counted twice.

Table 4 Studies on the Effects of NPs on Established Allergic Asthma

NPs	Species	Allergen	NPs Exposure				Result	Reference
			Dose Per Time	Time	Route	Order
MWCNTs	Male B6C3F1/N mice	HDM	0.06, 0.2, 0.6 mg/m^3	30	Whole-body inhalation	Before sensitization phase	MWCNTs pre-exposure altered the immune response to allergens.	[22]
MWCNTs	C57BL/6 mice	HDM	50 µg	1	Intratracheal instillation	After challenge phase	MWCNTs had adverse inflammatory effects in individuals suffering from atopic asthma.	[23]
MWCNTs	Male C57BL/6 mice	HDM	2 mg/kg	1	Oropharyngeal aspiration	After sensitization phase	MWCNTs exacerbated the allergen-induced airway fibrosis via suppressing inflammasome activation and IL-1β in the lung.	[24]
MWCNTs	Male wild-type mice and Stat1^−/− mice	OVA	4 mg/kg	1	Oropharyngeal aspiration	After challenge phase	MWCNTs exacerbated airway remodeling and transcription factor STAT1 played a protective role in allergen-induced airway inflammation.	[25]
MWCNTs	Male Balb/cByJ mice	HDM	75 or 225 μg	3 or 10	Intranasal instillation	During sensitization phase	MWCNTs exhibited a dose-dependent manner in enhancing systemic immune response, as well as airway inflammation and remodeling.	[26]
MWCNTs	Wild-type C57BL/6J mice and COX-2^−/− mice	OVA	4 mg/kg	1	Oropharyngeal aspiration	After challenge phase	The exacerbating effects of MWCNTs on OVA-induced airway inflammation and mucus-cell metaplasia were intensified via the deficiencies of COX-2.	[27]
MWCNTs	Male Balb/c mice	OVA	0.3, 3, 30 µg	6	Intranasal instillation	During sensitization phase	The combination of MWCNTs with OVA enhanced allergic asthmatic responses.	[28]
MWCNTs	Male ICR mice	OVA	25, 50 µg	7	Intratracheal instillation	During sensitization and challenge phases	MWCNTs could aggravate allergic airway inflammation probably via the inappropriate activation of antigen presenting cells.	[29]
MWCNTs	Male C57BL/6 mice	OVA	100 mg/m^3	1	Inhalation	After challenge phase	Pre-existing allergic inflammation caused by OVA could be susceptible to airway fibrosis under MWCNTs exposure.	[30]
SWCNTs	Male Wistar rats	OVA	0.02, 0.2, 2 mg/kg	13	Intratracheal instillation	Before and during sensitization phase	SWCNTs exacerbated OVA-sensitized rat asthma, which was antagonized by concurrent vitamin E.	[31]
SWCNTs, MWCNTs, Carbon nanofibers	Female Balb/c mice	OVA	200 µg (or 133.3 µg)	1 (or 3)	Injection into footpad (or intranasal instillation)	During sensitization phase	CNTs induced a stronger IgE response than carbon nanofibers, and promoted eosinophil lung inflammation rather than carbon nanofibers.	[32]
SWCNTs	Male ICR mice	OVA	25, 50 µg	7	Intratracheal instillation	During sensitization and challenge phases	SWCNTs exacerbated OVA-induced murine pulmonary inflammation and mucus hypersecretion.	[33]
CB	Female Balb/c mice	OVA	7 μg	2	Oropharyngeal application	During and after challenge phase	A low dose of CB NPs did not exacerbate allergic airway inflammation.	[34]
CB	Female Balb/c mice	OVA	2.5 mg/kg	4	Pharyngeal aspiration	Before and during sensitization phase	CB NPs enhanced the allergic airway inflammation and specific Th2 response in lymph nodes.	[35]
CB	Female Balb/cANNCrl mice	OVA	2, 20, 200 μg	3	Intranasal application	During sensitization phase	CB NPs caused early airway inflammation and had adjuvant activity in mouse allergic airway disease model.	[21]
GO	Male Balb/c mice	OVA	0.04, 0.4, 4 mg/kg	32	Intraperitoneal injection	Before and during sensitization phase	GO exacerbated the OVA-sensitized allergic asthma in mice.	[36]
GO	Female Balb/c mice	OVA	40, 80 μg	3	Pharyngeal aspiration	During sensitization and challenge phases	GO attenuated Th2 immune response in asthmatic mice while augment AHR and airway remodeling with chitinase induction.	[37]
C70-tetraglycolate	Female C57BL/6 and Balb/c mice	OVA	0.128 mg/kg	16	Inhalation	During sensitization and challenge phases	Bronchoconstriction, airway inflammation, and eosinophilia of mice with asthma were significantly alleviated by C70.	[38]
C60	C57BL/6 mice	2,4-dinitrophenol-albumin	50 ng	1	Intraperitoneal injection	Before challenge phase	C60 NPs inhibited allergic responses.	[39]
SiO2	Female Balb/c mice	OVA	10 mg/kg	7	Tail vein injection	Before and during challenge phase	SiO2 NPs exposure could exacerbate allergic inflammation.	[40]
SiO2	Female Balb/c mice	OVA	5, 10, 20 mg/kg	3	Intranasal instillation	Before and during challenge phase	SiO2 NPs aggravated asthma development via inflammasome activation.	[41]
SiO2	Female Balb/c mice	OVA	10 mg/kg	6	Intranasal inoculation	During sensitization and challenge phases	SiO2 NPs exerted adjuvant effect for OVA to induce allergic airway inflammation.	[42]
SiO2	Female Balb/c mice	OVA	200 μg	3	Intranasal instillation	During challenge phase	SiO2 NPs could give rise to airway inflammation which was not affected by the immunological status of mice.	[43]
SiO2	Female Balb/c mice	OVA	10, 100, 400 μg	4	Intranasal instillation	During sensitization phase	SiO2 NPs could facilitate allergen sensitization and the manifestation of airway disease.	[44]
SiO2	Female Balb/c mice	OVA	10, 50, 250 μg	3	Intranasal instillation	During sensitization phase	SiO2 NPs could induce Th2 type allergic immune responses depending on particle size.	[45]
SiO2	Male Wistar rats	OVA	4, 8 μg	30	Intratracheal instillation	Before and during sensitization phase	SiO2 NPs showed both developing and exacerbating effects on allergic asthma.	[46]
Ag	Female Balb/c mice	OVA	3.3 mg/m^3	7	Inhalation	Between sensitization and challenge phases	Ag NPs could exhibit respiratory risks to not only susceptible but also healthy individuals.	[47]
Ag	Female Balb/c mice	OVA	3.3 mg/m^3	7	Inhalation	Between sensitization and challenge phases	Ag NPs could provoke immune responses in normal and susceptible individuals.	[48]
Ag	Female Balb/c mice	OVA	40 mg/kg	5	Inhalation	During challenge phase	Signaling pathway of vascular endothelial growth factor was suppressed and airway inflammation was relieved by Ag NPs.	[49]
Ag	Female C57BL/6 mice	OVA	40 mg/kg	5	Inhalation	During challenge phase	Ag NPs moderated asthma symptoms and antioxidation could be a potential mechanism involved.	[50]
Au	Female Balb/c mice	OVA	20 μg	2	Intranasal instillation	Before and during challenge phase	Au NPs alleviated airway inflammation and AHR promoted by OVA.	[51]
Au	Swiss-Webster and A/J mice	OVA	6, 60 μg/kg	1	Intranasal instillation	Between sensitization and challenge phases	Au NPs prevented pivotal pathological changes in murine models of asthma.	[52]
Au, TiO2	Male Balb/c mice	Toluene-2,4-diisocyanate	0.8 mg/kg	1	Oropharyngeal aspiration	Between sensitization and challenge phases	Au and TiO2 NPs aggravated airway hyperreactivity and pulmonary inflammation.	[53]
TiO2	Female Balb/c mice	OVA	5, 10, 20 mg/kg	3	Intranasal instillation	During sensitization phase	TiO2 NPs exacerbated allergic airway inflammation.	[54]
TiO2	Female Balb/c mice	OVA	1.25 mg	2	Intranasal instillation	During challenge phase	TiO2 NPs exacerbated allergic airway inflammation.	[55]
TiO2	Female Balb/c mice	OVA	200 µg/m^3	3	Inhalation	During challenge phase	TiO2 NPs could exacerbate asthma via the release of neuromediator.	[56]
TiO2	Female Balb/c mice	OVA	50 µg/m^3	3	Inhalation	During challenge phase	TiO2 NPs contributed to inflammasome activation in asthmatic lung.	[57]
TiO2	Balb/c mice	OVA	8 mg/kg	1	Intraperitoneal injection	During sensitization phase	TiO2 NPs could augment the inflammatory responses in the lung via NF-κB pathway.	[58]
TiO2	Male DA/OlaHsd and BN/SsNOlaHsd rats	OVA	10 mg/mL	10	Aerosol inhalation	Before and during challenge phase	Influences of TiO2 NPs on murine immune and airway reactivity could depend on strain/genetics.	[59]
TiO2	Male Brown Norway rats	OVA	9.4, 15.7 mg/m^3	1	Inhalation	After challenge phase	TiO2 decreased lung inflammation in asthmatic rats.	[60]
TiO2	Female Balb/c mice	OVA	10 mg/m^3	12	Inhalation	During sensitization phase	TiO2 NPs could modulate airway inflammation which hinged on the immunological status of mice.	[61]
TiO2	Female Balb/c mice	OVA	2, 10, 50, 250 μg	1	Intraperitoneal injection	During sensitization phase	TiO2 NPs promoted allergic sensitization and lung inflammation in mice.	[62]
ZnO	Female Balb/c mice	OVA	16.67, 33.34 mg/mL	2	Inhalation or skin exposure	During sensitization phase	ZnO NPs played a limited role in the development of allergic airway inflammation.	[63]
ZnO	Female Balb/c mice	OVA	0.1, 0.5 mg/kg	2	Oropharyngeal aspiration	During sensitization phase	ZnO NPs could lead to eosinophilic airway inflammation with or without allergen.	[64]
Fe2O3	Female Balb/c mice	OVA	1.25, 2.5, 5 mg/kg	1	Intratracheal instillation	During challenge phase	The mice with established inflammation underwent cell death when exposed to Fe2O3 NPs.	[65]
Fe2O3	Female Balb/c mice	OVA	100, 250, 500 μg	4	Intratracheal instillation	Before and during sensitization phase	Influences of Fe2O3 NPs on allergic responses hinging on the particle dose.	[66]
Al2O3	Male Balb/c mice	OVA	0.5, 5, 50 mg/kg	11	Intratracheal instillation	Before and during sensitization phase	Al2O3 NPs aggravated the lung function damage in the OVA-induced allergic asthma model.	[67]
CuO	Female Balb/c mice	OVA	2.5, 10, 40 μg	4	Oropharyngeal aspiration	During challenge phase	CuO NPs deteriorated allergic airway inflammation via causing neutrophilia in the lung.	[68]
NiO	Female Balb/cJ mice	OVA	3, 40 μg	1	Oropharyngeal aspiration	Before sensitization phase	NiO NPs surface area was closely correlated with pulmonary injury and inflammation.	[69]
CeO2	Female Balb/c mice	HDM	75, 750 μg/kg	9	Intranasal instillation	During sensitization and/or challenge phases	CeO2 NPs exacerbated the HDM induced type II airway inflammation.	[70]

Table 5 The Role of Different Types of NPs in Allergic Asthma

NPs	MWCNTs	SWCNTs	CB	GO	Fullerene	SiO2	Ag	Au	TiO2	ZnO	Fe2O3	Al2O3	CuO	NiO	CeO2
Aggravating	✔	✔	✔	✔		✔				✔		✔	✔	✔	✔
Alleviating					✔
Dual							✔	✔	✔		✔

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