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Article ; Online: Perspective: The Lung, Particles, Fibers, Nanomaterials, and Autoimmunity.

Pollard, K Michael

2020 Volume 11, Page(s) 587136

Abstract: Studies have shown that a wide range of factors including drugs, chemicals, microbes, and other environmental agents can induce pre-clinical autoimmunity. However, only a few have been confidently linked to autoimmune diseases. Among these are exposures ... ...

Abstract	Studies have shown that a wide range of factors including drugs, chemicals, microbes, and other environmental agents can induce pre-clinical autoimmunity. However, only a few have been confidently linked to autoimmune diseases. Among these are exposures to inhaled particulates that are known to be associated with autoimmune diseases such as lupus and rheumatoid arthritis. In this article, the potential of particle, fiber, and nanomaterial exposures to induce autoimmunity is discussed. It is hypothesized that inhalation of particulate material known to be associated with human autoimmune diseases, such as cigarette smoke and crystalline silica, results in a complex interplay of a number of pathological processes, including, toxicity, oxidative stress, cell and tissue damage, chronic inflammation, post-translational modification of self-antigens, and the formation of lymphoid follicles that provide a milieu for the accumulation of autoreactive B and T cells necessary for the development and persistence of autoimmune responses, leading to disease. Although experimental studies show nanomaterials are capable of inducing several of the above features, there is no evidence that this matures to autoimmune disease. The procession of events hypothesized here provides a foundation from which to pursue experimental studies to determine the potential of other environmental exposures to induce autoimmunity and autoimmune disease.
MeSH term(s)	Animals ; Autoimmune Diseases/etiology ; Autoimmune Diseases/immunology ; Autoimmunity/immunology ; Humans ; Inhalation Exposure/adverse effects ; Lung/pathology ; Nanoparticles/adverse effects ; Particulate Matter/adverse effects ; Particulate Matter/immunology
Chemical Substances	Particulate Matter
Language	English
Publishing date	2020-12-18
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.587136
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Editorial: The Role of the Environment in Autoimmunity.

Pestka, James J / Pollard, K Michael / Rosenspire, Allen J

Frontiers in immunology

2021 Volume 12, Page(s) 641171

MeSH term(s)	Animals ; Autoimmunity/immunology ; Environmental Exposure/adverse effects ; Humans
Language	English
Publishing date	2021-02-22
Publishing country	Switzerland
Document type	Editorial ; Introductory Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.641171
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Article ; Online: Exposure to silicates and systemic autoimmune-related outcomes in rodents: a systematic review.

Janssen, Lisa M F / Ghosh, Manosij / Lemaire, Frauke / Michael Pollard, K / Hoet, Peter H M

Particle and fibre toxicology

2022 Volume 19, Issue 1, Page(s) 4

Abstract: Background: Autoimmunity can result from the interplay between genetic background and effects of environmental and/or occupational exposure to hazardous materials. Several compounds, including silica dust, have been linked with systemic autoimmunity and ...

Abstract	Background: Autoimmunity can result from the interplay between genetic background and effects of environmental and/or occupational exposure to hazardous materials. Several compounds, including silica dust, have been linked with systemic autoimmunity and systemic autoimmune diseases, based on epidemiological evidence. For asbestos, a strong link with systemic autoimmune diseases does not yet exist, however, several studies have documented features of autoimmunity following asbestos exposure. Even so, human studies are limited in their ability to identify and examine isolated exposures, making it difficult to demonstrate causation or to assess pathogenic mechanisms. Therefore, this systematic review examines the existing animal evidence regarding autoimmunity and exposure to silicates (silica and asbestos). Methods: PubMed and EMBASE were systematically searched for peer-reviewed studies examining systemic autoimmune disease-related outcomes after silicate exposure in rodents. Literature databases were searched up to September 2021 for studies written in English and where the full text was available. Search strings were established based on a PECO (Population, Exposure, Comparator, Outcome) format. After title, abstract, and full-text screening, thirty-four studies were identified for further analysis. Quality assessment through ToxR tool and qualitative analysis of the results was performed. Results: Although there was significant heterogeneity in the included studies in terms of exposure protocol and genetic background of the rodent models used, it was noted that both genetic background and exposure to silicates [(crystalline) silica and asbestos] are highly relevant to the development of (sub-) clinical systemic autoimmune disease. Conclusion: Parallels were observed between the findings from the animal (this review) and human (epidemiological) studies, arguing that experimental animal models are valuable tools for examining exacerbation or development of autoimmune disease after silicate exposure. However, genetic background and synergism between exposures should be considered in future studies.
MeSH term(s)	Animals ; Autoimmunity ; Dust ; Occupational Exposure/adverse effects ; Rodentia ; Silicates
Chemical Substances	Dust ; Silicates
Language	English
Publishing date	2022-01-07
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review ; Systematic Review
ZDB-ID	2170936-1
ISSN	1743-8977 ; 1743-8977
ISSN (online)	1743-8977
ISSN	1743-8977
DOI	10.1186/s12989-021-00439-6
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Article ; Online: An Emerging Fluorescence-Based Technique for Quantification and Protein Profiling of Extracellular Vesicles.

Dehghani, Mehdi / Montange, Rebecca K / Olszowy, Michael W / Pollard, David

SLAS technology

2020 Volume 26, Issue 2, Page(s) 189–199

Abstract: Robust and well-established techniques for the quantification and characterization of extracellular vesicles (EVs) are a crucial need for the utilization of EVs as potential diagnostic and therapeutic tools. Current bulk analysis techniques such as ... ...

Abstract	Robust and well-established techniques for the quantification and characterization of extracellular vesicles (EVs) are a crucial need for the utilization of EVs as potential diagnostic and therapeutic tools. Current bulk analysis techniques such as proteomics and Western blot suffer from low resolution in the detection of small changes in target marker expression levels, exemplified by the heterogeneity of EVs. Microscopy-based techniques can provide valuable information from individual EVs; however, they are time-consuming and statistically less powerful than other techniques. Flow cytometry has been successfully employed for the quantification and characterization of individual EVs within larger populations. However, traditional flow cytometry is not highly suited for the examination of smaller, submicron particles. Here we demonstrate the accurate and precise quantification of nanoparticles such as EVs using the Virus Counter 3100 (VC3100) platform, a fluorescence-based technique that uses the principles of flow cytometry with critical enhancements to enable the effective detection of smaller particles. This approach can detect nanoparticles precisely with no evidence of inaccurate concentration measurement from masking effects associated with traditional nanoparticle tracking analysis (NTA). Fluorescently labeled EVs from different sources were successfully quantified using the VC3100 without a postlabeling washing step. Moreover, protein profiling and characterization of individual EVs were achieved and have been shown to determine the expression level of target protein markers.
MeSH term(s)	Biomarkers ; Extracellular Vesicles ; Flow Cytometry ; Nanoparticles ; Proteomics
Chemical Substances	Biomarkers
Language	English
Publishing date	2020-11-13
Publishing country	United States
Document type	Journal Article
ZDB-ID	2900310-6
ISSN	2472-6311 ; 2472-6303
ISSN (online)	2472-6311
ISSN	2472-6303
DOI	10.1177/2472630320970458
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Article ; Online: Gender differences in autoimmunity associated with exposure to environmental factors.

Pollard, K Michael

Journal of autoimmunity

2011 Volume 38, Issue 2-3, Page(s) J177–86

Abstract: Autoimmunity is thought to result from a combination of genetics, environmental triggers, and stochastic events. Gender is also a significant risk factor with many diseases exhibiting a female bias. Although the role of environmental triggers, especially ...

Abstract	Autoimmunity is thought to result from a combination of genetics, environmental triggers, and stochastic events. Gender is also a significant risk factor with many diseases exhibiting a female bias. Although the role of environmental triggers, especially medications, in eliciting autoimmunity is well established less is known about the interplay between gender, the environment and autoimmunity. This review examines the contribution of gender in autoimmunity induced by selected chemical, physical and biological agents in humans and animal models. Epidemiological studies reveal that environmental factors can be associated with a gender bias in human autoimmunity. However many studies show that the increased risk of autoimmunity is often influenced by occupational exposure or other gender biased activities. Animal studies, although often prejudiced by the exclusive use of female animals, reveal that gender bias can be strain specific suggesting an interaction between sex chromosome complement and background genes. This observation has important implications because it argues that within a gender biased disease there may be individuals in which gender does not contribute to autoimmunity. Exposure to environmental factors, which encompasses everything around us, adds an additional layer of complexity. Understanding how the environment influences the relationship between sex chromosome complement and innate and adaptive immune responses will be essential in determining the role of gender in environmentally-induced autoimmunity.
MeSH term(s)	Animals ; Autoimmune Diseases/chemically induced ; Autoimmune Diseases/etiology ; Autoimmunity/drug effects ; Autoimmunity/immunology ; Disease Models, Animal ; Environmental Exposure ; Female ; Humans ; Male ; Sex Factors
Language	English
Publishing date	2011-12-03
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2011.11.007
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Article: Differential Pulmonary Toxicity and Autoantibody Formation in Genetically Distinct Mouse Strains Following Combined Exposure to Silica and Diesel Exhaust Particles.

Janssen, Lisa Mf / Lemaire, Frauke / Marain, Nora Fopke / Ronsmans, Steven / Heylen, Natasja / Vanstapel, Arno / Velde, Greetje Vande / Vanoirbeek, Jeroen Aj / Pollard, K Michael / Ghosh, Manosij / Hoet, Peter Hm

Research square

2023

Abstract: Background: Inhalation of airborne particulate matter, such as silica and diesel exhaust particles, poses serious long-term respiratory health risks. Silica exposure can lead to silicosis and systemic autoimmune diseases, while DEP exposure is linked to ...

Abstract	Background: Inhalation of airborne particulate matter, such as silica and diesel exhaust particles, poses serious long-term respiratory health risks. Silica exposure can lead to silicosis and systemic autoimmune diseases, while DEP exposure is linked to asthma and cancer. Combined exposure to silica and DEP, common in mining, may have more severe effects. This study investigates the separate and combined effects of silica and DEP on lung injury, inflammation, and autoantibody formation in two genetically distinct mouse strains, thereby aiming at understanding the interplay between genetic susceptibility, particulate exposure, and disease outcomes. Silica and diesel exhaust particles were administered to mice via oropharyngeal aspiration. Assessments of lung injury and host response included in vivo lung micro-computed tomography, lung function tests, bronchoalveolar lavage fluid analysis including inflammatory cytokines and antinuclear antibodies, and histopathology with particle colocalization. Results: Silica exposure elicited a well-established inflammatory response marked by inflammatory infiltrates, release of cytokines, and chemokines, alongside limited fibrosis, indicated by collagen deposition in the lungs of both C57BL/6J and NOD/ShilLtJ mice. Notably, these strains exhibited divergent responses in terms of respiratory function and lung volumes, as assessed through micro-computed tomography. Additionally, silica exposure induced airway hyperreactivity and elevated antinuclear antibody levels in bronchoalveolar lavage fluid, particularly prominent in NOD/ShiLtJ mice. Lung tissue analysis revealed DEP loaded macrophages and co-localization of silica and DEP particles. Conclusion: Mouse strain variations exerted a substantial influence on the development of silica induced lung alterations. Furthermore, the additional impact of diesel exhaust particles on these silica-induced effects was minimal.
Language	English
Publishing date	2023-10-09
Publishing country	United States
Document type	Preprint
DOI	10.21203/rs.3.rs-3408546/v1
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Article ; Online: Requirements for "Fire and ICE" differ between animal models of autoimmunity: comment on the article by Kahlenberg et al.

Pollard, K Michael / Kono, Dwight H

Arthritis & rheumatology (Hoboken, N.J.)

2014 Volume 66, Issue 8, Page(s) 2310–2311

MeSH term(s)	Animals ; Apoptosis/immunology ; Autoantibodies/immunology ; Caspase 1/immunology ; Endothelium, Vascular/physiology ; Humans ; Interferon Type I/immunology ; Lupus Erythematosus, Systemic/immunology ; Vascular Diseases/immunology ; Vasodilation/physiology
Chemical Substances	Autoantibodies ; Interferon Type I ; Caspase 1 (EC 3.4.22.36)
Language	English
Publishing date	2014-04-22
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	2756371-6
ISSN	2326-5205 ; 2326-5191
ISSN (online)	2326-5205
ISSN	2326-5191
DOI	10.1002/art.38678
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Article: Mercury-induced inflammation and autoimmunity

Pollard, K. Michael / Cauvi, David M / Toomey, Christopher B / Hultman, Per / Kono, Dwight H

Biochimica et biophysica acta. 2019 Feb. 01,

2019

Abstract: Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to ... ...

Abstract	Human exposure to mercury leads to a variety of pathologies involving numerous organ systems including the immune system. A paucity of epidemiological studies and suitable diagnostic criteria, however, has hampered collection of sufficient data to support a causative role for mercury in autoimmune diseases. Nevertheless, there is evidence that mercury exposure in humans is linked to markers of inflammation and autoimmunity. This is supported by experimental animal model studies, which convincingly demonstrate the biological plausibility of mercury as a factor in the pathogenesis of autoimmune disease.In this review, we focus on ability of mercury to elicit inflammatory and autoimmune responses in both humans and experimental animal models.Although subtle differences exist, the inflammatory and autoimmune responses elicited by mercury exposure in humans and experimental animal models show many similarities. Proinflammatory cytokine expression, lymphoproliferation, autoantibody production, and nephropathy are common outcomes. Animal studies have revealed significant strain dependent differences in inflammation and autoimmunity suggesting genetic regulation. This has been confirmed by the requirement for individual genes as well as genome wide association studies. Importantly, many of the genes required for mercury-induced inflammation and autoimmunity are also required for idiopathic systemic autoimmunity. A notable difference is that mercury-induced autoimmunity does not require type I IFN. This observation suggests that mercury-induced autoimmunity may arise by both common and specific pathways, thereby raising the possibility of devising criteria for environmentally associated autoimmunity.Mercury exposure likely contributes to the pathogenesis of autoimmunity.
Keywords	animal models ; antibody formation ; autoimmune diseases ; autoimmunity ; cytokines ; genes ; genome-wide association study ; humans ; immune system ; inflammation ; kidney diseases ; mercury ; pathogenesis
Language	English
Dates of publication	2019-0201
Publishing place	Elsevier B.V.
Document type	Article
Note	Pre-press version
ZDB-ID	840755-1
ISSN	0304-4165
ISSN	0304-4165
DOI	10.1016/j.bbagen.2019.02.001
Database	NAL-Catalogue (AGRICOLA)

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Article: Environmental triggers and autoimmunity.

Vojdani, Aristo / Pollard, K Michael / Campbell, Andrew W

Autoimmune diseases

2014 Volume 2014, Page(s) 798029

Language	English
Publishing date	2014-12-24
Publishing country	United States
Document type	Journal Article
ISSN	2090-0422
ISSN	2090-0422
DOI	10.1155/2014/798029
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Article ; Online: High throughput screening of ultrafiltration and diafiltration processing of monoclonal antibodies via the ambr® crossflow system.

Fernandez-Cerezo, Lara / Wismer, Michael K / Han, InKwan / Pollard, Jennifer M

Biotechnology progress

2019 Volume 36, Issue 2, Page(s) e2929

Abstract: As the biopharmaceutical industry moves toward high concentration of monoclonal antibody drug substance, additional development is required early on when material is still limited. A key constraint is the availability of predictive high-throughput low- ... ...

Abstract	As the biopharmaceutical industry moves toward high concentration of monoclonal antibody drug substance, additional development is required early on when material is still limited. A key constraint is the availability of predictive high-throughput low-volume filtration screening systems for bioprocess development. This particularly impacts final stages such as ultrafiltration/diafiltration steps where traditional scale-down systems need hundreds of milliliters of material per run. Recently, the ambr® crossflow system has been commercialized by Sartorius Stedim Biotech (SSB) to meet this need. It enables parallel high throughput experimentation by only using a fraction of typical material requirements. Critical parameters for predictive filtration systems include loading, mean transmembrane pressure (Δ
MeSH term(s)	Antibodies, Monoclonal/chemistry ; Antibodies, Monoclonal/isolation & purification ; Filtration ; Fractionation, Field Flow ; High-Throughput Screening Assays ; Pressure
Chemical Substances	Antibodies, Monoclonal
Language	English
Publishing date	2019-11-21
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	165657-0
ISSN	1520-6033 ; 8756-7938
ISSN (online)	1520-6033
ISSN	8756-7938
DOI	10.1002/btpr.2929
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