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Cellular Biology in Tissue Engineering
Published in Joseph W. Freeman, Debabrata Banerjee, Building Tissues, 2018
Joseph W. Freeman, Debabrata Banerjee
Before going into the clinical uses of hematopoietic growth factors, it may be useful to understand their biological actions. These factors are a class of growth factors that are responsible for the growth of blood cells and bone marrow proliferation. These hematopoietic growth factors are a diverse set of hormones with effects on hematopoietic lineages at various points in their developmental cycle.72 So far, they have entered clinical trials and have displayed encouraging results clinical situations. Currently, phase II and III clinical trials are trying to use these factors, either alone or in combinations, to modify disease states and to eradicate many of the side effects associated with other therapeutic agents, such as cytotoxic anticancer agents.72 Many other disease states can also be treated with these growth factors in a similar fashion. Not all hematopoietic growth factors have been studied in humans thus far. However, they show great promise because of the positive results provided from the other related growth factors. Some of these factors are used to clinically mobilize peripheral blood stem cells prior to harvesting the stem cells for transplantation (e.g., granulocyte colony-stimulating factor [GCSF] either alone or in combination with granulocyte macrophage colony-stimulating factor [GMCSF] is used to mobilize CD34+ peripheral blood stem cells).
Nanomaterial-induced toxicity in pathophysiological models representative of individuals with pre-existing medical conditions
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Sreejesh Sreedharan, Georgios Zouganelis, Samantha J Drake, Gyanendra Tripathi, Ali Kermanizadeh
In another study, healthy and OVA sensitized 7-week-old male ICR mice were exposed to MWCNT (approximately 65 nm; surface area, 26 m2/g; carbon purity, 99.8%; fiber length not specified) once a week for a total of 6 weeks via intratracheal instillation where each NM dose was 50 μg/animal (Inoue et al. 2009). Concurrently, OVA-sensitized T-cells isolated from the spleens of allergic mice were exposed to MWCNTs at concentration range of 0.1–1 μg/ml as well as 10 ng/ml recombinant mouse granulocyte macrophage-colony stimulating factor. The results showed aggravated inflammation in the lungs of diseased animals compared to control mice as evidenced by increased BALF total cell, neutrophil, and eosinophil numbers. Further, histological analysis demonstrated that in combined treatment with OVA and NMs increasing numbers of neutrophils and eosinophils was detected accompanied by lymphocyte sequestration into the lung parenchyma. Similarly, MWCNT exposure in asthmatic animals resulted in an elevated number of goblet cells in the bronchial epithelium which was not observed in the other treatment groups. The MWCNT and OVA exposure also amplified lung protein levels of inflammatory cytokines and chemokines, namely, IL4, IL5, IL13, IL18, IL33, and IFN-Ƴ. Finally, the in vitro exposure of MWCNT significantly enhanced allergen-specific syngeneic T-cell proliferation. Data from this study suggest that MWCNTs might potentially intensify allergic airway inflammation (Inoue et al. 2009).
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
Pulmonary alveolar proteinosis (PAP) is a relatively uncommon lung disease characterized by the accumulation of surfactant lipids and proteins within the alveolar space (Wang et al. 2012). Impaired clearance mechanisms are responsible for the buildup of these acellular components, which impair gas exchange, and eventually produce respiratory failure and death. Several different sources of PAP have been identified, and three corresponding variants of the disease were described to reflect these different origins of disease. Congenital PAP results from genetic mutations in innate immune cell receptors, autoimmune PAP involves adaptive immune-mediated interference with normal pulmonary clearance mechanisms, and secondary PAP emerges as a complication of infections, malignancies, or toxic exposures (Ben-Dov and Segel 2014; Santos et al. 2020). Accordingly, PAP is known to occur in both worker populations and the general public. The cytokine granulocyte macrophage-colony stimulating factor (GM-CSF) plays a central role in the pathogenesis of all three variants of PAP, as it mediates the terminal differentiation of alveolar macrophages, which are responsible for catabolizing the offending molecules and clearing them from the lower airways (Trapnell et al. 2019). Accordingly, disease onset corresponds with the introduction of disruptions in GM-CSF signaling and alveolar macrophage functionality.
Traffic-related particulate matter aggravates ocular allergic inflammation by mediating dendritic cell maturation
Published in Journal of Toxicology and Environmental Health, Part A, 2021
Moonwon Hwang, Sehyun Han, Jeong-Won Seo, Ki-Joon Jeon, Hyun Soo Lee
This procedure was previously described by Lee et al. (2015). The femurs of naıve BALB/c mice were removed and irrigated with a syringe to collect bone marrow dendritic cells (BMDC). The bone marrow cells were washed and plated (1 × 105/ml) in RPMI 1640 medium with 20 ng/ml mouse granulocyte-macrophage colony-stimulating factor (BioLegend), 10% fetal bovine serum, and 1% penicillin/streptomycin. The loosely adherent cells were collected on day 7. To stimulate T cells in vitro, ipsilateral cervical lymph nodes (LNs) were harvested after the topical challenge. T cells were enriched with magnetic-activated cell sorting using anti-CD90.2 antibodies (Miltenyi Biotec, Germany) and then T cells were counted via a trypan blue exclusion assay and plated in round-bottom 96-well plates at a concentration of 1 × 106/ml. The immature BMDCs as described above were plated with OVA at a concentration of 0.5 × 106/ml with T cells. All culture wells were plated in triplicate for up to 72 hr.