The Potential Contribution of Biopolymeric Particles in Lung Tissue Regeneration of COVID-19 Patients

The lung is a vital organ that houses the alveoli, which is where gas exchange takes place. The COVID-19 illness attacks lung cells directly, creating significant inflammation and resulting in their inability to function. To return to the nature of their job, it may be essential to rejuvenate the afflicted lung cells. This is difficult because lung cells need a long time to rebuild and resume their function. Biopolymeric particles are the most effective means to transfer developing treatments to airway epithelial cells and then regenerate infected lung cells, which is one of the most significant symptoms connected with COVID-19. Delivering biocompatible and degradable natural biological materials, chemotherapeutic drugs, vaccines, proteins, antibodies, nucleic acids, and diagnostic agents are all examples of these molecules‘ usage. Furthermore, they are created by using several structural components, which allows them to effectively connect with these cells. We highlight their most recent uses in lung tissue regeneration in this review. These particles are classified into three groups: biopolymeric nanoparticles, biopolymeric stem cell materials, and biopolymeric scaffolds. The techniques and processes for regenerating lung tissue will be thoroughly explored.

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Dung biomass smoke activates inflammatory signaling pathways in human small airway epithelial cells

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00183.2016 ◽

2016 ◽

Vol 311 (6) ◽

pp. L1222-L1233 ◽

Cited By ~ 18

Author(s):

Claire E. McCarthy ◽

Parker F. Duffney ◽

Robert Gelein ◽

Thomas H. Thatcher ◽

Alison Elder ◽

...

Keyword(s):

Epithelial Cells ◽

Human Lung ◽

Inflammatory Responses ◽

Airway Epithelial Cells ◽

Lung Cells ◽

Airway Epithelial ◽

Inflammatory Signaling ◽

Biomass Smoke ◽

Human Lung Cells ◽

Small Airway Epithelial Cells

Animal dung is a biomass fuel burned by vulnerable populations who cannot afford cleaner sources of energy, such as wood and gas, for cooking and heating their homes. Exposure to biomass smoke is the leading environmental risk for mortality, with over 4,000,000 deaths each year worldwide attributed to indoor air pollution from biomass smoke. Biomass smoke inhalation is epidemiologically associated with pulmonary diseases, including chronic obstructive pulmonary disease (COPD), lung cancer, and respiratory infections, especially in low and middle-income countries. Yet, few studies have examined the mechanisms of dung biomass smoke-induced inflammatory responses in human lung cells. Here, we tested the hypothesis that dung biomass smoke causes inflammatory responses in human lung cells through signaling pathways involved in acute and chronic lung inflammation. Primary human small airway epithelial cells (SAECs) were exposed to dung smoke at the air-liquid interface using a newly developed, automated, and reproducible dung biomass smoke generation system. The examination of inflammatory signaling showed that dung biomass smoke increased the production of several proinflammatory cytokines and enzymes in SAECs through activation of the activator protein (AP)-1 and arylhydrocarbon receptor (AhR) but not nuclear factor-κB (NF-κB) pathways. We propose that the inflammatory responses of lung cells exposed to dung biomass smoke contribute to the development of respiratory diseases.

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Ontogeny of the eotaxins in human lung

AJP Lung Cellular and Molecular Physiology ◽

10.1152/ajplung.00086.2007 ◽

2008 ◽

Vol 294 (2) ◽

pp. L214-L224 ◽

Cited By ~ 12

Author(s):

Kathleen J. Haley ◽

Mary E. Sunday ◽

Yolanda Porrata ◽

Colleen Kelley ◽

Anne Twomey ◽

...

Keyword(s):

Signaling Pathway ◽

Lung Tissue ◽

Human Lung ◽

Airway Epithelial Cells ◽

Pcr Analysis ◽

Mrna Levels ◽

Airway Epithelial ◽

Human Lung Tissue ◽

Qrt Pcr ◽

Explant Cultures

The ontogeny of the C-C chemokines eotaxin-1, eotaxin-2, and eotaxin-3 has not been fully elucidated in human lung. We explored a possible role for eotaxin in developing lung by determining the ontogeny of eotaxin-1 (CCL11), eotaxin-2 (CCL24), eotaxin-3 (CCL26), and the eotaxin receptor, CCR3. We tested discarded surgical samples of developing human lung tissue using quantitative RT-PCR (QRT-PCR) and immunostaining for expression of CCL11, CCL24, CCL26, and CCR3. We assessed possible functionality of the eotaxin-CCR3 system by treating lung explant cultures with exogenous CCL11 and analyzing the cultures for evidence of changes in proliferation and activation of ERK1/2, a signaling pathway associated with CCR3. QRT-PCR analyses of 22 developing lung tissue samples with gestational ages 10–23 wk demonstrated that eotaxin-1 mRNA is most abundant in developing lung, whereas mRNAs for eotaxin-2 and eotaxin-3 are minimally detectable. CCL11 mRNA levels correlated with gestational age ( P < 0.05), and immunoreactivity was localized predominantly to airway epithelial cells. QRT-PCR analysis detected CCR3 expression in 16 of 19 developing lung samples. Supporting functional capacity in the immature lung, CCL11 treatment of lung explant cultures resulted in significantly increased ( P < 0.05) cell proliferation and activation of the ERK signaling pathway, which is downstream from CCR3, suggesting that proliferation was due to activation of CCR3 receptors by CCL11. We conclude that developing lung expresses the eotaxins and functional CCR3 receptor. CCL11 may promote airway epithelial proliferation in the developing lung.

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Proteomic Analysis of Lung Tissue in a Rat Acute Lung Injury Model: Identification of PRDX1 as a Promoter of Inflammation

Mediators of Inflammation ◽

10.1155/2014/469358 ◽

2014 ◽

Vol 2014 ◽

pp. 1-14 ◽

Cited By ~ 10

Author(s):

Dongdong Liu ◽

Pu Mao ◽

Yongbo Huang ◽

Yiting Liu ◽

Xiaoqing Liu ◽

...

Keyword(s):

Acute Lung Injury ◽

Lung Injury ◽

Lung Tissue ◽

Critical Role ◽

Model Identification ◽

Airway Epithelial Cells ◽

High Morbidity ◽

Airway Epithelial ◽

Lps Challenge

Acute respiratory distress syndrome (ARDS) remains a high morbidity and mortality disease entity in critically ill patients, despite decades of numerous investigations into its pathogenesis. To obtain global protein expression changes in acute lung injury (ALI) lung tissues, we employed a high-throughput proteomics method to identify key components which may be involved in the pathogenesis of ALI. In the present study, we analyzed lung tissue proteomes ofPseudomonas aeruginosa-induced ALI rats and identified eighteen proteins whose expression levels changed more than twofold as compared to normal controls. In particular, we found that PRDX1 expression in culture medium was elevated by a lipopolysaccharide (LPS) challenge in airway epithelial cellsin vitro. Furthermore, overexpression of PRDX1 increased the expression of proinflammatory cytokines interleukin-6 (IL-6), interleukin-8 (IL-8), and tumor necrosis factor-α(TNF-α), whereas knockdown of PRDX1 led to downregulated expression of cytokines induced by LPS. In conclusion, our findings provide a global alteration in the proteome of lung tissues in the ALI rat model and indicate that PRDX1 may play a critical role in the pathogenesis of ARDS by promoting inflammation and represent a novel strategy for the development of new therapies against ALI.

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Immunohistochemical identification of lung cells responsive to beta-stimulation with a rise in cAMP

Journal of Applied Physiology ◽

10.1152/jappl.1987.63.1.434 ◽

1987 ◽

Vol 63 (1) ◽

pp. 434-439 ◽

Cited By ~ 4

Author(s):

T. B. Casale ◽

D. Wood ◽

S. Wescott ◽

M. Kaliner

Keyword(s):

Airway Epithelial Cells ◽

Beta Agonist ◽

Staining Procedure ◽

Immunoperoxidase Staining ◽

Airway Smooth Muscle Cells ◽

Lung Cells ◽

Type I ◽

Airway Epithelial ◽

Capillary Endothelial Cells

To identify specific lung cells possessing functional beta-adrenergic receptors, we developed an immunoperoxidase-staining procedure capable of in situ localization of cells responding to beta-agonist stimulation with a rise in adenosine 3′,5′-cyclic monophosphate (cAMP). Isoproterenol was instilled into the airways of excised intact guinea pig lungs for 5 min and resulted in a six to eightfold rise in cAMP. Immediately thereafter, the lungs were washed in and fixed with 10% buffered Formalin. Sections were then stained using immunoperoxidase techniques and monoclonal antibodies directed against cAMP. We found that isoproterenol-stimulated lungs had widespread increased staining for immunoreactive cAMP. The specific cells consistently demonstrating marked increases in staining were airway epithelial cells, airway smooth muscle cells, alveolar and parenchymal macrophages, and alveolar lining cells, including both type I and type II cells, and capillary endothelial cells. Of all tissues, the airway epithelium was the most intensely stained area for beta-agonist-induced immunoreactive cAMP. The techniques employed herein should make possible the in situ localization of cells responding to any stimuli capable of increasing cAMP, thereby allowing the specific identification of cells possessing functional adenylate cyclase-linked receptors.

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