Effect of Epithelial-Specific MyD88 Signaling Pathway on Airway Inflammatory Response to Organic Dust Exposure

Johnson, Amber N.; Dickinson, John; Nelson, Amy; Gaurav, Rohit; Kudrna, Katrina; Evans, Scott E.; Janike, Katherine; Wyatt, Todd A.; Poole, Jill A.

doi:10.1080/1547691X.2022.2148782

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Effect of Epithelial-Specific MyD88 Signaling Pathway on Airway Inflammatory Response to Organic Dust Exposure

12 2023
By Johnson, Amber N. ; Dickinson, John ; Nelson, Amy ; ...
Source: J Immunotoxicol. 20(1):2148782

Public Access Version Available on: December 01, 2024, 12:00 AM

Please check back on the date listed above.

English

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Alternative Title:

J Immunotoxicol
Personal Author:

Johnson, Amber N. ; Dickinson, John ; Nelson, Amy ; Gaurav, Rohit ; Kudrna, Katrina ; ... More +

Johnson, Amber N. ; Dickinson, John ; Nelson, Amy ; Gaurav, Rohit ; Kudrna, Katrina ; Evans, Scott E. ; Janike, Katherine ; Wyatt, Todd A. ; Poole, Jill A. Less -
Description:

The Toll-like receptor (TLR) adaptor protein MyD88 is integral to airway inflammatory response to microbial-enriched organic dust extract (ODE) exposures. ODE-induced airway neutrophil influx and release of pro-inflammatory cytokines was essentially abrogated in global MyD88-deficient mice, yet these mice demonstrate an increase in airway epithelial cell mucin expression. To further elucidate the role of MyD88-dependent responses specific to lung airway epithelial cells in response to ODE |, the surfactant protein C protein (SPC) Cre| embryologic expressing airway epithelial cells floxed for MyD88 to disrupt MyD88 signaling were utilized. The inducible club cell secretory protein (CCSP) Cre|, MyD88 floxed, were also developed. Using an established protocol, mice were intranasally instilled with ODE or saline once or daily up to 3 weeks. Mice with MyD88-deficient SPC| lung epithelial cells exhibited decreased neutrophil influx following ODE exposure once and repetitively for 1 week without modulation of classic pro-inflammatory mediators including tumor necrosis factor (TNF)-α, interleukin (IL)-6, and neutrophil chemoattractants. This protective response was lost after 3 weeks of repetitive exposure. ODE-induced Muc5ac mucin expression at 1 week was also reduced in MyD88-deficient SPC| cells. Acute ODE-induced IL-33 was reduced in MyD88-deficient SPC| cells whereas serum IgE levels were increased at one week. In contrast, mice with inducible MyD88-deficient CCSP| airway epithelial cells demonstrated no significant difference in experimental indices following ODE exposure. Collectively, these findings suggest that MyD88-dependent signaling targeted to all airway epithelial cells plays an important role in mediating neutrophil influx and mucin production in response to acute organic dust exposures.
Subjects:

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Animals Dust Inhalation Exposure Interleukin-6 Mice Mice, Inbred C57BL Mucins Myeloid Differentiation Factor 88 Signal Transduction Toll-Like Receptors Tumor Necrosis Factor-alpha
Keywords:

[+]

Adaptation Agriculture Airway Inflammation Environmental Respiratory Disease MyD88 Occupational Organic Dust
Source:

J Immunotoxicol. 20(1):2148782
Pubmed ID:

36538286
Pubmed Central ID:

PMC9912912
Document Type:

Journal Article
Funding:

R01 OH012045/OH/NIOSH CDC HHSUnited States/ ; IK6 BX005962/BX/BLRD VAUnited States/ ; P30 CA036727/CA/NCI NIH HHSUnited States/ ; R35 HL144805/HL/NHLBI NIH HHSUnited States/ ; R01 HL157269/HL/NHLBI NIH HHSUnited States/ ; ... More +

R01 OH012045/OH/NIOSH CDC HHSUnited States/ ; IK6 BX005962/BX/BLRD VAUnited States/ ; P30 CA036727/CA/NCI NIH HHSUnited States/ ; R35 HL144805/HL/NHLBI NIH HHSUnited States/ ; R01 HL157269/HL/NHLBI NIH HHSUnited States/ ; R01 ES019325/ES/NIEHS NIH HHSUnited States/ ; U54 OH010162/OH/NIOSH CDC HHSUnited States/ Less -
Volume:

20
Issue:

1
Collection(s):

CDC Public Access
Main Document Checksum:

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urn:sha-512:e6329ad11278331bebd97f255dd53ef7c53d061c03724969344e2e66d49f77f751ea19866bc31bd29cce790d6ca526d1d515659128e5114dde64c0173f63a46d
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