Cigarette Smoking Induced Inflammation accompany the earliest Acute
Brain Injury is the pathological basis of COPD comorbid MDD
Abstract
Background and Purpose: COPD is one of the most common
respiratory diseases worldwide with high comorbidities as major
depressive disorder(MDD). Cigarette smoking(CS) is the most major risk
factor and smokers tend to be more easy to get COPD and MDD, the
mechanisms still remained poorly defined. Experimental Approach: The
gene expression microarray analyzed between COPD lung tissues and MDD
brain tissues were conducted and enriching GO and KEGG pathways analysis
in R. CS exposure induced COPD animal model in mice was established and
followed the expression of hub-bottleneck genes. Key Results: Based on
microarray analysis, found some DEGs plays a prominent role in COPD and
MDD, such as Casitas B-lineage Lymphoma Proto-OncogeneB (CBLB) is
involved in the regulation of immune response. Myocyte enhancer factor
2C (MEF2C) have been associated with severe cognitive disability,
stereotypic movements and cerebral malformation. Mitogen-activated
protein kinase 7 (MAPK7) was involved in various cellular processes.
Furthermore, animal studies showed that mice exposure to CS whose airway
inflammation increased and inflammatory cells rise in bronchoalveolar
lavage fluid accompanied with markedly declined lung function. In
addition, CBLB and MAPK7 with abnormal expression in the brain tissue.
Even more important, mice exposure to CS whose brain was seriously
injured and the nerve cells morphological have changed, CBLB deficiency
increased the GM-CSF signal pathway related inflammatory reactions in
brain tissue. Conclusion and Implications: In conclusion, CS causes COPD
accompanied with early acute brain injury, GM-CSF and MAPK7 signal
pathway may be involved in it. To some extent, the study revealing that
inflammatory response accompany with the earliest acute brain injury is
the pathological basis of COPD complicating MDD