Smoker's macrophages

Smoker's macrophages are alveolar macrophages whose characteristics, including appearance, cellularity, phenotypes, immune response, and other functions, have been affected upon the exposure to cigarettes.[1] These altered immune cells are derived from several signaling pathways and are able to induce numerous respiratory diseases. They are involved in asthma, chronic obstructive pulmonary diseases (COPD), pulmonary fibrosis, and lung cancer.[2] Smoker’s macrophages are observed in both firsthand and secondhand smokers, so anyone exposed to cigarette contents, or cigarette smoke extract (CSE), would be susceptible to these macrophages, thus in turns leading to future complications.[3]

Alveolar macrophages are crucial in processing inhaled substances including cigarette chemicals and particulate matter.[4] The chemicals in tobacco, such as nicotine, tar, and carbon monoxide, stimulate several physiological pathways, which influence the recruitment and functions of these macrophages. Some of the smoker’s macrophages are recruited from the circulating monocytes while some are the original alveolar macrophages residing in the lung. The biochemical processes also lead to immunomodulation and dysregulated repair processes, so the malfunction of macrophages renders individuals more susceptible to infections.[5][2] In addition, these inhaled substances can enter the bloodstream, especially nicotine which is rapidly transported to the brain, leading to addiction; it will subsequently distributed throughout the body, leading to carcinoma in the future.[6]

The morbidity of cigarette smoking is nearly 50% with 7 million first-hand smokers and 1.2 millions second hand smokers killed each year.[8] Regardless of active or passive smokers, macrophage accumulation is found in the lungs.[3][5] The diagnostic methods for smoke-related diseases include bronchoalveolar lavage which can also be used for examining smoker's macrophages in addition to augmented inflammatory cells in the alveolar lumen.[1]

  1. ^ a b Monick, Martha M.; Powers, Linda S.; Walters, Katherine; Lovan, Nina; Zhang, Michael; Gerke, Alicia; Hansdottir, Sif; Hunninghake, Gary W. (2010-11-01). "Identification of an Autophagy Defect in Smokers' Alveolar Macrophages". The Journal of Immunology. 185 (9): 5425–5435. doi:10.4049/jimmunol.1001603. ISSN 0022-1767. PMC 3057181. PMID 20921532.
  2. ^ a b Yang, David C.; Chen, Ching-Hsien (November 2018). "Cigarette Smoking-Mediated Macrophage Reprogramming: Mechanistic Insights and Therapeutic Implications". Journal of Nature and Science. 4 (11): e539. ISSN 2377-2700. PMC 6383770. PMID 30801020.
  3. ^ a b Woodruff, Prescott G.; Ellwanger, Almut; Solon, Margaret; Cambier, Christopher J.; Pinkerton, Kent E.; Koth, Laura L. (April 2009). "Alveolar Macrophage Recruitment and Activation by Chronic Second Hand Smoke Exposure in Mice". COPD. 6 (2): 86–94. doi:10.1080/15412550902751738. ISSN 1541-2555. PMC 2873864. PMID 19378221.
  4. ^ Cite error: The named reference :1 was invoked but never defined (see the help page).
  5. ^ a b Wynn, Thomas A.; Vannella, Kevin M. (2016-03-15). "Macrophages in tissue repair, regeneration, and fibrosis". Immunity. 44 (3): 450–462. doi:10.1016/j.immuni.2016.02.015. ISSN 1074-7613. PMC 4794754. PMID 26982353.
  6. ^ Tega, Yuma; Yamazaki, Yuhei; Akanuma, Shin-ichi; Kubo, Yoshiyuki; Hosoya, Ken-ichi (2018). "Impact of Nicotine Transport across the Blood–Brain Barrier: Carrier-Mediated Transport of Nicotine and Interaction with Central Nervous System Drugs". Biological and Pharmaceutical Bulletin. 41 (9): 1330–1336. doi:10.1248/bpb.b18-00134. PMID 30175770. S2CID 52143978.
  7. ^ CDCTobaccoFree (2020-10-06). "Tobacco-Related Mortality". Centers for Disease Control and Prevention. Retrieved 2022-04-19.
  8. ^ "Tobacco". www.who.int. Retrieved 2022-04-17.
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