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Semi-protected edit request on 10 May 2022 - Genetics of Pneumonia
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It has been found that vulnerability to Pneumonia and its severity may be linked to underlying genetic mechanisms. These mechanisms, such as the CYP1A1 gene (CYP1A1) regulating inflammatory responses and sepsis, can influence the efficacy of the immune system which can either be detrimental or beneficial in combating Pneumonia.
Individuals with certain genetic variants can be at risk for a higher susceptibility to Pneumonia. For example, individuals with mutations in Bruton’s tyrosine kinase (BTK). These mutations lead to the development of a disease called X-linked agammaglobulinemia which inhibits the formation of white blood cells and mature B cells. Without functional BTK, the development cycle of B lymphocytes is stopped at the pre-B cell stage which results in the loss of mature lymphocytes in the bone marrow and lymphatic system. In BTK, the mutation of arg525 to gln was particularly responsible for the lowered functionality of BTK. Due to decreased white blood cell count, this immune deficiency increases one’s susceptibility to Pneumonia greatly.
A broad mapping study aimed at identifying loci associated with pulmonary function and Pneumonia in humans mapped 137 loci of interest. 116 of the 137 loci were found to be responsible for both pulmonary function and susceptibility to Pneumonia. Furthermore, 336/340 SNPs were shared between Pneumonia and pulmonary function . Genes that are responsible for pulmonary function play an integral role in overall lung development and inflammation pathways that are key to an immune response. Individuals with an impaired pulmonary function due to certain predisposed developmental, inflammatory, or cardiovascular traits were found to be at a higher risk for Pneumonia. This high degree of overlap of genes and the correlation between pulmonary function traits and susceptibility to Pneumonia could mean that there is a major genetic factor.
There are nine disease genes currently known to increase susceptibility to idiopathic interstitial Pneumonia. Three of the disease genes are responsible for the production of surfactant by alveoli in the lungs: Surfactant protein C (SFTPC), Surfactant protein A2 (SFTPA2), and Adenosine triphosphate-binding cassette subfamily A member 3 (ABCA3). Surfactant is a mixture of proteins and fats that helps keep the alveoli from collapsing when a person exhales and also protects lung cells from infection. Mutations at these loci have age-dependent effects, however, it is not yet possible to predict which family members will develop Pneumonia at what age. The other six disease genes are associated with telomeres: Telomerase reverse transcriptase , Telomerase RNA component , Dyskerin , Telomere repeat binding factor 1-interacting nuclear factor 2 , Regulator of telomere elongation helicase , Poly(A)-specific ribonuclease . Mutations in these genes impede the ability of the body to repair damage in the telomeres of chromosomes and thus they become shorter, which can also increase the risk of developing Pneumonia, amongst many other diseases. Currently, doctors do offer genetic testing for these 9 disease genes in cases where two or more individuals in the same family have Pneumonia.
During the COVID-19 pandemic, patients infected with COVID-19 were found to have twice the risk of developing pneumonia. Doctors have developed a DNA test that uses multiple polymerase chain reactions to detect DNA and antibiotic resistance of streptococcus pneumoniae in a patient’s blood sample. This can be done in the span of four hours which is much quicker than the conventional method of growing bacterial cultures which is prone to false negatives due to patients receiving antibiotics before the sample is collected. The test expedites the treatment procedure with doctors being able to prescribe antibiotics at an earlier stage and making it more effective in the treatment of Pneumonia.
References
Chen, Shaw, Petty, North. (2020, December 11). Host genetic effects in Pneumonia. Cell. https://www.cell.com/ajhg/fulltext/S0002-9297(20)30446-8
Genetics in community-acquired Pneumonia : Current Opinion in Pulmonary Medicine. (2019). LWW. https://journals.lww.com/co-pulmonarymedicine/Abstract/2019/05000/Genetics_in_community_acquired_Pneumonia.17.aspx
ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
Khadzhieva, Kuzovlev, Salnikova. (2019, December). Pneumonia: host susceptibility and shared genetics with pulmonary function and other traits. PubMed. https://pubmed.ncbi.nlm.nih.gov/31487037/
Kropski, YOung, Cogan, Mitchell, Lancaster, Worrell, Markin, Liu. (2017, June 1). Genetic Evaluation and Testing of Patients and Families with Idiopathic Pulmonary Fibrosis. National Library of Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470751/
Waterer, Wunderink. (2010). Genetic susceptibility to Pneumonia. PubMed. https://pubmed.ncbi.nlm.nih.gov/15802163/
Guin, Debleena, et al. “Human Genetic Factors Associated with Pneumonia Susceptibility, a Cue for Covid-19 Mortality.” MedRxiv, Cold Spring Harbor Laboratory Press, 1 Jan. 2021, https://www.medrxiv.org/content/10.1101/2021.06.03.21258106v1.full.
“DNA Test Can Quickly Identify Pneumonia in Patients with Severe COVID-19, Aiding Faster Treatment.” ScienceDaily, ScienceDaily, 15 Jan. 2021, https://www.sciencedaily.com/releases/2021/01/210115091340.htm.
- Guin, Debleena, et al. “Human Genetic Factors Associated with Pneumonia Susceptibility, a Cue for Covid-19 Mortality.” MedRxiv, Cold Spring Harbor Laboratory Press, 1 Jan. 2021, https://www.medrxiv.org/content/10.1101/2021.06.03.21258106v1.full.
- Genetics in community-acquired Pneumonia : Current Opinion in Pulmonary Medicine. (2019). LWW. https://journals.lww.com/co-pulmonarymedicine/Abstract/2019/05000/Genetics_in_community_acquired_Pneumonia.17.aspx
- Chen, Shaw, Petty, North. (2020, December 11). Host genetic effects in Pneumonia. Cell. https://www.cell.com/ajhg/fulltext/S0002-9297(20)30446-8
- Khadzhieva, Kuzovlev, Salnikova. (2019, December). Pneumonia: host susceptibility and shared genetics with pulmonary function and other traits. PubMed. https://pubmed.ncbi.nlm.nih.gov/31487037/
- Khadzhieva, Kuzovlev, Salnikova. (2019, December). Pneumonia: host susceptibility and shared genetics with pulmonary function and other traits. PubMed. https://pubmed.ncbi.nlm.nih.gov/31487037/
- ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
- ILD Colaborative. (2020). Genetics of Familial Idiopathic Interstitial Pneumonia. https://www.ildcollaborative.org/resources/genetics-of-familial-idiopathic-interstitial-Pneumonia
- Kropski, YOung, Cogan, Mitchell, Lancaster, Worrell, Markin, Liu. (2017, June 1). Genetic Evaluation and Testing of Patients and Families with Idiopathic Pulmonary Fibrosis. National Library of Medicine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5470751/
- “DNA Test Can Quickly Identify Pneumonia in Patients with Severe COVID-19, Aiding Faster Treatment.” ScienceDaily, ScienceDaily, 15 Jan. 2021, https://www.sciencedaily.com/releases/2021/01/210115091340.htm.
Editor3456123123 (talk) 00:26, 11 May 2022 (UTC)
Not done: it's not clear what changes you want to be made. Please mention the specific changes in a "change X to Y" format and provide a reliable source if appropriate. —Sirdog (talk) 05:46, 14 May 2022 (UTC)
Hypostatic pneumonia
On Misplaced Pages there are 5 links to "hypostatic pneumonia" which then redirects here, yet "hypostatic" does not appear anywhere within this article. The disambiguation for hypostasis only gives one medically relevant definition: "Hypostasis (livor mortis), corpse's discoloration". That might be helpful, but it's for a different organ. I can only take an educated guess at what hypostatic pneumonia means, and I wouldn't be sure the right place to describe it if I knew. DAVilla (talk) 20:12, 26 September 2022 (UTC)
Cause section should probably be updated to take into account the prevalence of SARS-CoV-2 amongst pneumoniae causes
This is important because such beliefs may lead the public to not consiser SARS-CoV-2 as a potential cause of pneumonia and lead to unjustified intakes of antibiotics. MathieuSchopfer (talk) 06:09, 29 September 2023 (UTC)
Wiki Education assignment: LLIB 1115 - Intro to Information Research
This article was the subject of a Wiki Education Foundation-supported course assignment, between 21 August 2023 and 8 December 2023. Further details are available on the course page. Student editor(s): Lions.2223 (article contribs).
— Assignment last updated by Lions.2223 (talk) 17:15, 4 October 2023 (UTC)
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