The new policy for COVID was implemented in our country and many people developed and even died from pneumonia caused because of it. One of the many types of pneumonia described in this article is -- Community Acquired Pneumonia（CAP).
One of types of pneumonia -- Community-acquired pneumonia (CAP) refers to infectious parenchymal inflammation (CAP) that occurs outside the hospital, including pneumonia that develops within 48 hours of a patient's admission to hospital from a pathogen with a defined incubation period. With an ageing population, antibiotic overuse and pathogens with drug resistance, new challenges is faced in the prevention and treatment of CAP. However, new antibiotics and gene sequencing technologies are also offering the promise of reducing mortality. This article will only focus on the pathological causes of CAP to provide an understanding of the underlying mechanisms behind it. The underlying mechanisms can be summarised in two main points: 1. immune response triggered by the invasion of pathogens into the body 2. genetic changes that lead to an increased susceptibility to CAP. Therefore, research into the genetic variation of CAP is valuable in furthering our understanding of the pathogenesis of CAP. However, most of them have not been studied and need to be further investigated. It is hopeful to be used in the future to prevent CAP or to reduce CAP mortality.
immune response, cytokines, genes, mutation
Point 1: Immune response leading by pathogens
Community-acquired pneumonia(CAP) is an infectious inflammation of the lung parenchyma that develops outside the hospital, including pneumonia that develops within 48 hours of a patient's admission to hospital from a pathogenic infection with a defined incubation period. It is a common infectious disease of the lower respiratory tract with a high incidence and burden of disease, high rates of death and treatment failure increaseing with the age of the patient. One of the pathological causes is a variety of pathogens such as bacteria such as Streptococcus pneumoniae, Staphylococcus aureus, Mycoplasma pneumoniae and Gram-negative enterobacteria, fungi such as Histoplasma, Bacillus and Coccidioides or viruses such as influenza virus and adenovirus. The lower respiratory tract is usually reached by four mechanisms: 1. inhalation of diseased aerosols 2. inadvertent aspiration of oropharyngeal secretions into the trachea and entry into the lower airways via the trachea 3. blood-borne transmission from a locally infected site 4. direct spread of nearby infected lesions. The pathogen invades and overgrows in the lung parenchyma, which exceeds the host's defence limits and causes exudate to develop in the alveolar cavity. Normally, in the body's defence system, the immune response is triggered when foreign unrecognisable agents are encountered. The foreign cells release chemical factors and the white blood cells are the first to reach the pathogen and engulf it and signal more white blood cells to kill the pathogen. But it is the immune response of the leukocytes that leads to the outcome in pneumonia. A type of leukocyte -- mast cell releases cytokines which cause the blood vessels to dilate and become more permeable, as more fluid will facilitate the leukocytes to kill the pathogens, but this also creates a build-up of fluid in the lungs. Similarly, an increase in temperature, for example, is beneficial to the white blood cells in their fight which will increase the inefficiency. Also, like coughing is designed to drive pathogens out of the body to protect our body.
Point 2: Gene mutations
Scientists have also discovered that the pathology of CAP is genetically related through techniques such as Luminex. The influence of CAP. In the respiratory tract, motile cilia are responsible for the removal of mucus, thereby protecting it from infection and ensuring mucociliary clearance. Some scientists have identified genes such as ARMC4 as playing an important role in ciliary motility in anchoring the outer dynein arms. In defective cases, affected cilia exhibit reduced beating frequency and amplitude or become immobile, and malfunctions in the coordinated movement of cilia can impede the clearance of invading microorganisms from the airways and promote respiratory infections. As a result, patients with autosomal recessive disorders like primary ciliary dyskinesia often develop recurrent pneumonia. Scientists have found that the 250-base ACE gene is also associated with CAP, and elderly patients from long-term care facilities who carry a pure combination of this gene are more likely to develop pneumonia over eight months (excluding winter). Several recent prospective longitudinal observational studies have shown that the use of ACE inhibitors is associated with a lower incidence of pneumonia. Variants in TLR4, a gene that identifies the molecule, appear to increase the risk of severe Gram-negative infection to trigger CAP. A cytokine called Tumor Necrosis Factor (TNF) is critical to the immune response to infection, and experimental animals who lack TNF could not survive in the challenge of infection. The A allele of TNF-308 is associated with an increased risk of multiple infectious diseases.
Further understanding of the pathogenesis of CAP would be valuable through the study of CAP gene variants. Many other cytokines and chemokines are important in the immune response to infection, but most have not been well studied and require further research.
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