Immunoinflammatory mechanism of severe pneumonia and the application of inflammatory markers in clinical practice

  • Yanxin Xu The Fourth Affiliated Hospital of Harbin Medical University
  • Lixia Qian The Fourth Affiliated Hospital of Harbin Medical University
  • Feiyan Wu The Fourth Affiliated Hospital of Harbin Medical University
  • Yuanyuan Liu The Fourth Affiliated Hospital of Harbin Medical University
  • Shoude Jin The Fourth Affiliated Hospital of Harbin Medical University
Keywords: Severe Pneumonia; Immune Inflammation; Inflammatory Markers


Pneumonia is a common disease and one of the leading causes of morbidity and mortality worldwide. [1] Severe pneumonia is a unique clinical disease that is highly life-threatening, characterized by severe sepsis, septic shock, or respiratory failure. Usually, treatment is required in the intensive care unit (ICU). Approximately 10% of community-acquired pneumonia (CAP) patients require hospitalization, with a mortality rate of 21% -47%. Most patients with severe community-acquired pneumonia have complications, including chronic obstructive pulmonary disease, diabetes and coronary heart disease. Streptococcus pneumoniae, Staphylococcus aureus, Mycoplasma pneumoniae, aaLe_x005fgionella, Klebsiella pneumoniae, Haemophilus influenzae, novel coronavirus, respiratory virus and Pseudomonas aeruginosa are important pathogenic microorganisms for severe CAP. [2] Host autoimmune factors, patient clinical manifestations, and laboratory and imaging examination results at admission can help identify high-risk populations for this disease. Early identification and timely empirical application of antibiotics are particularly important for the prognosis of patients.


[1] Lanks CW, Musani AI, Hsia DW (2019) Community-acquired Pneumonia and Hospital-acquired Pneumonia. Med Clin North Am

103: 487-501.

[2] Ewig S, Torres A (1999) Severe community-acquired pneumonia. Clin Chest Med 20: 575-587.

[3] Mizgerd JP (2012) Respiratory infection and the impact of pulmonary immunity on lung health and disease. Am J Respir Crit Care

Med 186: 824-829.

[4] Marshall NB, Swain SL (2011) Cytotoxic CD4+ T cells in antiviral immunity. J Biomed Biotechnol 2011: 954602.

[5] Lumeng CN (2016) Lung Macrophage Diversity and Asthma. Ann Am Thorac Soc 13 Suppl 1: S31-34.

[6] Hussell T, Bell TJ (2014) Alveolar macrophages: plasticity in a tissue-specific context. Nat Rev Immunol 14: 81-93.

[7] Takabayshi K, Corr M, Hayashi T, et al. (2006) Induction of a homeostatic circuit in lung tissue by microbial compounds. Immunity 24: 475-487.

[8] Mizgerd JP (2008) Acute lower respiratory tract infection. N Engl J Med 358: 716-727.

[9] Park BV, Pan F (2015) Metabolic regulation of T cell differentiation and function. Mol Immunol 68: 497-506.

[10]Niedzwiedzka-Rystwej P, Tokarz-Deptula B, Deptula W (2013) [Characteristics of T lymphocyte subpopulations]. Postepy Hig

Med Dosw (Online) 67: 371-379.

[11]Zhu J, Paul WE (2008) CD4+ T cells: fates, functions, and faults. Blood 112: 1557-1569.

[12]Zhou L, Chong MM, Littman DR (2009) Plasticity of CD4++ T cell lineage differentiation. Immunity 30: 646-655.

[13]Luckheeram RV, Zhou R, Verma AD, et al. (2012) CD4+(+)T cells: differentiation and functions. Clin Dev Immunol 2012: 925135.

[14]De Carli M, D’Elios MM, Zancuoghi G, et al. (1994) Human Th1 and Th2 cells: functional properties, regulation of development

and role in autoimmunity. Autoimmunity 18: 301-308.

[15]Peiris JS, Hui KP, Yen HL (2010) Host response to influenza virus: protection versus immunopathology. Curr Opin Immunol 22:


[16]Chang YJ, Kim HY, Albacker LA, et al. (2011) Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity. Nat Immunol 12: 631-638.

[17]Bilate AM, Lafaille JJ (2012) Induced CD4++Foxp3+ regulatory T cells in immune tolerance. Annu Rev Immunol 30: 733-758.

[18]Fu B, Zhang P, Zhang J (2023) Diagnosis and Prognosis Evaluation of Severe Pneumonia by Lung Ultrasound Score Combined

with Serum Inflammatory Markers. Mediterr J Hematol Infect Dis 15: e2023057.

[19]Wang C, Deng R, Gou L, et al. (2020) Preliminary study to identify severe from moderate cases of COVID-19 using combined

hematology parameters. Ann Transl Med 8: 593.

[20]Howie SR, Morris GA, Tokarz R, et al. (2014) Etiology of severe childhood pneumonia in the Gambia, West Africa, determined by

conventional and molecular microbiological analyses of lung and pleural aspirate samples. Clin Infect Dis 59: 682-685.

[21]Wu Y, Potempa LA, El Kebir D, et al. (2015) C-reactive protein and inflammation: conformational changes affect function. Biol

Chem 396: 1181-1197.

[22]Coelho LM, Salluh JI, Soares M, et al. (2012) Patterns of c-reactive protein RATIO response in severe community-acquired pneumonia: a cohort study. Crit Care 16: R53.

[23]Velazquez-Salinas L, Verdugo-Rodriguez A, Rodriguez LL, et al. (2019) The Role of Interleukin 6 During Viral Infections. Front

Microbiol 10: 1057.

Review Article