Pleural Empyema pathophysiology: Difference between revisions
Jump to navigation
Jump to search
Prince Djan (talk | contribs) No edit summary |
Prince Djan (talk | contribs) No edit summary |
||
| Line 10: | Line 10: | ||
Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of pro-inflammatory cytokines, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.<ref name="pmid8144895">{{cite journal| author=Broaddus VC, Boylan AM, Hoeffel JM, Kim KJ, Sadick M, Chuntharapai A et al.| title=Neutralization of IL-8 inhibits neutrophil influx in a rabbit model of endotoxin-induced pleurisy. | journal=J Immunol | year= 1994 | volume= 152 | issue= 6 | pages= 2960-7 | pmid=8144895 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8144895 }} </ref><ref name="pmid1416405">{{cite journal| author=Broaddus VC, Hébert CA, Vitangcol RV, Hoeffel JM, Bernstein MS, Boylan AM| title=Interleukin-8 is a major neutrophil chemotactic factor in pleural liquid of patients with empyema. | journal=Am Rev Respir Dis | year= 1992 | volume= 146 | issue= 4 | pages= 825-30 | pmid=1416405 | doi=10.1164/ajrccm/146.4.825 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1416405 }} </ref><ref name="pmid9387973">{{cite journal| author=Kroegel C, Antony VB| title=Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy. | journal=Eur Respir J | year= 1997 | volume= 10 | issue= 10 | pages= 2411-8 | pmid=9387973 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9387973 }} </ref> | Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of pro-inflammatory cytokines, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.<ref name="pmid8144895">{{cite journal| author=Broaddus VC, Boylan AM, Hoeffel JM, Kim KJ, Sadick M, Chuntharapai A et al.| title=Neutralization of IL-8 inhibits neutrophil influx in a rabbit model of endotoxin-induced pleurisy. | journal=J Immunol | year= 1994 | volume= 152 | issue= 6 | pages= 2960-7 | pmid=8144895 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=8144895 }} </ref><ref name="pmid1416405">{{cite journal| author=Broaddus VC, Hébert CA, Vitangcol RV, Hoeffel JM, Bernstein MS, Boylan AM| title=Interleukin-8 is a major neutrophil chemotactic factor in pleural liquid of patients with empyema. | journal=Am Rev Respir Dis | year= 1992 | volume= 146 | issue= 4 | pages= 825-30 | pmid=1416405 | doi=10.1164/ajrccm/146.4.825 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=1416405 }} </ref><ref name="pmid9387973">{{cite journal| author=Kroegel C, Antony VB| title=Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy. | journal=Eur Respir J | year= 1997 | volume= 10 | issue= 10 | pages= 2411-8 | pmid=9387973 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=9387973 }} </ref> | ||
These mediators induce changes in the permeability of the mesothelial cell monolayer, which contributes to fluid accumulation in the pleural space. Murine studies of infection with S. aureus suggest pleural mesothelial cells express early response genes c-fos and c-jun, followed by the expression of pro-apoptotic genes Bak and Bad during late stage infection.<ref name="pmid17929089">{{cite journal| author=Mohammed KA, Nasreen N, Antony VB| title=Bacterial induction of early response genes and activation of proapoptotic factors in pleural mesothelial cells. | journal=Lung | year= 2007 | volume= 185 | issue= 6 | pages= 355-65 | pmid=17929089 | doi=10.1007/s00408-007-9046-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17929089 }} </ref This leads to pleural mesothelial cell apoptosis and loss of monolayer integrity, which may contribute to loss of the normal fibrinolytic milieu of the pleural space with conversion to a more pro-fibrinogenic, anti-fibrinolytic environment, with release of TNF-α from mesothelial cells | These mediators induce changes in the permeability of the mesothelial cell monolayer, which contributes to fluid accumulation in the pleural space. Murine studies of infection with S. aureus suggest pleural mesothelial cells express early response genes c-fos and c-jun, followed by the expression of pro-apoptotic genes Bak and Bad during late stage infection.<ref name="pmid17929089">{{cite journal| author=Mohammed KA, Nasreen N, Antony VB| title=Bacterial induction of early response genes and activation of proapoptotic factors in pleural mesothelial cells. | journal=Lung | year= 2007 | volume= 185 | issue= 6 | pages= 355-65 | pmid=17929089 | doi=10.1007/s00408-007-9046-6 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=17929089 }} </ref This leads to pleural mesothelial cell apoptosis and loss of monolayer integrity, which may contribute to loss of the normal fibrinolytic milieu of the pleural space with conversion to a more pro-fibrinogenic, anti-fibrinolytic environment, with release of TNF-α from mesothelial cells and concurrent upregulation of antifibrinolytic mediators, such as plasminogen activator inhibitor-1 and -2<ref name="pmid2064128">{{cite journal| author=Idell S, Girard W, Koenig KB, McLarty J, Fair DS| title=Abnormalities of pathways of fibrin turnover in the human pleural space. | journal=Am Rev Respir Dis | year= 1991 | volume= 144 | issue= 1 | pages= 187-94 | pmid=2064128 | doi=10.1164/ajrccm/144.1.187 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=2064128 }} </ref>. Infection of mesothelial cells with live mycobacteria bacille Calmette–Guerin (BCG) results in enhanced vascular endothelial growth factor release<ref name="pmid12953144">{{cite journal| author=Mohammed KA, Nasreen N, Hardwick J, Van Horn RD, Sanders KL, Antony VB| title=Mycobacteria induces pleural mesothelial permeability by down-regulating beta-catenin expression. | journal=Lung | year= 2003 | volume= 181 | issue= 2 | pages= 57-66 | pmid=12953144 | doi=10.1007/s00408-003-1006-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12953144 }} </ref> and both live BCG and S. aureus infection increase permeability across the mesothelial monolayer, in part via downregulation of β-catenin. <ref name="pmid12953144">{{cite journal| author=Mohammed KA, Nasreen N, Hardwick J, Van Horn RD, Sanders KL, Antony VB| title=Mycobacteria induces pleural mesothelial permeability by down-regulating beta-catenin expression. | journal=Lung | year= 2003 | volume= 181 | issue= 2 | pages= 57-66 | pmid=12953144 | doi=10.1007/s00408-003-1006-1 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=12953144 }} </ref><ref name="pmid11404254">{{cite journal| author=Mohammed KA, Nasreen N, Hardwick J, Logie CS, Patterson CE, Antony VB| title=Bacterial induction of pleural mesothelial monolayer barrier dysfunction. | journal=Am J Physiol Lung Cell Mol Physiol | year= 2001 | volume= 281 | issue= 1 | pages= L119-25 | pmid=11404254 | doi= | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=11404254 }} </ref> | ||
With persistent inflammation, increased vascular and mesothelial permeability leads to increased plasma extravasation into the pleural cavity. Activation of the coagulation cascade within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion, with fibrin deposition over both pleural surfaces and characteristic fibrinous septae producing loculated effusions. | With persistent inflammation, increased vascular and mesothelial permeability leads to increased plasma extravasation into the pleural cavity. Activation of the coagulation cascade within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion, with fibrin deposition over both pleural surfaces and characteristic fibrinous septae producing loculated effusions. | ||
Revision as of 20:27, 4 January 2017
|
Empyema Microchapters |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Prince Tano Djan, BSc, MBChB [2]
Overview
Pathophysiology
The process leading to the formation of empyema involves migration of organisms into the pleural cavity. This may be via direct extension/contiguous route. Contiguous infection {synpneumonic infection} leading to increased polymorphs to the pleura space and release of inflammatory cellular components and toxic oxygen species. This promotes endothelial injury resulting in increased pleural membrane permeability and increased osmotic pressure.[1] The resultant empyema may spontaneously burrowed through the parietal pleura into the chest wall to form a subcutaneous abscess that may eventually rupture through the skin leading to formation of empyema necessitans.[2]
Lung parenchymal infection stimulates local pleural immune activation, neutrophil migration and release of pro-inflammatory cytokines, such as IL-6, IL-8 and tumour necrosis factor (TNF)-α.[3][4][5] These mediators induce changes in the permeability of the mesothelial cell monolayer, which contributes to fluid accumulation in the pleural space. Murine studies of infection with S. aureus suggest pleural mesothelial cells express early response genes c-fos and c-jun, followed by the expression of pro-apoptotic genes Bak and Bad during late stage infection.. Infection of mesothelial cells with live mycobacteria bacille Calmette–Guerin (BCG) results in enhanced vascular endothelial growth factor release[6] and both live BCG and S. aureus infection increase permeability across the mesothelial monolayer, in part via downregulation of β-catenin. [6][7]
With persistent inflammation, increased vascular and mesothelial permeability leads to increased plasma extravasation into the pleural cavity. Activation of the coagulation cascade within the pleural cavity contributes to the development of a “fibrinopurulent” or “complicated” parapneumonic effusion, with fibrin deposition over both pleural surfaces and characteristic fibrinous septae producing loculated effusions.
References
- ↑ Strange C, Tomlinson JR, Wilson C, Harley R, Miller KS, Sahn SA (1989). "The histology of experimental pleural injury with tetracycline, empyema, and carrageenan". Exp Mol Pathol. 51 (3): 205–19. PMID 2480911.
- ↑ Ahmed SI, Gripaldo RE, Alao OA (2007). "Empyema necessitans in the setting of pneumonia and parapneumonic effusion". Am J Med Sci. 333 (2): 106–8. PMID 17301589.
- ↑ Broaddus VC, Boylan AM, Hoeffel JM, Kim KJ, Sadick M, Chuntharapai A; et al. (1994). "Neutralization of IL-8 inhibits neutrophil influx in a rabbit model of endotoxin-induced pleurisy". J Immunol. 152 (6): 2960–7. PMID 8144895.
- ↑ Broaddus VC, Hébert CA, Vitangcol RV, Hoeffel JM, Bernstein MS, Boylan AM (1992). "Interleukin-8 is a major neutrophil chemotactic factor in pleural liquid of patients with empyema". Am Rev Respir Dis. 146 (4): 825–30. doi:10.1164/ajrccm/146.4.825. PMID 1416405.
- ↑ Kroegel C, Antony VB (1997). "Immunobiology of pleural inflammation: potential implications for pathogenesis, diagnosis and therapy". Eur Respir J. 10 (10): 2411–8. PMID 9387973.
- ↑ 6.0 6.1 Mohammed KA, Nasreen N, Hardwick J, Van Horn RD, Sanders KL, Antony VB (2003). "Mycobacteria induces pleural mesothelial permeability by down-regulating beta-catenin expression". Lung. 181 (2): 57–66. doi:10.1007/s00408-003-1006-1. PMID 12953144.
- ↑ Mohammed KA, Nasreen N, Hardwick J, Logie CS, Patterson CE, Antony VB (2001). "Bacterial induction of pleural mesothelial monolayer barrier dysfunction". Am J Physiol Lung Cell Mol Physiol. 281 (1): L119–25. PMID 11404254.