Pro-inflammatory agents released by pathogens, dying host cells, and neutrophils act synergistically to destroy host tissues: a working hypothesis.
bacterial toxin
bacteriolysis
cationic proteins
sepsis
synergism
tissue damage
Journal
Journal of inflammation research
ISSN: 1178-7031
Titre abrégé: J Inflamm Res
Pays: New Zealand
ID NLM: 101512684
Informations de publication
Date de publication:
2019
2019
Historique:
entrez:
19
2
2019
pubmed:
19
2
2019
medline:
19
2
2019
Statut:
epublish
Résumé
We postulate that the extensive cell and tissue damage inflicted by many infectious, inflammatory and post-inflammatory episodes is an enled result of a synergism among the invading microbial agents, host neutrophils and dead and dying cells in the nidus. Microbial toxins and other metabolites along with the plethora of pro-inflammatory agents released from activated neutrophils massively recruited to the infectious sites and high levels of cationic histones, other cationic peptides, proteinases and Th1 cytokines released from activated polymorphonuclear neutrophils (PMNs) and from necrotized tissues may act in concert (synergism) to bring about cell killing and tissue destruction. Multiple, diverse interactions among the many potential pro-inflammatory moieties have been described in these complex lesions. Such infections are often seen in the skin and aerodigestive tract where the tissue is exposed to the environment, but can occur in any tissue. Commonly, the tissue-destructive infections are caused by group A streptococci, pneumococci,
Identifiants
pubmed: 30774411
doi: 10.2147/JIR.S190007
pii: jir-12-035
pmc: PMC6350637
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
35-47Déclaration de conflit d'intérêts
Disclosure The authors report no conflicts of interest in this work.
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