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Inflammation aiguë I : phase cellulaire
La phase cellulaire de l’inflammation aiguë est une séquence d’événements étroitement orchestrée qui recrute des leucocytes, principalement des neutro…
La phase cellulaire de l’inflammation aiguë implique des étapes qui recrutent les leucocytes vers le site de la blessure.
La première est la margination, où les leucocytes se déplacent vers la paroi du vaisseau à mesure que le flux sanguin ralentit et que la viscosité augmente. Cela est suivi par le roulement, où elles se lient et se délient lâchement aux sélections endothéliales.
Ensuite, lors d’une adhésion ferme, les intégrines leucocytaires se lient étroitement aux molécules d’adhésion endothéliales telles que l’ICAM-1 et le VCAM-1.
Ensuite, dans la diapédèse, les leucocytes se pressent entre les cellules endothéliales pour pénétrer dans le tissu.
À l’intérieur du phagolysosome, les agents pathogènes sont décomposés par des espèces réactives de l’oxygène et des enzymes protéolytiques.
Après avoir accompli leur rôle, les neutrophiles subissent une apoptose et sont normalement éliminés discrètement par les macrophages.
Si l’élimination est retardée, leurs enzymes peuvent s’infiltrer dans les tissus environnants et poursuivre le processus inflammatoire.
Si le stimulus nuisible est éliminé, les signaux anti-inflammatoires et les médiateurs pro-résolution restaurent l’homéostasie tissulaire.
Une inflammation persistante ou non résolue peut évoluer vers une inflammation chronique.
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Q1: What is margination in the cellular phase of acute inflammation?
Margination is the first step of leukocyte recruitment where reduced blood flow causes leukocytes to move toward the vessel wall as blood viscosity increases. This positioning along the endothelium prepares cells for the subsequent rolling and adhesion phases, enabling their eventual migration into inflamed tissue.
Q2: How do leukocytes move from rolling to firm adhesion?
During rolling, leukocytes loosely bind and unbind to endothelial selectins. Firm adhesion occurs when leukocyte integrins such as LFA-1 and Mac-1 bind tightly to endothelial adhesion molecules like ICAM-1 and VCAM-1. This tight binding halts rolling motion and anchors cells in preparation for tissue entry through diapedesis.
Q3: What happens during diapedesis in acute inflammation?
Diapedesis is the process where leukocytes squeeze between endothelial cells to enter tissue. Molecules such as PECAM-1 facilitate this transmigration. Once in the interstitial space, leukocytes respond to chemoattractants including IL-8, C5a, and leukotriene B4, which guide them to the precise injury site.
Q4: How do neutrophils destroy pathogens inside phagolysosomes?
Neutrophils engulf pathogens into phagosomes that fuse with lysosomes to form phagolysosomes. Inside, reactive oxygen species and proteolytic enzymes break down and destroy the pathogens. After completing their antimicrobial role, neutrophils undergo apoptosis and autophagy, then are normally cleared quietly by macrophages.
Q5: What causes tissue damage when neutrophil clearance is delayed?
If macrophage clearance of apoptotic neutrophils is delayed, neutrophil enzymes may leak into surrounding tissue and continue the inflammatory process, causing additional damage. This enzyme release extends inflammation beyond its intended protective role and can worsen tissue injury at the inflammation site.
Q6: How does acute inflammation resolve when the injury is eliminated?
When the injurious stimulus is eliminated, anti-inflammatory signals and pro-resolving mediators restore tissue homeostasis, allowing inflammation to resolve. If the cause persists or inflammation remains unresolved, it may transition into chronic inflammation, requiring different immune mechanisms for resolution and management.
Q7: What is the role of chemotaxis in leukocyte recruitment?
Chemotaxis is the directed migration of leukocytes in response to chemoattractants released at injury sites. Key chemotactic agents include interleukin-8, complement component C5a, and leukotriene B4. These chemical signals guide neutrophils and other leukocytes precisely to the location of tissue damage or infection.