positive regulation of neutrophil migration

Definition

Target type: biologicalprocess

Any process that activates or increases the frequency, rate or extent of neutrophil migration. [GO_REF:0000058, GOC:TermGenie, PMID:1826836]

Positive regulation of neutrophil migration is a complex and tightly regulated process that involves a cascade of molecular events. It is essential for the innate immune response, enabling neutrophils to effectively reach sites of infection or inflammation to combat pathogens.

**Initiation:**

* **Chemoattractant sensing:** Neutrophils express a variety of receptors on their cell surface that recognize and bind to chemoattractants, such as chemokines, bacterial products (e.g., N-formylmethionine peptides), and complement components. These receptors include G protein-coupled receptors (GPCRs), such as CXCR1, CXCR2, and formyl peptide receptors (FPRs).
* **Signal transduction:** Upon binding of chemoattractants, GPCRs activate intracellular signaling pathways, including the phosphoinositide 3-kinase (PI3K) pathway and the mitogen-activated protein kinase (MAPK) pathway. These pathways lead to the production of second messengers, such as diacylglycerol (DAG) and inositol trisphosphate (IP3), which play crucial roles in downstream events.

**Migration:**

* **Polarization:** The intracellular signaling events triggered by chemoattractants induce a polarized morphology in neutrophils, characterized by the formation of a leading edge and a trailing edge. The leading edge is characterized by the assembly of actin filaments and the formation of lamellipodia, which are thin, sheet-like protrusions that extend towards the chemoattractant source.
* **Chemotaxis:** Neutrophils move towards the chemoattractant gradient by a process called chemotaxis, which is mediated by the coordinated assembly and disassembly of the cytoskeleton. The leading edge extends towards the chemoattractant, while the trailing edge retracts, resulting in a net movement towards the source.
* **Adhesion:** Neutrophils adhere to the endothelium, the lining of blood vessels, through interactions between adhesion molecules expressed on both the neutrophil and the endothelial cell surface. These interactions are essential for slowing down the neutrophil's movement and allowing them to migrate through the endothelium into the tissues.

**Termination:**

* **Apoptosis:** After reaching the site of infection or inflammation, neutrophils undergo apoptosis, a programmed cell death process. This prevents excessive inflammation and tissue damage.
* **Phagocytosis:** Neutrophils engulf and destroy pathogens, such as bacteria and fungi, through a process called phagocytosis. This process is essential for clearing the infection.

**Regulation:**

* **Cytokine modulation:** The production and release of cytokines, such as TNF-alpha, IL-1, and IL-6, can modulate neutrophil migration by regulating the expression of chemokine receptors and adhesion molecules.
* **Immune cell interactions:** Neutrophils interact with other immune cells, such as lymphocytes and macrophages, to fine-tune their migration and function.
* **Microenvironment:** The local environment, including pH, oxygen tension, and presence of extracellular matrix components, can influence neutrophil migration.

In summary, positive regulation of neutrophil migration is a multifaceted process involving a complex interplay of signaling pathways, cytoskeletal rearrangements, and interactions with the surrounding environment. It is crucial for the rapid and effective recruitment of neutrophils to sites of infection or inflammation, enabling them to combat pathogens and protect the host.'
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Proteins (1)

Compounds (11)