neutrophilattracting

Neutrophil-attracting describes substances and signals that recruit neutrophils to sites of infection or tissue injury. This recruitment relies largely on chemotaxis, the directed movement of cells along chemical gradients. Neutrophils are among the first immune responders and play a key role in early antimicrobial defense.

Mechanisms involve receptors on neutrophils that sense chemoattractants and trigger migration. Key receptors include CXCR1 and CXCR2 for the chemokine interleukin-8/CXCL8, the formyl peptide receptor FPR1 for N-formyl peptides from bacteria, the C5a receptor (C5AR1) for the complement component C5a, and receptors for leukotriene B4 (LTB4).

Major neutrophil attractants include IL-8 (CXCL8) and related ELR+ CXC chemokines such as CXCL1, CXCL2 and CXCL3 in humans; lipid mediators like leukotriene B4; the anaphylatoxin C5a; and bacterial products such as formylated peptides (e.g., fMLP).

Sources include host cells such as macrophages, epithelial and endothelial cells, mast cells, and platelets that release chemokines and lipid mediators in response to infection or tissue damage; pathogens themselves can contribute via surface molecules and toxins that stimulate host cells to release attractants.

Physiological and pathological roles: neutrophil-attracting signals are essential for rapid microbial clearance but excessive or prolonged recruitment can cause tissue damage and contribute to inflammatory diseases such as ARDS, sepsis, inflammatory bowel disease and rheumatoid arthritis.

Regulation and resolution: anti-inflammatory mediators such as lipoxins and resolvins help terminate neutrophil recruitment and promote clearance of neutrophils from tissues, restoring homeostasis.