Bacteria at the infection site are a steady-state chemical source. In three dimensions, a point source diffusing at rate D reaches a steady concentration that falls off as 1/r:
C(r) = Q / (4πD·r)
∇C ∝ -(p - src) / r³ (points toward the source)
|∇C| ∝ 1 / r²
Each neutrophil sums that gradient contribution from every live bacterium, then blends it with random thermal jitter using the chemotactic sensitivity s:
v = normalize( s·Σ ∇C_i + (1-s)·jitter ) · speed
This is the classic biased-random-walk model of leukocyte chemotaxis: at s = 0 the cell explores blindly; at s = 1 it beelines for the strongest gradient.
- Phagocytosis — a neutrophil that comes within its capture radius of a bacterium engulfs and destroys it with a per-frame probability, exactly like real granulocyte engulfment.
- NETosis — if the local bacterial density around a neutrophil exceeds the NETosis threshold, the cell is overwhelmed: it stops moving, ruptures, and releases a web of decondensed chromatin (a NET) that immobilises every bacterium inside its radius, which then decay over time instead of being individually engulfed.
- Infection severity controls the bacterial spawn rate at the wound site; recruitment controls how fast fresh neutrophils arrive from the vessel margin.
Real-world relevance: this two-tier response — fast one-by-one phagocytosis backed by a "scorched earth" NET release once a cell is outnumbered — is exactly how innate immunity buys time against a bacterial infection before antibodies and antibiotics can act.