Alkali-burned collagen produces a locomotory and metabolic stimulant to neutrophils.

Polymorphonuclear leukocytes (PMNs) invade the cornea following an alkali burn apparently undergoing a respiratory burst and degranulation, which is thought to lead to corneal ulceration. The supernatant obtained from burned Sigma collagen (Miller type 1) or from bovine cornea produced a significant locomotory stimulus to PMNs. Citrate inhibited this locomotory stimulus by 69.5% and 98%, respectively. PMNs were stimulated to undergo a respiratory burst without the concomitant release of beta-glucuronidase when exposed to the supernatant from alkali-burned commercial collagens, or from bovine or porcine corneas. This stimulation is reduced by 72% (Sigma collagen) or 89% (bovine cornea) when the supernatant is dialyzed against distilled water and reinstated when the osmolality is increased. The degree of the respiratory burst is partially dependent on the volume of the supernatant, the duration of alkali exposure, and/or the concentration of NaOH used. The respiratory burst of PMNs stimulated by alkali-burned Sigma collagen supernatant is inhibited by trifluoperazine but not by citrate or EDTA. Light and electron microscopy of these stimulated PMNs show many large blebs and hairlike projections. The authors hypothesize that collagen breakdown product(s) from alkali burning might be the initial, or one of the initial stimuli, for PMN invasion into the cornea and the subsequent activation of the respiratory burst.