Evidence that neutrophil accumulation induced by interleukin‐1 requires both local protein biosynthesis and neutrophil CD18 antigen expression in vivo

Abstract

Mechanisms involved in neutrophil accumulation induced by intradermal injection of interleukin‐1 (IL‐1) in the rabbit were investigated using intravenously‐injected 111In‐labelled neutrophils. C5a des Arg, N‐formyl‐methionyl‐leucyl‐phenylalanine (FMLP) and leukotriene B4 (LTB4) were included for comparison. Local inhibition of protein biosynthesis in the skin using actinomycin‐D or cycloheximide blocked 111In‐neutrophil accumulation induced by IL‐1, but not that induced by the other mediators. Actinomycin‐D and cycloheximide had no effect on local plasma protein leakage induced by intradermally‐injected C5a des Arg, or that induced by zymosan. 111In‐neutrophil accumulation induced by zymosan was, however, partially suppressed. A monoclonal antibody, MoAb 60.3, recognising neutrophil surface CD18 antigen, was preincubated with 111In‐neutrophils before intravenous injection. This pretreatment did not affect circulating numbers of radiolabelled cells, but it inhibited their accumulation in response to IL‐1, C5a des Arg and the other mediators. The results suggest that neutrophil accumulation induced by IL‐1, but not the other mediators, requires local protein biosynthesis, probably in the microvascular endothelium. Neutrophil accumulation to IL‐1 and the other mediators appears to require neutrophil surface antigen, CD18. The inflammatory response to zymosan may be mediated by both endogenous C5a des Arg and IL‐1.

Neurokinin-1 Receptor Agonists Are Involved in Mediating Neutrophil Accumulation in the Inflamed, But Not Normal, Cutaneous Microvasculature: An In Vivo Study Using Neurokinin-1 Receptor Knockout Mice

“…The proinflammatory cytokine IL-1␤ is a potent mediator of neutrophil accumulation in vivo, inducing local neutrophil accumulation after injection into a range of specific tissue sites (21)(22)(23). In 1989, Osborn et al (24) reported that IL-1 was able to augment the adhesiveness of the vascular endothelium.…”

Role of adhesion glycoproteins CD 18 and intercellular adhesion molecule‐1 in complement‐mediated reactions of rabbit skin

“…The CD18/P2 integrin family of adhesion molecules has been extensively studied both in vitro (Springer, 1990) and in vivo (Rampart & Williams, 1988;Nourshargh et al, 1989;1993a,b;Argenbright & Barton, 1992;Williams & Hellewell, 1992). Two members of the P2 integrin family, CDlIa/CD18 (LFA-1) and Cllb/CD18 (Mac-i) are widely held to be important in neutrophil adhesion at and migration to inflammatory sites.…”

“…Studies have shown that antibodies raised against these molecules can be effective blockers of neutrophil adhesion in vitro (Sanchez-Madrid et al, 1983;Rothlein et al, 1986), and of inflammation in vivo (Arfors et al, 1987;Rampart & Williams, 1988;Barton et al, 1989;. Recently it has been shown that the Shwartzman reaction, a phenomenon that models disseminated intravascular coagulation, and non-immune complex mediated vasculitis, is both CD18 and ICAM-1 dependent (Argenbright & Barton, 1991).…”

A role for endogenous histamine in interleukin‐8‐induced neutrophil infiltration into mouse air‐pouch: investigation of the modulatory action of systemic and local dexamethasone

“…ing DNA-dependent RNA synthesis (Rampart & Williams, 1988;Colditz et al, 1989;Foster et al, 1989;Rampart et al, 1989). In this respect, IL-8 is considered to be a direct chemoattractant as are C5a and leukotriene B4.…”