Lymphocyte-Neutrophil Interactions: Opposite Effects of Interleukin-2 and Tumour Necrosis Factor-Beta (Lymphotoxin) on Human Neutrophil Adherence

Seow, W.K.; Thong, Y H; McCormack, J. G.; Fèrrante, Antonio

doi:10.1159/000234475

Cited by 17 publications

(14 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The mechanism of this inhibition could be related to increased adhesiveness of neutrophils induced by TNF for the substratum of the chamber [19,20,42,43]. However, in the present experiments, the rates of random motility of neutro phils on polycarbonate membrane were not reduced, so that increased adhesion which is so excessive as to inhibit migration seems an unlikely mechanism of re duced chemotactic movement to FMLP.…”

Section: Discussioncontrasting

confidence: 51%

Studies of Chemotactic, Chemotactic Movement-Inhibiting and Random Movement-Inhibiting Effects of Interleukin-1 Alpha and Beta, Tumor Necrosis Factors Alpha and Beta and Interferon Gamma on Human Neutrophils in Assays Using ‘Sparse-Pore’ Polycarbonate (Nuclepore) Membranes in the Boyden Chamber

Bignold

Fèrrante²,

Haynes³

1990

Int Arch Allergy Immunol

View full text Add to dashboard Cite

Interleukin-1 alpha and beta (IL-1α and β), tumour necrosis factors alpha and beta (TNFα and β) and interferon gamma (IFNγ) were tested for their chemotactic effects, their effects on chemotactic movement towards N-formyl-methionyl-leucyl-phenylalanine (FMLP) and their effects on random locomotion of human peripheral blood neutrophils through polycarbonate membranes in Boyden-type chambers. Both IL-1α and β, but no other cytokine tested were chemotactic for neutrophils using ‘sparse-pore’ polycarbonate membrane. Both TNFs, but no other cytokine, inhibited neutrophil chemotactic movement towards FMLP using the same membrane. No cytokine influenced random migration of neutrophils through polycarbonate membrane of standard pore density. These results suggest that IL-1 may have a role as a chemotactic mediator of inflammation, but that TNFs may inhibit chemotactic migration of neutrophils into inflammatory lesions.

show abstract

Section: Discussioncontrasting

confidence: 51%

Studies of Chemotactic, Chemotactic Movement-Inhibiting and Random Movement-Inhibiting Effects of Interleukin-1 Alpha and Beta, Tumor Necrosis Factors Alpha and Beta and Interferon Gamma on Human Neutrophils in Assays Using ‘Sparse-Pore’ Polycarbonate (Nuclepore) Membranes in the Boyden Chamber

Bignold

Fèrrante²,

Haynes³

1990

Int Arch Allergy Immunol

View full text Add to dashboard Cite

show abstract

“…It is likely that endothelial damage and the CLS are multifactorial in origin with adherent lymphokine activated killer and natural killer cells together with widespread activation of endothelial cells by other cytokines also playing a role (Slow et al, 1988;Aronson et al, 1988;Damle & Doyle, 1989). Our study demonstrates that activation of PMN and of the complement system contribute substantially to these processes and may be one of the initiating events.…”

Section: Discussionmentioning

confidence: 99%

The activation of polymorphonuclear neutrophils and the complement system during immunotherapy with recombinant Interleukin-2

Baars

Hack²,

Pinedo³

et al. 1992

Br J Cancer

View full text Add to dashboard Cite

Summary The toxicity due to interleukin-2 (IL-2) strongly resembles the clinical picture seen during septic shock. In septic shock activation of polymorphonuclear neutrophils (PMN) and the complement system contribute significantly to the pathophysiology of the condition. We therefore investigated whether similar events contributed to the toxicity observed with IL-2.Four patients received seven cycles of escalating dose IL-2 (18.0 to 72.0 x 106 IU m-2 day-') and 16 were treated with 20 cycles of fixed dose IL-2 (12.0 or 18.0 x 106 IU m-2 day-'). Toxicity, as judged by hypotension (P = <0.005) and capillary leakage (fall in serum albumin 18.2 vs 4.0 gm 1'; P = <0.0005 and weight gain 4.0 vs 1.2 kg; P = <0.025) were worse with the esc. dose protocol.PMN became activated following IL-2 with mean peak elastase/a,-antitrypsin (Ea,A) and lactoferrin values of 212 (SEM = 37) and 534 (SEM = 92) ng ml-' respectively occurring 6 h after the IL-2. Peak values for the esc. dose IL-2 group being generally higher than 500 ng ml-'. Activation of the complement cascade was evidenced by a dose dependent elevation of peak C3a values (fixed dose 9.1 (SEM = 0.6); esc. dose 25.7 (SEM = 6.33); P = <0.005) on day 5 of IL-2.There was a significnt correlation between C3a levels and the degree of hypotention during the first 24 h after IL-2 (r = 0.91) and parameters of capillary leakage such as weight gain and fall in serum albumin (r = 0.71).These data suggest that activation of PMN initiates endothelial cell damage which subsequently leads to activation of the complement cascade. This latter system then contributes to the haemodynamic changes and capillary leakage seen in IL-2 treated patients.

show abstract

“…Thus far, those basic mechanisms partially defined for cytokine-induced modifications in PMN function derive primarily from experiments using formylmethionylleucylphenylalanine (FMLP), phorbol myristate acetate (PMA), immunoglobulin (Ig) G-coated particles (11)(12)(13)(14)(15)(16)(17)(18)(19). However, our previous comparisons of responses to different stimuli by unprimed PMN indicate that C. albicans hyphae may elicit disparate patterns of early cellular events linked to PMN respiratory burst activation (39)(40)(41)(42).…”

mentioning

confidence: 99%

Disparate effects of interferon-gamma and tumor necrosis factor-alpha on early neutrophil respiratory burst and fungicidal responses to Candida albicans hyphae in vitro.

Diamond

Lyman²,

Wysong³

1991

J. Clin. Invest.

View full text Add to dashboard Cite

We examined effects of priming with recombinant human interferon-y (IFN) or tumor necrosis factor-a (TNF) on neutrophil responses to Candida albicans hyphae. Both cytokines increased early superoxide generation after hyphal stimulation. The more pronounced effects of TNF were accompanied by an augmented surface membrane depolarization rate and were insensitive to both pertussis toxin and calcium ion chelation, but were negated by concomitant incubation with puromycin or cycloheximide during priming. IFN augmented hyphal killing despite its only minor enhancement of early respiratory burst responses, but TNF reduced neutrophil fungicidal activity to nearly 40% below those by unprimed control cells even though it enhanced early superoxide responses more dramatically. Though TNF-primed neutrophils killed hyphae at normal initial rates, IFN-primed or even unprimed cells manifested more fungicidal sustained activity. These disparate consequences of cytokine priming on hyphal destruction were paralleled by differences in late generation of potentially candidacidal oxidants, hydrogen peroxide, and hypochlorous acid. IFN added during priming failed to correct TNF-associated functional defects in neutrophil anti-Candida responses. Thus, augmentation of early respiratory burst responses to oxidant-sensitive organisms need not necessarily reflect concomitant salutary effects on microbicidal activity. (J. Clin. Invest. 1991. 87:711-720.)

show abstract

Lymphocyte-Neutrophil Interactions: Opposite Effects of Interleukin-2 and Tumour Necrosis Factor-Beta (Lymphotoxin) on Human Neutrophil Adherence

Cited by 17 publications

References 15 publications

Studies of Chemotactic, Chemotactic Movement-Inhibiting and Random Movement-Inhibiting Effects of Interleukin-1 Alpha and Beta, Tumor Necrosis Factors Alpha and Beta and Interferon Gamma on Human Neutrophils in Assays Using ‘Sparse-Pore’ Polycarbonate (Nuclepore) Membranes in the Boyden Chamber

Studies of Chemotactic, Chemotactic Movement-Inhibiting and Random Movement-Inhibiting Effects of Interleukin-1 Alpha and Beta, Tumor Necrosis Factors Alpha and Beta and Interferon Gamma on Human Neutrophils in Assays Using ‘Sparse-Pore’ Polycarbonate (Nuclepore) Membranes in the Boyden Chamber

The activation of polymorphonuclear neutrophils and the complement system during immunotherapy with recombinant Interleukin-2

Disparate effects of interferon-gamma and tumor necrosis factor-alpha on early neutrophil respiratory burst and fungicidal responses to Candida albicans hyphae in vitro.

Contact Info

Product

Resources

About