Protease Inhibitor Eglin-C Affects Superoxide Anion Release but not Bacterial Killing by Human Polymorphonuclear Leukocytes

1988 ◽  
Vol 14 (6) ◽  
pp. 743-756 ◽  
Author(s):  
Anthony L. Esposito ◽  
Carolyn A. Clark ◽  
William J. Poirier ◽  
Phyllis A. Kephart
Keyword(s):  
Protease Inhibitor ◽  
Superoxide Anion ◽  
Polymorphonuclear Leukocytes ◽  
Bacterial Killing ◽  
Eglin C ◽  
Human Polymorphonuclear Leukocytes

scholarly journals Immunoglobulin A-Mediated Protection against Bordetella pertussis Infection

2001 ◽  
Vol 69 (8) ◽  
pp. 4846-4850 ◽  
Author(s):  
Sandra M. M. Hellwig ◽  
Annemiek B. van Spriel ◽  
Joop F. P. Schellekens ◽  
Frits R. Mooi ◽  
Jan G. J. van de Winkel
Keyword(s):  
Transgenic Mice ◽  
Bordetella Pertussis ◽  
Polymorphonuclear Leukocytes ◽  
Whooping Cough ◽  
Immunoglobulin A ◽  
Pertussis Infection ◽  
Bacterial Killing ◽  
Effector Functions ◽  
Human Polymorphonuclear Leukocytes

ABSTRACT Infection with Bordetella pertussis, the causative agent of pertussis (whooping cough) in humans, is followed by the production of antibodies of several isotypes, including immunoglobulin A (IgA). Little is known, however, about the role of IgA in immunity against pertussis. Therefore, we studied targeting ofB. pertussis to the myeloid receptor for IgA, FcαRI (CD89), using either IgA purified from immune sera of pertussis patients or bispecific antibodies directed against B. pertussis and FcαRI (CD89 BsAb). Both IgA and CD89 BsAb facilitated FcαRI-mediated binding, phagocytosis, and bacterial killing by human polymorphonuclear leukocytes (PMNL) and PMNL originating from human FcαRI-transgenic mice. Importantly, FcαRI targeting resulted in enhanced bacterial clearance in lungs of transgenic mice. These data support the capacity of IgA to induce anti-B. pertussis effector functions via the myeloid IgA receptor, FcαRI. Increasing the amount of IgA antibodies induced by pertussis vaccines may result in higher vaccine efficacy.

scholarly journals Hexachlorocyclohexanes, potent stimuli of O2- production and calcium release in human polymorphonuclear leukocytes

Blood ◽  
1986 ◽  
Vol 68 (2) ◽  
pp. 535-540
Author(s):  
DB Kuhns ◽  
SS Kaplan ◽  
RE Basford
Keyword(s):  
Superoxide Anion ◽  
Polymorphonuclear Leukocytes ◽  
Calcium Release ◽  
Divalent Cations ◽  
Calcium Mobilization ◽  
New Class ◽  
Human Polymorphonuclear Leukocytes ◽  
O2 Production

alpha-, gamma-, and delta-Hexachlorocyclohexane (HCCH), but not the beta-isomer, are shown to be potent stimuli for the production of superoxide anion (O2-) and the release of calcium in human polymorphonuclear leukocytes (PMNs). Although O2- production occurs in the absence of exogenous divalent cations, calcium (0.5 mmol/L) enhances O2- production by 50%. In addition, gamma-HCCH-induced O2- production is sensitive (IC50–30–40 mumol/L) to inhibition by the putative intracellular antagonist, 8-(diethylamino)octyl-3,4,5- trimethoxybenzoate hydrochloride (TMB-8). Furthermore, it is shown that gamma-HCCH induces a marked loss of membrane-associated calcium as monitored by chlortetracycline fluorescence. This pool of calcium appears to encompass the same pool released by the formylated tripeptide, formylmethionylleucylphenylalanine (FMLP). We suggest that the HCCHs represent a new class of stimuli of O2- production and calcium mobilization in PMNs.

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