EFFECTS OF GROWTH-HORMONE AND INSULIN-LIKE-GROWTH-FACTOR-I ON OPSONINRECEPTOR EXPRESSION ON LOCAL AND SYSTEMIC PHAGOCYTES IN A LETHAL PERITONITIS MODEL
T. Inoue et al., EFFECTS OF GROWTH-HORMONE AND INSULIN-LIKE-GROWTH-FACTOR-I ON OPSONINRECEPTOR EXPRESSION ON LOCAL AND SYSTEMIC PHAGOCYTES IN A LETHAL PERITONITIS MODEL, Critical care medicine, 26(2), 1998, pp. 338-343
Objective: To investigate the effects of pretreatment with growth horm
one (GH) and insulin like growth factor I (IGF-I) on phagocyte exudati
on and bacterial clearance, focusing on CD11b and CD32/CD16 expression
on local and systemic phagocytes, in a lethal peritonitis model. Desi
gn: Prospective randomized experimental study. Setting: Research labor
atory in a university hospital. Subjects: Balb/c mice (n = 21). Interv
entions: Mice were challenged intraperitoneally with 1 x 10(8) Escheri
chia coli, after 6 days of pretreatment with saline (control), GH (4.8
mg/kg/day), or IGF-I (24 mg/kg/day). Samples were harvested at 4 hrs
after the challenge. Measurements and Main Results: Viable bacterial c
ounts in peritoneal lavage fluid (PLF) and blood were determined. Peri
toneal exudative cells and peripheral blood leukocytes were counted an
d analyzed for receptor expressions by flow cytometry. GH reduced viab
le bacterial counts in PLF, as compared with the saline control. GH (t
hree fold) and IGF I (two fold) increased the number of peritoneal exu
dative neutrophils (PENs), as compared with the saline control. The nu
mber of PENs showed an inverse correlation with PLF viable bacterial c
ounts. By contrast, there were no differences in peripheral blood neut
rophil (PN) counts among the three groups, nor was there a correlation
between PN and PEN counts. CD11b expression was greater on PENs than
on PNs in all three groups. CD11b expression on PNs did not differ amo
ng the three groups. However, GH increased CD11b expression on PENs, a
s compared with saline and IGF-I, and this expression showed a positiv
e correlation with PEN numbers and an inverse correlation with PLF via
ble bacterial counts. CD11b expression on peritoneal macrophages and p
eripheral blood monocytes did not differ among the three groups. There
were no differences in phagocyte CD32/CD16 expression among the three
groups. Conclusions: GH pretreatment enhanced CD11b expression on PEN
s, but not PNs, possibly in association with enhanced neutrophil recru
itment, phagocytosis, and bacterial elimination by PENs, without activ
ation of PNs. GH prophylaxis may be useful for reducing the frequency
rate and severity of septic complications, via modulation of CD11b exp
ression on local and systemic neutrophils.