Elevation by muroctasin of the serum level of the complement subcomponent C1q in mice and of its biosynthesis by cultured mouse peritoneal macrophages.

Augmentative effects of muroctasin (N2-[(N-acetylmuramoyl)-L-alanyl-D-isoglutaminyl]-N6-stearoyl-L-lysine, (MDP-Lys(L18] on the production of a subcomponent of the first complement component, C1q, in mice were examined. The serum level of C1q in mice treated subcutaneously with muroctasin was found to be elevated significantly at 24 h (p less than 0.1) and 48 h (p less than 0.01). At 24 h, samples of peritoneal macrophages were derived from mice, and incubated with Dulbecco's Modified Eagle Medium (MEM) at 37 degrees C for 24 h. At 19 h of incubation, the C1q concentration in the supernatant of the culture also increased significantly (p less than 0.05). Moreover, when the peritoneal macrophages from non-treated mice were cultured in MEM containing muroctasin (0.001 microgram/ml), the amount of C1q in the culture supernatants also increased significantly 3 h (p less than 0.01) after cultivation. These results indicate that muroctasin activated C1q generation by macrophages in mice through direct and/or indirect mechanisms.

Stimulation of plasma fibronectin production in mice by muroctasin.

The production of plasma fibronectin (PFN) in mice treated subcutaneously with N2-[(N-acetylmuramoyl)-L-alanyl-D-isoglutaminyl]-N6-stearoyl-L-lysine (MDP-Lys(L18), muroctasin), was examined. The plasma levels of PFN in mice increased significantly by treatment with a single dose of 10 to 100 micrograms/mouse of MDP-Lys(L18). A slight strain difference in the PFN levels among Std: ddY, C3H/He, and DBA 2 mice was observed: the percent increases at the maximal level in Std: ddY, C3H/He, and DBA/2 mice were 21.6, 19.9, and 10.4, respectively. In Std: ddY mice, the concentration of PFN reached the maximal level at 15 h post-treatment, and decreased gradually of the normal level by 48 h. These results indicate that MDP-Lys(L18) stimulates the PFN production in mice.

Outbreak of nosocomial urinary tract infections caused by Serratia marcescens.

A prolonged outbreak (December 1980 to July 1982) of nosocomial urinary tract infections appeared to be due to strains of Serratia marcescens that were resistant to currently available antibiotics. The serotyping and antibiotic susceptibility patterns suggested a few endemic strains of serotypes O13, O2/3, O12/14, and nontypable strains. These strains were isolated from the urine samples of inpatients with urinary tract infections in the urology ward and in other wards. The strains of O12/14 (gentamicin susceptible) were replaced with those of O2/3 (gentamicin resistant) between June and September 1981, whereas the other serotypes were isolated continuously. They were resistant to sulbenicillin, cefmetazole, gentamicin, and amikacin, and susceptible to micronomicin and of loxacin, a new quinolone antibiotic. Most of them were also resistant to the disinfectant chlorhexidine, which had been used widely for hand washing in the hospital.

Stimulation of complement production in mice by N alpha-(N-acetylmuramyl-L-alanyl-D-isoglutamine)-N epsilon-stearoyl-L-lysine.

N alpha-(N-acetylmuramyl-L-alanyl-D-isoglutamine)-N epsilon-stearoyl-L-lysine, a synthetic muramyl dipeptide analog, stimulated the production of the third component of complement (C3) in mice. The serum concentration of C3 was elevated significantly by subcutaneous treatment with a single dose (10 to 100 micrograms per mouse) of the adjuvant 24 h before assay of the serum. Thereafter, the concentration decreased gradually with time and returned to the normal level on day 4 to 5. Immunoelectrophoretic analysis of the serum revealed that the decrease in serum C3 could not be accounted for by the cleavage to C3a and C3b. By intermittent treatment with the adjuvant on every fifth day, a significant increase in serum C3 was repeated. However, no continuous retention of the serum level of C3 was established even during continuous treatment with the adjuvant once a day for 10 consecutive days. Instead, in this case, the level of C3 increased repeatedly at almost 5-day intervals.

Typing of O antigens of Vibrio parahaemolyticus by a slide agglutination test.

O antigens of Vibrio parahaemolyticus can be detected by a slide agglutination test.