Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “BACTERIOLYSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMedDate not supplied

Role of complement in host resistance against members of the Bacteroidaceae.

Considerable evidence has been reported in recent years suggesting that complement plays an important role in host resistance against members of the Bacteroidaceae. Most of the investigations in this area have focused on the genus Bacteroides because of its clinical importance. Various species of Bacteroides have been shown to activate the complement system in vitro via the classical and alternative pathways. Complement activation results in the generation of chemotactic factors that mobilize polymorphonuclear leukocytes to sites of infection. Activated complement also facilitates bacteriolysis and opsonophagocytic killing by polymorphonuclear leukocytes and macrophages. Strains possessing dense fibrillar polysaccharide capsules are resistant to both of these defense mechanisms. The putative importance of complement-dependent bacteriolysis and opsonophagocytic killing in resistance against Bacteroides infections in vivo requires confirmation. In addition, the role of complement in synergistic interactions between Bacteroides and facultative bacteria remains to be elucidated.

Antibodies, Bacterial↗
PubMed1990

Induction of autolysis in Enterococcus faecalis S-47 by peptide AS-48.

In addition to its bactericidal mode of action, the peptide antibiotic AS-48 exhibits a bacteriolytic effect on Enterococcus faecalis S-47 that is associated with autolysin activation. Bacteriolysis induced by the antibiotic can be modulated by addition of EDTA, divalent cations and autolysin activators (trypsin) or inhibitors (cardiolipin), suggesting that topologic regulation of the autolysins is involved in the process. In addition, inhibitors of protein and RNA synthesis interfere markedly with bacteriolysis, as do ionophores and the ATPase inhibitor DCCD, suggesting the participation of an internal messenger in autolysin activation in the presence of AS-48.

Anti-Bacterial Agents↗
PubMed1985

Differentiation among closely related organisms of the Actinobacillus-Haemophilus-Pasteurella group by means of lysozyme and EDTA.

Bacteriolysis in Tris-maleate buffer (0.005 M, pH 7.2) supplemented with EDTA (0.01 M) and hen egg white lysozyme (HEWL, 1.0 microgram/ml) was set up to assist differentiation between the taxonomically closely related Actinobacillus actinomycetemcomitans and Haemophilus aphrophilus. A. actinomycetemcomitans was more sensitive to lysis in this system than H. aphrophilus. The standard method for bacteriolysis separated the 10 tested strains of A. actinomycetemcomitans into two groups (I and II) based on their lysis patterns, whereas the 7 strains of H. aphrophilus examined were homogeneous. In group I of A. actinomycetemcomitans, EDTA displayed a considerable lytic effect, which was not increased by supplementation with HEWL. In group II, the lytic effect of EDTA was much less, but HEWL had a considerable supplementary lytic effect. When the turbidity of A. actinomycetemcomitans (ATCC 29522) or H. aphrophilus (ATCC 33389) suspended in Tris buffer was monitored at close pH intervals (0.2) from pH 5.2 to 9.2, maximal lysis of ATCC 29522 occurred with EDTA at pH 8.0 and with EDTA-HEWL at pH 7.6, while ATCC 33389 lysed with EDTA at pH 9.0 and with EDTA-HEWL at pH 9.2. When other members of the family Pasteurellaceae (Haemophilus influenzae type b, Haemophilus paraphrophilus, Pasteurella multocida, Pasteurella haemolytica, and Pasteurella ureae) were included for comparison, the group I strains of A. actinomycetemcomitans were the most rapidly lysed by EDTA. H. paraphrophilus was the least sensitive of the gram-negative strains tested, but not as resistant as Micrococcus luteus (control). M. luteus was the organism most sensitive to lysozyme, followed by P. ureae and the group II strains of A. actinomycetemcomitans, while the group I strains of A. actinomycetemcomitans, H. paraphrophilus, and P. haemolytica were the least sensitive organisms.

Actinobacillus↗
PubMed1998

Staphylococcal cell wall: morphogenesis and fatal variations in the presence of penicillin.

The primary goal of this review is to provide a compilation of the complex architectural features of staphylococcal cell walls and of some of their unusual morphogenetic traits including the utilization of murosomes and two different mechanisms of cell separation. Knowledge of these electron microscopic findings may serve as a prerequisite for a better understanding of the sophisticated events which lead to penicillin-induced death. For more than 50 years there have been controversial disputes about the mechanisms by which penicillin kills bacteria. Many hypotheses have tried to explain this fatal event biochemically and mainly via bacteriolysis. However, indications that penicillin-induced death of staphylococci results from overall biochemical defects or from a fatal attack of bacterial cell walls by bacteriolytic murein hydrolases were not been found. Rather, penicillin, claimed to trigger the activity of murein hydrolases, impaired autolytic wall enzymes of staphylococci. Electron microscopic investigations have meanwhile shown that penicillin-mediated induction of seemingly minute cross wall mistakes is the very reason for this killing. Such "morphogenetic death" taking place at predictable cross wall sites and at a predictable time is based on the initiation of normal cell separations in those staphylococci in which the completion of cross walls had been prevented by local penicillin-mediated impairment of the distribution of newly synthesized peptidoglycan; this death occurs because the high internal pressure of the protoplast abruptly kills such cells via ejection of some cytoplasm during attempted cell separation. An analogous fatal onset of cell partition is considered to take place without involvement of a detectable quantity of autolytic wall enzymes ("mechanical cell separation"). The most prominent feature of penicillin, the disintegration of bacterial cells via bacteriolysis, is shown to represent only a postmortem process resulting from shrinkage of dead cells and perturbation of the cytoplasmic membrane. Several schematic drawings have been included in this review to facilitate an understanding of the complex morphogenetic events.

Bacteriolysis↗
PubMed1976

[Human monocyte function in normal subjects and in certain states of immunologic deficiency].

The functions of peripheral blood monocytes (phagocytosis, bacteriolysis, the metabolism, and catabolism of a protein antigen) have been studied in 12 normal subjects and in 23 patients suffering from either primary or secondary immune deficiency. Phagocytosis and bacteriolysis were altered in 1/3-2/3 of patients with either Hodgkin's disease, sarcoidosis or pulmonary tuberculosis, whereas catabolism of the protein antigen were found to be abnormal in practically all cases of agammaglobulinemia. These results show that monocytes may have intrinsic functional abnormalities in some conditions.

Agammaglobulinemia↗
PubMed1992

Failure to trigger the autolytic enzymes in minicells of Escherichia coli.

Minicells from Escherichia coli P678-54 are refractory towards procedures known to induce bacteriolysis of DNA-containing E. coli cells. Although still engaged in murein synthesis, minicells could not be lysed by penicillin G. Likewise, endogenous overproduction of the cloned soluble lytic transglycosylase, the predominant murein hydrolytic activity in E. coli, failed to lyse minicells. Furthermore, induction of the phage MS2 lysis protein, a hydrophobic protein assumed to trigger the autolytic system of the host, did not result in bacteriolysis. It is concluded that the murein hydrolases present in minicells are under a tight cellular control.

Autolysis↗
PubMed2000

Permeability barrier of the gram-negative bacterial outer membrane with special reference to nisin.

The effect of nisin pretreatment on organic acid-induced permeability increase in strains of Escherichia coli, Pseudomonas aeruginosa, P. marginalis, and Salmonella enterica sv. Typhimurium was investigated, using assays based on the uptake of a fluorescent dye 1-N-phenylnaphthylamine (NPN) and on the bacterial susceptibility to detergent-induced bacteriolysis. The outer membrane of bacteria which had been pretreated with nisin was shown to be less stable against 1 mM EDTA, as indicated by their significantly higher NPN uptake levels as compared to untreated bacteria. Upon challenge with a tenfold lower concentration of EDTA (0.1 mM) some nisin-treated strains (Typhimurium, P. marginalis) exhibited, however, NPN uptake levels which were lower than those seen in control bacteria, suggesting that nisin had stabilized their outer membrane. Nisin pretreatment also decreased the NPN uptake induced by citric or lactic acid or both in E. coli, P. marginalis, and Typhimurium, whereas in P. aeruginosa the pretreatment resulted in increased NPN uptake in response to citric and lactic acid. These results suggest that, with the exception of P. aeruginosa, nisin could protect bacteria from the outer membrane-disrupting effect caused by the acids. P. aeruginosa was, however, shown to be protected against bacteriolysis induced by the detergents sodium dodecylsulfate and Triton X-100. With a pair of isogenic mutants of Typhimurium differing in their cell surface charge it was shown that the NPN uptake response to I mM EDTA of the abnormally cationic strain was not significantly affected by nisin, whereas in the normal anionic strain nisin strongly strengthened the uptake. Our hypothesis based on these findings is that the normally anionic cell surface of Gram-negative bacteria has a tendency to bind the cationic nisin. The binding of nisin to the surface does not proceed to the cytoplasmic membrane, but in the outer membrane the bound nisin actually stabilizes its structure through electrostatic interactions. With the exception of EDTA, the organic acids at pH 4 did not cause leakage of cell contents from Typhimurium, indicating that these acids do not permeabilize the outer membrane to an extent required for cytoplasmic pore formation by nisin.

Anti-Bacterial Agents↗
PubMed1997

Local and systemic complement activity in small intestinal bacterial overgrowth.

It is unknown whether bacteriolysis due to luminal complement activation contributes to local defense mechanisms against small intestinal bacterial overgrowth, particularly with gram-negative bacteria. This study addressed this issue. Thirty adult subjects were investigated with culture of luminal secretions adherent to proximal small intestinal mucosa. Luminal and plasma concentrations of C3 and C3d and C3d/C3 ratios were determined. Activated terminal complement complex was sought in surface epithelium to which aspirated secretions had been adherent. Small intestinal bacterial overgrowth with gram-negative bacteria was present in 12/30 (40.0%) subjects. C3, C3d, and C3d/C3 profile indicated that increased local but not systemic C3 activation occurs in this group. Conversely, no activation of terminal complement complex was evident in this circumstance. Thus, complement-mediated bacteriolysis is unlike to contribute to local defense mechanisms against small intestinal bacterial overgrowth, even when overgrowth flora includes gram-negative bacteria. Factors preventing full local activation of the complement cascade in this circumstance require investigation.

Adult↗
PubMed1995

Complement-mediated bactericidal activity of human antibodies to poly alpha 2-->8 N-acetylneuraminic acid, the capsular polysaccharide of Neisseria meningitidis serogroup B.

Serum antibodies to Neisseria meningitidis group B (MenB) polysaccharide are reported not to elicit bacteriolysis in the presence of human complement. To reexamine this question, we evaluated the ability of two human IgM anti-MenB polysaccharide monoclonal antibodies (MAbs) and seven human MenB polysaccharide-reactive human IgM paraproteins to elicit bacteriolysis. In the presence of human complement, both MAbs and five of the seven paraproteins were bactericidal at antibody concentrations of 0.25-9.6 micrograms/mL (50% killing). Activity of the respective antibodies was enhanced 200- to > 10,000-fold when rabbit complement was used instead of human complement. With rabbit complement, the bactericidal activity of human IgM polyclonal antibody or MAb to Haemophilus influenzae type b (Hib) polysaccharide but not human IgG polyclonal antibody or MAb to Hib polysaccharide was similarly augmented. Thus, for both MenB and Hib, IgM antipolysaccharide antibodies elicit complement-mediated bactericidal activity in the presence of human complement, and the use of rabbit complement yields spuriously high activity.

Animals↗
PubMed1994

The effect of Triton X-100 on the in-vitro susceptibility of methicillin-resistant Staphylococcus aureus to oxacillin.

The effect of the non-ionic detergent, Triton X-100, on the in-vitro activity of oxacillin against methicillin-resistant (MRSA) and methicillin-susceptible (MSSA) strains of Staphylococcus aureus was investigated. In the presence of Triton X-100, the MICs of oxacillin for both MRSA and MSSA isolates were reduced; this enhancing effect was particularly marked for the MRSA strains. Triton X-100 therefore counteracted the resistance to methicillin encoded by mecA. In the presence of oxacillin at subinhibitory concentrations, Triton X-100 induced the bacteriolysis of MRSA and potentiated the autolysis of these organisms. However, the detergent had no effect on the bacteriolytic enzyme profile or the susceptibility of the bacterial cell wall to bacteriolytic enzymes, nor did it promote the binding of oxacillin to the penicillin-binding protein (PBP) 2A. On the other hand, it stimulated the release from the bacteria of acylated lipoteichoic acid (LTA), a putative endogenous regulator of autolysins. Autolytic enzyme-deficient MRSA mutants were equally as sensitive as the parent strain to the effect of Triton X-100 on susceptibility to oxacillin. These results indicate that the enhanced in-vitro activity of oxacillin against MRSA in the presence of Triton X-100 cannot be accounted for simply by the induction of bacteriolysis following activation of autolytic enzymes by the detergent-stimulated release of LTA.

Autolysis↗
PubMed1994

Evidence for lipopolysaccharide as the predominant proinflammatory mediator in supernatants of antibiotic-treated bacteria.

Lipopolysaccharide (LPS), purified from gram-negative bacteria, is well known to induce proinflammatory responses in monocytes and macrophages, and release of LPS from the microbial surface has been suggested to be an important initiating event in the sepsis syndrome. However, numerous studies have documented that a variety of constituents present in the outer cell membrane of gram-negative bacteria have the capacity to activate cells of the immune system. Given that the majority of immunotherapeutic approaches designed to intervene in gram-negative sepsis have to date targeted the LPS molecule, it would be of value to assess the relative proinflammatory properties of LPS and other gram-negative structures. Experiments were therefore undertaken to assess stimulation of human monocytes by components released from Escherichia coli following bacteriolysis by the cell wall-active antibiotic ceftazidime. As assessed by both induction of procoagulant activity and release of tumor necrosis factor, bacterial culture supernatants contain significant proinflammatory activity. When culture supernatants are fractionated via either velocity sedimentation in sucrose gradients or isopycnic density gradient ultracentrifugation in cesium chloride, the predominant monocyte-stimulating activity is identified in LPS-containing fractions. Further, such activity can be readily abrogated by the addition of polymyxin B. These results provide support for the hypothesis that LPS may be responsible for the majority of the proinflammatory activity released from E. coli following bacteriolysis in vitro.

Antigens, Bacterial↗
PubMed1997

Bactericidal antibody responses of juvenile rhesus monkeys immunized with group B Neisseria meningitidis capsular polysaccharide-protein conjugate vaccines.

Reports on the bactericidal activities of antibodies to group B Neisseria meningitidis capsular polysaccharide (B PS) are conflicting. Using three different complement sources, we analyzed the bactericidal activities of sera of juvenile rhesus monkeys immunized with five conjugate vaccines of B PS synthesized by different schemes, an Escherichia coli K92 conjugate, and a noncovalent complex of B PS with group B meningococcal outer membrane vesicles (B+OMV) (S. J. N. Devi, W. D. Zollinger, P. J. Snoy, J. Y. Tai, P. Costantini, F. Norelli, R. Rappuoli, and C. E. Frasch, Infect. Immun. 65:1045-1052, 1997). With rabbit complement, nearly all preimmune sera showed relatively high bactericidal titers, and all vaccines, except the K92 conjugate, induced a fourfold or greater increase in bactericidal titers in most of the monkeys vaccinated. In contrast, with human complement, most prevaccination sera showed no bactericidal activity and in most of the vaccine groups, little or no increase in bactericidal titer was observed. However, the covalent conjugation of P BS and OMV (B-OMV) administered with and without the Ribi adjuvant induced relatively high bactericidal titers which persisted up to 30 weeks. An analysis of the specificities of bactericidal antibodies revealed that absorption with E. coli K1 cells did not change the bactericidal titer with human complement but reduced the titers observed with the rabbit and monkey complements. A significant increase in anti-lipopolysaccharide (LPS) antibodies was elicited by the B-OMV conjugates, and nearly all of the bactericidal activity with human complement could be inhibited with the purified group B meningococcal L3,7,8 LPS. B-OMV covalently coupled via adipic acid dihydrazide elicited significantly elevated levels (P < or = 0.02) of anti-OMV antibodies compared to those of the noncovalently complexed B+OMV. An initial small-scale evaluation of B PS conjugates in adult human males appears feasible, with careful monitoring, to settle the inconsistent reports of the importance of source of complement in eliciting bacteriolysis. Subsequent analysis of resultant human antibodies for bacteriolysis, opsonophagocytosis, and protective efficacy in animal models may be the first step toward answering safety- and efficacy-related concerns about B PS conjugate vaccines.

Animals↗
PubMed1985

Bactericidal activity and induction of cell volume alterations of cephalosporins in Escherichia coli.

The bactericidal efficacy of cefuroxime and cephacetril on Escherichia coli cultures was measured by killing curves. Simultaneously bacterial cell volumes were analysed by electronic particle counting using a Coulter Counter Channelanalyser system in order to study the relationship between bactericidal activity and bacterial cell volume alterations. Various concentrations (2-120 mg/l cefuroxime and 16-120 mg/l cephacetril) and different exposure times (over a time period of 12 h) were used. Growth medium was human plasma ultrafiltrate. The bactericidal activity of cefuroxime, as measured by the rate of killing of the E. coli culture, was independent of the concentration and constant in the range 4-120 mg/l. The characteristic cefuroxime-induced change in bacterial cell volume was a marked volume increase up to a maximum of 5-fold after 160-200 min exposure with a low-grade bacteriolysis following. The cefuroxime-induced bacterial volume changes were, in accordance with the bactericidal testing, almost independent of the concentration. In contrast, the killing curves for cephacetril strongly depended on the drug concentration. However, this effect was short-lived and regrowth of the E. coli culture followed. The typical cephacetril-induced volume distribution curves were also highly concentration-dependent. With increasing drug levels bacterial cell volume increased up to 20-fold, and regrowth of a persisting bacterial population occurred at lower antibiotic concentrations. Bacteriolysis started earlier than with cefuroxime. The relationship between loss of viability and cell volume increase was more marked with cefuroxime than with cephacetril.

Autoanalysis↗
PubMed2002

Complement regulator-acquiring surface proteins of Borrelia burgdorferi: a new protein family involved in complement resistance.

The innate immune system, particularly the host complement system, plays an important role in the elimination of invading pathogens. Borrelia burgdorferi, like other human pathogens, has developed strategies to prevent complement-mediated bacteriolysis. It is now well established that Borrelia differ in their complement resistance. In general terms, B. afzelii isolates are mainly resistant to complement-mediated bacteriolysis, whereas the majority of B. burgdorferi s.s. isolates display an intermediate complement-resistant phenotype. Most of the B. garinii isolates, in contrast, are efficiently killed by complement and, therefore, are classified as complement-sensitive. Complement resistance of B. afzelii and B. burgdorferi s.s. isolates correlates directly with the acquisition of the fluid-phase human complement regulators FHL-1/reconectin and factor H. To date, five distinct complement regulator-acquiring surface proteins (CRASPs) have been identified in B. afzelii and B. burgdorferi s.s. isolates. The individual CRASPs can be differentiated according to their size and their binding properties to FHL-1/reconectin and factor H. The domains that interact with CRASPs are localized at the C-terminal ends of these complement regulators. Thus, CRASPs represent a family of functional proteins involved in complement resistance of Borrelia. Furthermore, an alterable pattern of gene expression was observed for three CRASPs of B. afzelii: BaCRASP-1, BaCRASP-2, and BaCRASP-5 are up-regulated at 37 degrees C and down-regulated at 20 degrees C. The continued characterization of CRASPs at the molecular level is expected to identify new virulence factors and potential vaccine candidates.

Animals↗
PubMed1990

Inhibition of the bacteriolytic effect of beta-lactam-antibiotics on Staphylococcus aureus by the polyanionic drugs suramin and Evans Blue.

The anionic polyelectrolytes suramin and Evans Blue inhibited different autolytic systems involved in wall growth and wall turnover of growing staphylococci and in wall autolysis of resting bacteria. Moreover, both substances lowered the beta-lactam-induced pre-lytic release of cytoplasmic constituents from staphylococci, and inhibited the beta-lactam-induced bacteriolysis as well as the loss of viability. The protective effects of these sulfonated drugs against bacteriolysis were also monitored by electron microscopy. Some medical implications of our results are discussed.

Anti-Bacterial Agents↗
PubMed1994

A novel, "hidden" penicillin-induced death of staphylococci at high drug concentration, occurring earlier than murosome-mediated killing processes.

In log-phase cells of staphylococci, cultivated under high, "non-lytic" concentrations of penicillin G, there occurred a novel killing process hitherto hidden behind seemingly bacteriostatic effects. Two events are essential for the appearance of this "hidden death": (i) the failure of the dividing cell to deposit enough fibrillar cross-wall material to be welded together, and (ii) a premature ripping up of incomplete cross walls along their splitting system. "Hidden death" started as early as 10-15 min after drug addition, already during the first division cycle. It was the consequence of a loss of cytoplasmic constituents which erupted through peripheral slit-like openings in the incomplete cross walls. The loss resulted either in more or less empty cells or in cell shrinkage. These destructions could be prevented by raising the external osmotic pressure. In contrast, the conventional "non-hidden death" occurred only much later and exclusively during the second division cycle and mainly in those dividing cells, whose nascent cross walls of the first division plane had been welded together. These welding processes at nascent cross walls, resulting in tough connecting bridges between presumptive individual cells, were considered as a morphogenetic tool which protects the cells, so that they can resist the otherwise fatal penicillin-induced damages for at least an additional generation time ("morphogenetic resistance system"). Such welded cells, in the virtual absence of underlying cross-wall material, lost cytoplasm and were killed via ejection through pore-like wall openings or via explosions in the second division plane and after liberation of their murosomes, as it was the case in the presence of low, "lytic" concentrations of penicillin. Bacteriolysis did not cause any of the hitherto known penicillin-induced killing processes.

Bacteriolysis↗
PubMed1982

Effect of leukocyte hydrolases on bacteria XVI. Activation by leukocyte factors and cationic substances of autolytic enzymes in Staphylococcus aureus: modulation by anionic polyelectrolytes in relation to survival of bacteria in inflammatory exudates.

The mechanisms involved in the activation of autolytic enzymes in Staphylococcus aureus, by leukocyte extracts, cationic proteins, phospholipase A2, amines, and membrane-damaging agents was studied in a resting cell system as well as by growing staphylococci. The bacteria were labeled with [14C]N-acetylglucosamine and were subjected to a variety of agents either in 0.1 M acetate buffer, pH 5.0, or in phosphate buffer, pH 7.4. While intact log-phase cultures were found to undergo partial autolysis at pH 5.0 and almost complete lysis at pH 7.4, both heat-killed bacteria and bacterial cell walls were completely resistant to autolysis in buffers. Autolysis at pH 5.0 can be further activated by leukocyte extracts, nuclear histone, crystalline ribonuclease, egg-white and human lysozyme, phospholipase A2, as well as by spermine, spermidine, and polymyxins B and E. The addition of viable log-phase bacteria to radiolabeled heat-killed staphylococci or to radiolabeled cell walls which had been cleaned off autolytic enzymes resulted in degradation of the radiolabeled targets. The data suggest that the various inducers of autolysin activation caused leakage of autolytic enzymes from the intact bacteria which attacked the depolymerized the bacterial cell walls. Anionic polyelectrolytes like heparin, dextran sulfate, suramine, polyglutamic acid, and liquid (polyanethole sulfonic acid) markedly inhibited both spontaneous and induced lysis. Staphylococci which had grown in the presence of anionic polyelectrolytes became highly resistant to lysis triggered by any of the inducers of autolysis. Since inflammatory exudates are known to be rich in anionic polyelectrolytes, it is suggested that the prolonged survival of intact bacterial cells in such a milieu may be due to the inactivation of autolytic enzymes. It is also postulated that the degradation of certain bacterial species following phagocytosis or extracellular degradation may not be the result of the action of hydrolytic enzymes but rather the result of activation by leukocyte factors of autolytic enzymes which lead to bacteriolysis.

Bacteriolysis↗
PubMed1983

Effect of human leukocyte extracts and gingival exudate on periodontopathic bacteria.

The effect of leukocyte hydrolytic enzymes on periodontopathic bacteria was examined in vitro. A frozen and thawed extract of human peripheral blood leukocytes (LE) and human gingival crevicular exudate (GE) were shown to be able to cause the release of 50% of the radioactivity from a leukotoxic strain of Actinobacillus actinomycetemcomitans (Aa Y4), labeled by 14C. A nonleukotoxic strain (Aa 653) was shown to be more susceptible to both LE and GE, up to 68% of the total radioactivity was solubilized by LE at pH 7.4. Both bacterial strains were found to be resistant to the activity of lysozyme, but highly susceptible to lysolecithin and mixtures of lysolecithin and lysozyme or LE. Capnocytophaga sputigena strain 4 was also found to be partially susceptible to the effect of LE and GE. The possible role of leukocyte hydrolytic enzymes in bacteriolysis and release of bacterial products in relation to periodontal disease is discussed.

Actinobacillus↗