| First Author | Markart P | Year | 2004 |
| Journal | Biochem J | Volume | 380 |
| Issue | Pt 2 | Pages | 385-92 |
| PubMed ID | 14977423 | Mgi Jnum | J:90269 |
| Mgi Id | MGI:3042773 | Doi | 10.1042/BJ20031810 |
| Citation | Markart P, et al. (2004) Comparison of the microbicidal and muramidase activities of mouse lysozyme M and P. Biochem J 380(Pt 2):385-92 |
| abstractText | Lysozyme is one of the most abundant antimicrobial proteins in the airspaces of the lung. Mice express two lysozyme genes, lysozyme M and P, but only the M enzyme is detected in abundance in lung tissues. Disruption of the lysozyme M locus significantly increased bacterial burden and mortality following intratracheal infection with a Gram-negative bacterium. Unexpectedly, significant lysozyme enzyme activity (muramidase activity) was detected in the airspaces of uninfected lysozyme M-/- mice, amounting to 25% of the activity in wild-type mice. Muramidase activity in lysozyme M-/- mice was associated with increased lysozyme P mRNA and protein in lung tissue and bronchoalveolar lavage fluid respectively. The muramidase activity of recombinant lysozyme P was less than that of recombinant M lysozyme. Recombinant P lysozyme was also less effective in killing selected Gram-negative bacteria, requiring higher concentrations than lysozyme M to achieve the same level of killing. The lower antimicrobial activity of P lysozyme, coupled with incomplete compensation by P lysozyme in lysozyme M-/- mice, probably accounts for the increased susceptibility of null mice to infection. Recombinant lysozyme M and P were equally effective in killing selected Gram-positive organisms. This outcome suggests that disruption of both M and P loci would significantly increase susceptibility to airway infections, particularly those associated with colonization by Gram-positive organisms. |
