It is generally recognized that hog gastric mucin is capable of markedlv increasing the apparent virulence of many bacteria. Recently, it has been realized that this is due in large part to the decreased resistance of the host rather than to some virulence-enhancing property of the mucin itself. Although the viscosity of mucin evidentlv has a physically protective role toward the bacteria, other factors acting on the host are of at least equal, if not greater, importance. The work of Smith and his associates (Smith, 1950a, b, 1951; Smith et al., 1951; 1952a, b; 1953; Smith and Gallop, 1953) has identified some of these fractions as heparin, chondroitin sulfuric acid and blood group A mucoid. Although Lambert and Richley (1952) have shown that mucin is anticomplementary in vitro and have identified the anticomplementary fac-tor as heparin, the importance of complement to in vivo resistance is still relatively unknown. Their studies, as well as those of Engley (1954) and Engley and Scott (1954) have again demonstrated an inhibitory action by mucin on the nonspecific bactericidins of serum. Following the discovery of the properdin system (Pillemer et al., 1954) numerous reports have appeared which relate this normal serum bactericidin to properdin and it has been shown that mucin is indeed active against the properdin system both in the test tube and in the host (Pillemer et al., 1954, 1955; Pillemer and Ross, 1955; Kiser et al., 1956). The importance of this activity in the over-all infecti-on promoting action of mucin is unknown, however. It is well recognized that hog gastric mucin vxaries with the commercial source and even from lot to lot from a single source in its resistance lowering activity (Nungester et al., 1936; Smith, 1950a, b; Engley, 1954). In this report it is sought to relate in vitro and in vivo antiproperdin activity to the in vivo antiresistance activity of hog gastric mucin. The phenomenon of increasing host riesistance to gram-negative bacteria following preinfection treatment with mucin has also been investigated with respect to its possible relation-ship to the properdin svstem.
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Charles W. Dewitt (1958) studied this question.
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